Epigenetic Regulation of Immunity

welcome to the everything epigenetics podcast where we discuss DNA regulation and the insights it can tell you about

your health I’m Hannah w and I’m the founder of everything EP gentics today my guest

is Dr Andrew dinardo he is an infectious disease specialist investigating

Immunology of co-infection tuberculosis epigenetic regulation of

immunity of course what I am personally most interested and we will be chatting about today HIV and Global Health uh

just to name a few of of his Specialties we are really going to dive into what we can learn about immunity through the

lens of epigenetics uh he has a lot of great papers that we’re going to dive into and really understand how we can uh

apply these and and and push these to application in real world case scenarios a quick introduction to my

guest Andrew attended Wayne State school of medicine from 2003 to

2007 his internship and residency in global health and Internal Medicine was completed at the hospital of the

University of Pennsylvania in philadel Philadelphia from 2007 to

2010 he practiced Primary Care in an underserved community in southwest Philadelphia from 2010 to 2012 and

completed an infectious disease fellowship at Baylor College of Medicine

Andrew has been studying tuberculosis immunology and epigenetics for the past

decade and he completed and became an assistant professor at Baylor College of Medicine in 2015 and he also has his PhD

in the epigenetic regulation of host immunity I am telling you he is the

expert on immunity and and all things epigenetics I hope you enjoy and now for

my guest Dr Andrew dinardo welcome to the everything epigenetics podcast Dr

dinardo I appreciate you being here today it’s my pleasure to be here with

you yeah so i’ I’d love to hear a little bit more about your background and uh

you know how you you ended up where you are today and and you know we’ll talk about things that you’re studying currently and and kind of the next

question but can you just talk about yeah your journey I’d love to love to learn a little bit more about your

background uh my journey sure um I did uh an internal medicine residency and I

knew I was interested in global health and tuberculosis um and I was falling in

love with the Immunology of tuberculosis and and interestingly um there has been a lot of

work on Helman and tuberculosis co-infection showing that helments increase the risk

for tuberculosis and outside of the United States is a large population that’s

uh affected by both helmets and tuberculosis um and I’m

also married to an oncologist and I remember one night um going to bed and

my wife was showing me what she was working on and it was uh idh Inhibitors and um these idh mutations

that they found in leukemia and gasto uh that lead to epigenetic changes

and then lead um either to Cleo blastoma or or leukemia uh and she was walking me

through this and and I had just read a paper by Indie Malhotra from uh from

Kenya a really interesting paper they they uh were looking at the BCG induced

vaccine response in children that never had schistosomiasis but when they were

in utero their moms had schistosomiasis and the kids born to moms who had chisos has had a 26-fold

lower BCG induced interfer on gamma response compared to the kids who were

born to moms that didn’t have chisos smasis and I just put these two things together my my wife’s work that she was

explaining to me on epigenetic changes in leukemia uh and I said hey I I really

want to study this I want to see if helmets result in epigenetic changes um

that are predisposing people to having an increased risk of tuberculosis and and eventually that um led me to my

first major studies uh I finished my infectious disease Fellowship this is what I worked on during my infectious

disease Fellowship um and it’s been what I’ve been working on now for about the

past 10 years yeah yeah no thanks for for that that background that’s that’s super fascinating especially you said

you know the story of of you and your wife kind of you were looking at some of the work that she’s doing I think that’s always interesting um seeing you kind of

you know both both take a a lead in in the field so yeah you’re you’re an infectious disease specialist

investigating Immunology of of co-infection tuberculosis epigenetic regulation of immunity HIV and Global

Health just to to name a few that I I pulled off of your website there um can you talk a little bit more just about

the the current work you’re doing and and what you’re studying we’ll get into some of the the specifics and in the

papers that you published here soon but um yeah you know what are you most excited on or or looking at and studying

currently um well we’re looking forwards and backwards a little bit is one one way to explain it so in terms of looking

forwards we’re looking um at children and Adolescence H we did a school-based

deworming program so um in eswatini uh we went to different schools uh and

every other year they’re supposed to get dewormed based off of international and

National guidelines and and uh what we did is we added to this a randomized

control trial of revaccinated them so the standard TB vaccine is given at

Birth um and it works great and not so great so the standard TB vaccine uh BCG

uh prevents disseminated tuberculosis in kids but loses its effect uh and doesn’t

really protect against pulmonary tuberculosis in adults so the question

we wanted to ask here was um do these kids who have schistosomiasis and we

already know that kids with schistosomiasis um lose their BCG vaccine immunity they also lose

hepatitis vaccine immunity almost any vaccine that’s been studied um when you

when you have you know so these asymptomatic Helman infections they’re asymptomatic but they’re

ruining uh vaccine efficacy so we just finished that study

um we’re just getting started now on the analysis and looking at the immune

response to see um were we able to revitalize the immune response in these

kids um and what was the epigenetic landscape of the kids um

who did develop an improved vac vaccine immune response versus those who didn’t

so I’m quite excited that’ll probably be at least a year of analysis and staring

at a computer to to to get to the bottom of that um so that’s that’s kind of

thinking about how we’re going forward um looking at looking at um how how one

infection leads to DNA hypermethylation changes and affecting the immune response uh in terms of looking

backwards um one of our other findings and now it doesn’t seem

that unexpected but at the time I think it was a little bit uh was that even after

after successful therapy for tuberculosis the epigenetic landscape

doesn’t go back to normal and we’ve seen this you know if you look the most common Mouse model for this is uh

chronic lcmv infection so once you have a chronic lcmv uh infection in the mice

the the uh epigenetic landscape stays perturbed for a very long

time so our previous paper showed that the same thing happened with individuals

who are successfully treated for tuberculosis so now the big question is so what what’s the clinical impact um

well we know that individuals who have tuberculosis even after successful therapy and it’s same

thing for covid it’s the same thing for severe pneumonia it’s the same thing for for sepsis and and there’s a

long-standing history um I think Charles Von perette was one of the first people

that identified this in 1907 seven um that kids with uh measles never

recovered their TB immune response and were increased risk of TB um well

individuals with tuberculosis their inflammatory State doesn’t go back to normal so they’re increased risk of

cardiovascular disease their increased risk of cancer they have recurrent infections um so the other big thing

we’re working on right now is following people after so-called therapy uh to

look at which are the DNA methylation changes

associated with a bad cardiovascular event afterwards um and hopefully that can

help shed some light on the path of physiology uh and hopefully from there we can uh find some ways to mitigate

that risk yeah definitely I I’ll be excited to follow along that that that study and

I liked how you mentioned it you know kind of in in the future and and you know uh the the history of everything

you’ve done so far we’ll be able to compound and learn more and more on this I think you’re absolutely right the next

question and one of the questions I always get J day from from Mostly these healthcare providers that I’m working with is hey what’s the clinical use

right how can I make this clinically applicable so we’re we’re getting there um like you said you know you’re gonna

have to do some data analysis for the first study you mentioned sitting in front of a computer for a year or so um

we’re kind of just uh with my work getting getting done with with a two-year study and again most of that

was sitting in front of a computer making sure things are um you know working correctly I should say in in in

processing um so so that’s great to hear hear about some of your work Dr jardo and I I appreciate those explanations um

you know we we’ve been kind of chatting uh about your your main focus being that epigenetic regulation of of immunity

which uh of course is is why we’re having this conversation today and what I’m most interested in so you’re you’re

doing all this great work uh what if we push the boundaries a little bit you know what else can we really learn about

immunity through the lens of epigenetics um I know you talked about some some things currently in the clinical impact

but is there anything else you you would want to add there W I think when I think when this

field opened up 10 to 20 years ago it was a brand new field I think

now I don’t think anyone’s going to argue that the entire immune responses

is regulated through epigenetics it’s one of the many ways that host immunity

is regulated but it’s a it’s a pretty significant one and it seems like every day especially

now with the Advent of single cell technology you know we’re we’re

identifying a new subset of immune cells um and a subset of a subset of a subset

of immune cells for some of them for I mean uh one of the subsets that we’re studying is okay well cd8 cells are a

subset of of t T cells but but then you have exhausted cd8 T cells oh well hold

on a second now there’s um progenitor exhausted cdat cells um and the

progenitor CDA the progenitor exhausted uh cd8 T cell has an epigenetic

landscape that’s different from an exhausted um cd8 T Cell so you know we

are technology is allowing us to Define these different immune um subsets at

much higher resolution and clearly um our bioinformatic friends are helping us

a lot with that um I think combining that high resolution the

high resolution that we can do now in the lab

with well delineated clinical cohorts to uh Pro to understand the applicability

of what we’re looking at I think that’s the exciting thing um or one of the most exciting things moving forward for you

know for me it’s what’s the which is the immune cell and what’s the epigenetic

landscape of that specific immune cell that’s going to tell me this TB patient only needs two months of therapy and I

don’t have to worry about cardiovascular disease afterwards or this TB therapy this TB patient needs nine months of

therapy and they’re at really high risk of post TB lung cancer um so you know

and and I I can be a little jealous here I’ve seen the cancer

field and it’s developed into Precision medicine and they look at molecular

medicine and based on somebody’s idh status and their Flip

3 status you know they get different therapy we’re not there for infectious diseases yet um certainly not infectious

diseases uh of the global nature that tends to affect people in resource constrainted settings um but I think we

can get there yeah yeah well I I love the you know you you being super hopeful

I think we can get there too and you’re exactly right you know with the the epigenetics and the single cell and all

these different immune cell subset types that we’re getting into if you think epigenetics is an entirely New Field I

think you know the immune cells in epigenetics is going to be its own own field as well I mean there’s just so

many things to to unfold there um one question I I I have for you based based on that answer and a lot of your data

analyses of um looking at epigenetics and and these different diseases and outcomes are you separating out the

immune cell subsets in in a lot of those and looking at that or um you know can you maybe talk about some of that data

analysis I’m just I’m just curious as well uh the short answer is yes and no

and and not good enough um so sheesh it

feels so long ago but it wasn’t to me so the chismis paper that I had

mentioned earlier uh we had isolated CD4 so from peripheral blood mononuclear

cells so from the immune cells circulating in somebody’s blood we

isolated CD4 T cells and then we implemented DNA methylation analysis

using an alumin based um sequencing method called the DNA methal opic array but then also

using msre qpc R um where you digest the DNA uh with enzymes that can only digest

under certain uh DNA methylation conditions and and running PCR so we we

validate it in two different ways and I was super proud of the work that we did and I remember presenting it uh a few

months later and they said but you didn’t control for the different CD4 subsets I said yep we did um and so then

the next paper was on tuberculosis and in this case we actually

used an insilico approach where we took all of the pbmc’s and ran the DNA methyl epic array

and then used a bioinformatic and silico approach to identify cd8 CD4 cd14 and

cd56 uh DNA methylation status for each one of those cell types and then again

we were discussing it and that was still a pretty a major Advance at the time and

someone said ah but you didn’t account for the different subsets of each of those so so now we’re now we’re doing

single cell technology and with single cell technology I mean this is a bit of a curse because yeah you can hey I found

a subset of two cells what the heck is a subset of of only two cells so we have

to be careful at what resolution we now look at things and we’re in um a place

that that uh we’re going to get pushed off a cliff if we’re not careful with our bio informaticians

um and then and then this comes up well is all of the premature epigenetic aging

stuff that you do um is that really just seeing a a loss of um naive cells and a

a progression towards uh exhausted cells and and more developed cells a and that

um there are experts I hope there are some experts listening to this that will that will know how to answer it better

than me um but it’s something we’re going to have to work on and we’re gonna have to try and explain better in the future yeah I I think so as well yeah

you know there’s a lot of um thought and effort that goes into these pre-processing steps and kind of taking out those immune cell subsets and

stratifying and it seems like with your work you’re very well aware of that and you know you’re doing that but then

people are asking you to dig deeper and deeper and deeper so you’re you know picking away at this and um excited to

see what you you find out there and and you know hopefully we’ll we’ll get an answer on that as well um the the last

question you you kind of pondered on there um I want to take into to one of the specific papers that that you’ve

you’ve published um it’s titled the the post infectious epigenetic immune modifications a double-edged sword um

you know I really like the the title of this this uh paper and and I want to dive into that statement a little bit

better can you can you maybe describe what you did there what you wrote and and what you mean by the double-edged

sword sure um so the term the double-edged sword was was uh Dan musher

one of the co-authors suggested that and I guess the whole the whole manuscript

really started with him in 2017 at at at our local Journal Club I presented a

Cutting Edge paper from Mii natia group um Rob Arts was the first author and

they showed that innate training was not only epigenetically mediated but it was

mediated specifically by the kreb cycle and changes that happened in the kreb cycle were inducing changes in uh

epigenetic landscape that were leading to inate training I was so proud of

presenting a very complicated um manuscript to journal Club um and Dan

musher who is currently 82 years old um you know waved away my explanation and

said ah we’ve known this for 40 years I said Dr musher we didn’t know

about epigenetics 40 years ago what are you talking about and he walked me through um some old Studies by George

mckinness some other studies from the 1960s the 1970s that showed the phenomenon that we didn’t know um the

epigenetic mechanisms but we knew the phenomenon that non lymphocytes and

lymphocytes um had a different response to a second pathogen after an exposure

to a first pathogen or something similar so that manuscript then was a way to try

and explain and Link the historical context

um from that we’ve known for for at least a hundred years some of the

studies back to the 1890s early 1900s um link them to Modern epigenetic

mechanisms and you know so the first half of the manuscript was okay if you have a monoy that sees BCG or beta

glucan it then has a better immune response a couple months later if it sees a a different pathogen and a lot of

live attenuated vaccines have this effect uh and during covid a lot of

people were looking to see well until a covid specific vaccine comes out what can we do to uh improve aate immunity um

uh in order to fight fight covid well the second half of the manuscript was the dark side um if you have a severe

pneumonia if you have tuberculosis if you have severe sepsis if you have severe covid um there are longlasting

detrimental effects that that we’ve discussed um increased rate of cardiovascular disease after covid is

very high increase rate um the all cause mortality uh after you survive sepsis um

is more than twofold higher than propensity match controls um for tuberculosis after surviving

tuberculosis and after so-called successful therapy you have a 3.7-fold increased risk of death compared to um

uh age and propensity Mass controls um wow and there are there are detrimental

epigenetic changes that occur after each one of those severe infections um so the

double-edged sword is there are epigenetic changes that regulate a beneficial immune response after a mild

uh uh immune exposure such as after BCG or after immune cells are exposed to

Beta glucan and then the opposite uh occurs um after a severe

infection uh and the point of that article was to discuss how we might be able to

manipulate that in the future uh as part of improved care yeah that was my my

leading question okay so you have these you know parts that are pulling away from each other do they cancel each

other out do they compound you know how does that kind of look as as a result so I thought that was that was an interesting find um in in your work

there so yeah wanted wanted you to to elaborate on on that further um another

paper I saw of yours I was really excited about this one we again been been chatting about all all these things kind of throughout our our uh

conversation here you have a paper titled uh increased DNA methylation cellular inessence and premature

epigenetic aging in in guinea pigs and humans with tuberculosis so uh yeah can you go ahead and and and

describe this one uh Dr dinardo this was a super fun one

so before the pandemic when we were still having fun in-person

meetings um I went to a tuberculosis conference and they were two of us that were presenting posters uh on on DNA

methylation and I was presenting my work uh that TB patients had DNA

hypermethylation and the the negative effect that had on the il12

interfer and Gamma pathway uh well across across the poster aisle from me was Karly boback from

Dartmouth who had done this beautiful work uh data mining publicly available

trans cryptomic data and her conclusion was TB is going to affect DNA

methylation and I was like yeah look it does um and we got the joke about that and we started talking

about how how we could understand this this better and um a brilliant post talk

in my group uh Abby Manu Dr ABI Manu uh worked with Carly to to data mine uh a

little bit more and there were some previous papers um

about oxidative stress um and cellular inessence and and we hypothesized that

they would that they would correlate with DNA hypermethylation and they did they very very strong

correlated um and so then we pulled in Jeff seral from Texas A&M to help us

with the guinea pig studies so we have a nice paper that shows an association and a correlation between those different

phenomena so that leads the question of well can can we manipulate one of those

so initially when we found the DNA hypermethylation in tuberculosis I said

okay well if you have DNA hypermethylation of these critical immune genes can we use hypomethylating

drugs to reverse the DNA hypermethylation and that seemed like an

obvious Next Step well the problem is most DNA hypermethylation DNA hypomethylating

drugs um they’re used for one thing and one thing only right now which is chemotherapy for people with um

myoblastic syndrome and Leukemia uh we don’t know how targeted they are we don’t know what they’re um they’re

really not studied in people who are’t extremely sick with with Cancers uh so

we were unclear about their safety profile um and they’re actually quite hard to work with in in vitro systems

and there were enough studies that had come out that showed uh as I mentioned previously that intracellular metabolism

is directly leading to epigenetic changes so we came up and we we put a

position paper out a few years ago at least three different metabolic epigenetic riats

that we identified and we started testing could we manipulate the metabol

intracellular metabolism uh so that’s what we’ve been studying in vitro and we’ve got very

exciting um findings there that we’re trying to make public but

ultimately it seems um if you try and

improve redo homeostasis um if you try and slow down

the TCA cycle from going into overdrive because when the immune system is activated the so-called warberg effect

occurs and the TCA cycle ramps up and what we can see from inv vitro studies

at least um is that that is driving a lot of uh the DNA hypermethylation

changes sure yeah very very interesting um and and pretty cool is how how uh

then you you said you met Carly from that that conference right and that’s how kind of the paper started was that correct yeah correct that’s pretty

neat there’s the advantage I complained about the pandemic the the advantage about the pandemic is we’re all very um

capable of interacting from from long distance so we met on zoom on a regular

basis and uh Carly’s really did some some some fantastic work for that and I

know she’s she’s still doing a lot of very nice TV work um and I hope to see her more on Zoom yeah that’s great I

always love how how papers start and hearing those stories and you know as you ask more questions things start to

unfold so you get some really interesting background that um no one really knows about so I thought that I I

wanted to to kind of ask that there um the advantage of going to in-person meetings and sitting at the coffee

station sitting at the cold drink station and just chat and talking turns

into really good science absolutely I not a doubt in my mind with with that um

so no that that’s a really interesting paper you have there and um I know when you know I had you fill out my little

podcast guest sheet I don’t know if you remember was a while back but you also kind of entered um a topic you you may

have wanted to go over so mtor right did did does that have anything to do with this study and um I actually haven’t

talked about mtor at all with anyone on the podcast so far so um if you could give our listeners like an introduction

to that I think that would be a really good place to start oh man there’s so many good introductions to mour that’s such a such

a responsibility um well what I would probably say is is um listen I think it

was the DA’s podcast on on mtor but mtor uh Mamon Target of rap ay and what’s so

much fun here is there’s so much history behind this target how it was Des

discovered the lab that discovered it and everything that happened um uh so

they discovered this they oh so um rapanui Island in one of the Easter

Islands and and um

it’s an immune I hate to say immune suppressive drug it’s an immune um

modulating drug maybe is a better terminology uh but it controls

intracellular metabolis ISM so as I mentioned earlier when immune cells are stimulated in order for the immune cells

to do their affector function and for them to proliferate they need a lot of

intracellular intermediate metabolites and the TCA cycle acts as a hub for

these critical metabolites that have to be produced to replicate your DNA and

and proliferate um to to do all the affector functions that immune cells need so mtor is one of the

critical proteins that regulates metabolism and yeah so it’s been studied

a lot in with the immune system and um I believe John War’s group has a nice

article from a few years ago showing that mtor Inhibitors can prevent uh t- cell immune exhaustion in

in an lcmv model there’s a lot of new studies on on using mtor inhibitors for

tuberculosis and that’s why I hate to call them immune suppressive drugs

because they seem to both decrease inflammation but improve immune

responsiveness so while they improve decrease basil inflammation they allow

the immune system to respond when activated again in the future uh and we’ve been

studying how they affect uh DNA methylation landscape in the

setting of IM um immune exhaustion and immune tolerance in vro models with the

hope that if we slowed down the TCA

cycle that that slowing down of the TCA cycle would lead to less DNA

hypermethylation in the setting of a severe chronic infection yeah that makes sense no thank

you I think you did a wonderful job um and and I can put some of the assets that you you know noted and uh link

those out in case anyone wants to to learn a little bit more but I think um you know mtor rap ayin rapamune these

are all buzzwords in the space right now people really want to know how how rap ayin is uh is affecting a lot of the

epigenetic biological age clocks and you know we I don’t think we exactly know yet there are still a lot of questions

about that there is the Pearl trial I believe it’s it’s called where where

they’re trying to you know use rap amyas in from Interventional standpoint um you

know for anti-aging purposes um and and see how it affects the clock so hopefully more to come with with that

trial soon but I I don’t think it’s I think it’s still ongoing um so so yeah Dr dinardo uh focusing more on on on

your work and and everything that that we’ve been discussing um what about the the applications uh can you tell me uh

you know is anything close to commercialization to more of that clinical use what else can we we know

about all the wonderful work that you’re doing o commercialization um in terms of a

signature no the the

cohorts in infectious diseases uh sometimes feel embarrassingly small um

so if you think of the are you familiar with the tcga um the cancer genome Atlas

nice punon word with using tcj but it’s thousands of cancer patients with

transcriptomics with epigenomics proteomics and clinical followup um yeah

I’m not I’m not familiar actually yeah so it has

revolutionized every single type of cancer so you name a cancer out there and the tcga is one of modern medicine’s

um greatest achievements it has there’s probably five New England

journals just on breast cancer so by making this giant repository of all of

this data so many papers now start off by saying hey we data mined this public

data we found this signal we tested it in this model and look we found a new drug and hey we tried this new drug on

patients and hey this new drug actually works on this subset of breast cancer or

this subset of leem um we don’t have anything like that for

infectious diseases show me an equivalency for bacterial pneumonia show me an equivalency for for sepsis for

tuberculosis for any of the major infections um there is no single

organizing repository um so if you ask me my wishes

um one because I could use it but I think you know anybody with a computer

and access would be able to make use of a similar Atlas for infectious diseases

um so if we know infectious diseases are one of the things that leads to increase morbidity and mortality outside of the

problem of infectious diseases because it increases cardiovascular disease because it induces premature aging

because it increases the risk for cancers um this this could be

um a major project to to improve there and help identify what are the

signatures that we need what are the gentic signatures that we need to be able to identify uh to prevent those things and

then to learn from them uh so that’s probably one of the things I’m I’m most excited about the other one uh as I

mentioned earlier is our findings that we might be able to manipul manipulate

metabolism to improve the immune response and improve epigenetics

um my colleagues have been teasing me recently because uh every single presentation I give and up with me

saying eat your vegetables um but we’ve been studying lycopene we’ve been studying

carotenoids um and uh different carotenoids really seem to be quite

impressive in their ability uh to prevent some of the epigenetic scars that we’re seeing in

inv vitro models so um if you asked me you know you can you can only do one

study one Interventional study over the next five years um it would be using

these really cool new devices that are cutaneous spectrometers that you know

you can just flash on the palm of your hand and it can tell you if you have enough carotenoids in your body I would

love to apply that to a post-infectious model and say hey you’re not eating

enough vegetables I can tell you right here based on the pigment I can detect on your hand

um and see if we can actually intervene right there wow yeah super interesting I

I don’t want to know I know I need to eat more vegies um but I think that’s a good application right for someone and

and you have to tell us now Dr darno if you had to pick one vegetable that we had to eat or or catenoid which one

would you say according I don’t know according to the data or what you think we should do o unfair unfair but I’m

going to have to go with my Japanese postto who has introduced all of

us I’m going to cheat I’m going to say seaweed because it’s not one vegetable

it’s hundreds of vegetables but our our our Japanese postto has introduced our

team to the um the benefits of of seaweed and uh um I know people some

people just don’t have the taste for that but whatever you like I mean um we joked we started with lycopene in the

lab um uh because I have Italian origin we we’ve looked at many different ones I

mean uh Alpha and beta carotenoids look look fantastic so um we get a lot of

carrots passed around um I don’t think there’s a single one but if you had to make me choose seaweed looks pretty

amazing interesting yeah no I I currently don’t have seaweed in in my diet whatsoever so I’m going to maybe

look up some recipes after this or see you know how you can can eat it and and try to incorporate that more um no

that’s great that’s great I’m I’m excited for for your work that’s coming out the the applications I think think I

I I’ve said this multiple times as you know researchers and and we we need to

be collaborative we need to create these kind of these these minds of of of data these these repertoire so people can

come and we can learn new new insights so I’m excited to uh see your work there and and hopefully put together some type

of database just like you said for for the cancer one um you led me perfectly into my next question for you um

basically just being you know um you also mentioned there’s there’s a lack of data in in in the Infectious induced

premature aging what we were just mentioning what about other limitations in this field is there anything if you said hey I if I had this one thing or if

if you know I could I could choose something then my work would be a lot easier any any other

limitations I think what we just discussed I think the Limited in infectious disease research there um we

just have a shortcoming of publicly available data compared to other fields

and um so so I think building that out um

would probably be my number one and I I’m really lucky to have uh Christian

karfa as a bioinformatic partner with all of this work um and

the I think hand inand with that goes that we need clinicians and clinical

investigators and wet lab um investigators that can work hand inand

with bioinformaticians um a uh AI American

Association of Immunology has a fellowship every year that they call the intersect Fellowship just to do this

because they recognize how critical it is that we bring those those two Fields

together uh and I think that’s one of the things that can exponentially imp uh help us um identify new findings uh what

has happened with big data um over the past decade and a half is truly

amazing yeah I couldn’t agree more again I always say this too but if I’m G to say it again if I could go back and

choose something because I I you know I just have a general science background I would definitely do bioinformatics computer science computer training like

I I have no coding experience but when I get a free second or you know I I have a

free weekend or something I’m going to spend time um messing with chat GPT or taking some of those free classes where

I mean you know you can learn from those tools now which make them um easy accessible and and free right for for

the most part so um you know hopefully I’ll increase my skill set with with those here soon 100% yeah yeah well um

you know we’re almost coming to the end of this this podcast here I I know you mentioned you were excited about kind of

the the device uh and scanning with with the um different you know kind of CR Nord levels and if you need to eat more

more vegetable by looking on the the pigment of the skin um what else are you excited about and anything anything

coming up next I know you have so many so many different you know studies and and things you’re looking at but any

anything else you want to add there those are the critical ones I’m I’m excited to see the field there’s a

lot of Metformin studies um in the Infectious Disease field there’s uh um

Harvey cornfeld is running a really nice metformin study on TB uh Bob Wallace has

a couple um that I’m really excited to see come out so I think this the the

intersection between metabolism and epigenetics um has a chance to to push

us forward and what’s really nice and maybe it even has a chance to push us

forward um with food rather than drugs so that’s those are the things I I’m

eager to see in the coming years yeah yeah I like that as well right um You

always hear like uh food is medicine right things like cliche saying like that so it definitely has truth behind

it um all right the last question I I usually ask um it’s a curveball has

nothing to do with your work but Dr dinardo if you could be any animal in the world what would you be and why

oh I have always wanted to fly so I think I would have to go

with Oh either a screech owl they’re so cute or a paragan falcon because they’re

so fast one of those I love it you knew it you knew the answer um and yeah I I

would be curious to learn to learn how to fly a little bit as well but I don’t think anyone has ever said an an owl so

that’s yeah that’s really unique I like it um here in we have really cute

screech owls they they look like um uh they they you know they’re only

like six six inches and they look like little teddy bears and so you go out at night and you can you can catch them

pretty well oh cool yeah I didn’t know that little little fun fact added there as well well um again appreciate all all

you’ve uh taught us here on on this this podcast today um we’re you know coming to the end uh for listeners who want to

connect with you or learn a little bit more you know I I’ll link everything but uh yeah are you active on you know Twitter or or where can people find and

learn more about your work I am not active on Twitter I’m so sorry um that’s

okay like maybe my boss is right when she tells me I should be um but I have

tried to um be active in my analysis and not so active in um in Twitter uh email

um reach out to me by email I’d love to chat um I I’d love to meet in person at

meetings and and discuss more it really has led to some great collaborations um

but throw throw my email in meeting notes perfect well do and I think that’s

totally okay you’re not on Twitter and more into your analysis and doing that work I think that’s what of course

people are most interested in so yeah thanks again uh everyone for listening to everything epigenetics podcast

remember you have control over your epigenetics so tune in next time to learn more thanks Dr dinardo absolutely

my pleasure thanks for having me