Publication: Minimal Impact of Prior Common Cold Coronavirus Exposure on Immune Responses to Severe Acute Respiratory Syndrome Coronavirus 2 Vaccination or Infection Risk in Older Adults in Congregate Care

Link to publication here.

Link to Bluesky “Skeetorial” here and reproduced below without images:

New paper! “Minimal Impact of Prior Common Cold Coronavirus Exposure on Immune Responses to Severe Acute Respiratory Syndrome Coronavirus 2 Vaccination or Infection Risk in Older Adults in Congregate Care”. For those of you who follow our #COVID work, read on for the story behind the story. 1/n

Remember reports like this one from the beginning of the pandemic? How could some older adults show such resilience to COVID compared to their peers? Some thought that they might have cross reactive immunity due to exposure to the related ‘seasonal’ or ‘common cold’ coronaviruses. 2/n
https://www.cbc.ca/news/canada/ottawa/102-year-old-woman-recovers-from-covid-19-1.5567189

After all, our @mcmasteru.bsky.social colleagues, Dr. Mark Loeb & team had shown years earlier that seasonal/common cold coronaviruses caused a lots of infections in long-term care and others had investigated whether these might protect kids from COVID…. 3/n
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0108481

….while others have shown that can be very deadly in residents of long-term care (reminding us that words matter and calling them ‘common colds’ minimizes risk – common viruses can still make people very sick, but that is rant for another day). So could pre-existing immunity be protective? 4/n
https://www.thelancet.com/journals/lanhl/article/PIIS2666-7568(23)00018-1/fulltext

Alternatively, maybe older adults got so sick because a life of exposure to these viruses ‘used up’ all the immune cells that could be used to respond to SARS-CoV-2 or COVID vaccines(i.e. ‘immune imprinting’, a phrase I came to hate along with ‘original antigenic sin’ as it was so misused) 5/n

To find out we tested whether antibody levels for the coronaviruses OC43, HL63, and 229E were higher/lower in people whose first COVID infection was an early Omicron variant and found they were not. Therefore it is unlikely these are either protective or problematic 6/n

What about pre-existing anti-coronavirus T cells? We looked at memory CD4+ and CD8+ T cells against the M & N proteins (indicates prev infections) and Spike (vaccine and infections). No evidence that these differed between those who did/did not get an infection (7/n)

What was a correlate of protection? Anti-RBD-IgG & neutralizing antibodies to the ancestral virus (which is all the residents would have been vaccinated to at that point). Unlike others we didn’t find that (serum) IgA was a correlate of protection. 8/n

Pre-existing immunity to common cold coronaviruses didn’t protect against SARS-CoV-2/COVID but might our vaccines and immunity alter immune responses to seasonal coronaviruses? Antibodies to other coronaviruses increased a bit (‘back-boosting’) after COVID infection or vaccination…. 9/n

But I doubt this will have much effect on the prevalence of other coronaviruses who follow a pretty consistent yearly/biennial or big wave/small wave pattern in the Northern hemisphere. We don’t know why but we do know that immunity doesn’t last long so a small boost from COVID infection/vaccination is not likely to make a difference 10/n
https://www.nature.com/articles/s41591-020-1083-1

Caveats: Only measured peoples first infections in the early Omicron era, only older adults living in LTC and retirement homes, vaccines would have been against the ancestral virus – things might be different in other populations/variants/vaccines. 11/n

Huge shout out to Braeden Cowborough for doing all those titres – that’s a lot of plates – and to Dr Jessica Breznik (former @miramcmaster.bsky.social currently @mcmasternexus.bsky.social PDF) for analytic skills. Thanks to the rest of the COVID-in-LTC team @mcmasteriidr.bsky.social

Post-doctoral position in Human Immunology Available

About the project

              The Bowdish lab has received funding from the Canadian Institute for Health Research (CIHR) to study immune responses to SARS-CoV-2 infections and vaccinations in older adults including those living in long-term care. The applicant will use over 10,000 biobanked saliva, PBMCs, and serum from over 500 participants in addition to participant metadata and detailed infection records to;

  1. Uncover novel correlates of protection in older and frail adults, including, but not limited to, ACP, ADCC, and cellular immune responses.
  2. To understand why immune responses are not always protective in older adults and may contribute to subsequent infections.

The successful applicant will have significant leeway to develop an independent research project based on their interests and expertise.  The applicant will work closely with an experienced technician and a graduate student, external collaborators, and will have access to biostatistics expertise.  If interested, there will be opportunities to teach undergraduate courses.

The initial contract will be for one year, with the possibility of extending for more years, depending on productivity. The position is funded, but the applicant will also apply for internal and external funding sources.

About the Bowdish Lab

              The Bowdish Lab is situated at Canada’s most research-intensive university, McMaster University in Hamilton, Ontario Canada. We are a diverse group of undergraduate students, graduate students, technicians and post-doctoral fellows committed to uncovering how the aging immune system changes and understanding why this alters immune responses to vaccination and respiratory infection. For more details on our lab’s philosophy see http://www.bowdish.ca/lab/lab-philosophy/ . We emphasize teamwork, career development, and leadership. Many of our former PDFs have gone on to independent faculty positions in Canada and abroad.

   
Must have;Passion for discovery & evidence of leadership in the form of first-author publications in a relevant field.Team-player with history of collaboration and mentorshipFlow cytometry experienceDeep knowledge of immunity   Nice to have;Experience in human immunology/vaccinologyExperience in antibody quantitation and functional antibody assays (e.g., ADCC, ADP)Experience in intracellular cytokine staining or Experience in science communication with vulnerable populations.

Application process

Please send Dr. Bowdish (bowdish@mcmaster.ca);

  1. A cover letter explaining your interest, skills and career goals and potential start-dates.
  2. A sample of your writing (e.g., first author publication, thesis, other)
  3. C.V.
  4. Names and email addresses of 2 references

Click here for .doc of posting

The Bowdish lab is no longer accepting thesis student applications for the 2025/26 academic year.

Thank you for your interest in our lab. Unfortunately we have received over 200 applications for 2 thesis positions and so we have no stopped accepting applications. Interviews will occur in January and if you have not heard from us, you have not been selected for an interview. This is not a reflection on the quality of your application or your credentials but simply the sheer volume of applications. Dr. Bowdish will not be able to respond to your emails directly. Very best of luck with your search.

Publication: Canadian Immunity Task Force (CITF) Hema-Net Serosurveillance Meeting

Serosurveillance describes using blood samples to determine what percentage of the population has been exposed to a pathogen or has been vaccinated by measuring the presence or absence of antibodies to the pathogen or vaccination. During the COVID-19 pandemic Dr. Bowdish and team built a network of long-term care homes to measure vaccine responses and infection rates, but this infrastructure could have been used to measure virtually any infection or any antibody response. The Hema-Net community came together February 14-16 to present data and share experiences using serosurveillance and published this report. Unfortunately, no funds were made available to continue Dr. Bowdish’s or others serosurveillance networks.

See the CITF website here.

See the English report here.

See the French Report here.

“The Perils of Being Born in the Fall” will be at the Zoetic Theatre November, 12, 2024

Missed the first run of ‘The Perils of Being Born in the Fall’ at the 2024 Hamilton Fringe Festival? Fear not, there is a repeat performance as part of the McMaster Institute for Research on Aging’s “Sage Conversations” series (and there’s free popcorn, drinks & parking – what’s not to love!)

What’s the show about? Well if you are born in September, Dr. Dawn Bowdish has got bad news for you.
Tour through the wackiness of early 19th century psychiatry, stealth mid-century reproductive rights activism and the climate/pregnancy connection; in the end you’ll learn why cold & flu season has an outsize impact on mental health.
You might laugh, but you’ll definitely learn.
Reserve a spot by clicking here
https://www.eventbrite.ca/e/sage-conversations-see-a-one-woman-show-featuring-dawn-bowdish-tickets-1016877456847

Also see other events in this series….

https://www.eventbrite.ca/e/sage-conversations-see-a-one-woman-show-featuring-dawn-bowdish-tickets-1016877456847

Dr. Bowdish speaks at the 2024 Innovation Nation Conference & Student Innovation Showcase

Dr. Bowdish presented “Ageism, infections & vaccinations: Lessons learned from the pandemic” at the 2024 Innovation Nation Conference & Student Innovation Showcase.

Publication: Reassuring humoral and cellular immune responses to SARS-CoV-2 vaccination in participants with systemic sclerosis

Benoit JM, Breznik JA, Huynh A, Cowbrough B, Baker B, Heessels L, Lodhi S, Yan E, Bhakta H, Clare R, Nazy I, Bramson JL, Larché MJ, Bowdish DM. Reassuring humoral and cellular immune responses to SARS-CoV-2 vaccination in participants with systemic sclerosis. Immunol Lett. 2024 Sep 19;270:106929. doi: 10.1016/j.imlet.2024.106929. 

Below is a Bluesky thread that summarizes and explains our manuscript. Click here to read it on Bluesky.

New publication alert! “Reassuring humoral and cellular immune responses to SARS-CoV-2 vaccination in participants with systemic sclerosis” Read on to learn why we did this study and why it is important. 1/n https://www.sciencedirect.com/science/article/pii/S0165247824001032?via%3Dihub

https://bsky.app/profile/msmacrophage.bsky.social/post/3l5zdipjxwe2o

Systemic Sclerosis(SSc) is a rare autoimmune disorder that causes fibrosis of the organs. Because it is caused an immune system gone awry, patients and their doctors were concerned that their immune systems might not respond to the vaccine and leave them less protected 2/n

Because SSC is an autoimmune condition, people generally take immunosuppressive drugs, which can also lead to lower vaccine responses and higher risk of infection. We investigated whether antibody or T cell responses to vaccination were affected in SSC. 3/n

Good news! People with SSC made the same amount of antibodies to the receptor binding domain of the Spike protein (i.e, the bit of the virus that the virus uses to get into us) after their second, third, and fourth SARS-CoV-2 vaccinations. 4/n

More good news! T cell responses to vaccines are thought to help with severe disease and may offer some cross-variant protection. Following the second, third, and fourth SARS-CoV-2 vaccinations, participants with SSc had T cell responses = those without SSC. 5/n

For the immunology geeks: People living with SSc have elevated levels of serum cytokines associated with T cell differentiation. Could this change Th1/2/17/reg mix posts vaccination? Nope. 6/n

Caveat#1: This is a small study (because a rare disease) and we couldn’t investigate all the different drugs that people are on. For more info on how drugs affect vaccination responses see our other studies 7/n https://acrjournals.onlinelibrary.wiley.com/doi/full/10.1002/acr2.11697

Caveat #2: This is very much a comparison of the quantity of immune responses, not the quality. There could still be qualitative differences in immune responses that we didn’t catch but… 8/n

…even though there is very little data on whether SSC is associated with higher infection risk or poorer outcomes what little exists doesn’t find a massive difference compared to the general population 9/n https://acrjournals.onlinelibrary.wiley.com/doi/full/10.1002/acr.25226

Take home message #1: Participants with SSc mount similar responses to SARS-CoV-2 vaccination as controls who do not have autoimmune conditions. 10/n

Take home message #2: Many ppl with autoimmune conditions are afraid that vaccination is unsafe for them because they know their immune system is a bit wonky. It is not the disease that affects immune responses, rather it’s some, not all, drugs at some, not all, doses. 11/n

Thanks to emerging leader & 1st author Jenna Benoit (graduating & looking for a job next year – hint), rheumatologist extraordinaire, Dr. Maggie Larche, cellular immunologist Dr. J. Breznik & J Bramson, team Antibody (Nazy, Huynh) & with special thanks to…..12/n

….our participants. People with SSC often have skin changes which makes blood draws especially hard. Thank you for your commitment to our study and huge props to our exceptional phlebotomist/RC Braeden Cowbrough – our unsung hero. 13/n Fin.

Publication: “Monocyte-driven inflamm-aging reduces intestinal barrier function in females”

Click here to access: Monocyte-driven inflamm-aging reduces intestinal barrier function in females published in Immunity and Ageing, September 2024.

This publication by former PDF, Dr Candice Quin and team, discovers that inflammatory markers and gut permeability increase with age, but the leaky gut seems to be a female specific phenomena in both mice and humans.

Bluesky explainer thread below and here https://bsky.app/profile/msmacrophage.bsky.social/post/3l5ethyexgp2u

New publication alert! “Monocyte-driven inflamm-aging reduces
intestinal barrier function in females” by lead author Dr Candice Quin @uniofaberdeen.bsky.social. Read on for some surprising insights into sex differences in aging, the microbiome, inflammation, and the ‘leaky gut’ hypothesis….1/n

With age levels of inflammatory mediators (cytokines, CRP, & others) increase in the blood and tissues. This is often called ‘inflamm-aging’, and higher than age-average levels of these mediators are associated with chronic disease, frailty, and other age-associated ills. 2/n

Men & women age differently (‘men die quicker, women live sicker’)so it stands to reason they might ‘inflam-age’ differently, but very few studies on aging investigate sex differences in the aging trajectory. We looked at cellular & soluble inflammatory markers and saw sex differences! 3/n

We were surprised by the magnitude of sex differences but immunology is literally one of the worst disciplines when it comes to reporting by sex https://elifesciences.org/articles/70817
By why do we ‘inflamm-age’ in the first place? Might the mechanisms of inflamm-aging differ by sex 4/n

One of the major theories is that with age a dysbiotic microbiota causes the gut to become leaky (alternatively, the gut gets leaky with age and this alters the microbiota). Bacterial products leak out and cause inflammation. We’ve published in mice, others in other model organisms 5/n https://www.cell.com/cell-host-microbe/fulltext/S1931-3128(17)30112-9?elsca1=etoc&elsca2=email&elsca3=1931-3128_20170412_21_4_&elsca4=Cell%20Press

Evidence for the ‘leaky gut’ hypothesis is weak in healthy humans (despite what the probiotic industry might say). Leakiness is generally found in people who have comorbidities, or are frail so we looked at healthy/non-frail male (41) females (54) btw 20-102 yrs and were surprised to find…6/n

…that women appeared to have leakier guts over the life course (as measured by the serum marker zonulin- imperfect), and only women had evidence of an age-associated increase in the bacterial product LPS in their serum. Could the leaky gut hypothesis be female specific? 7/n

Human studies are observational so we turned to mice to understand the chain of causality. Old female, but not male, mice did indeed have leakier guts and this seemed to be caused by TNF produced by the elevated number of circulating inflammatory monocytes. 8/n

Tl;dr The age-related leaky gut -> increased circulating bacterial products -> systemic inflammation hypothesis may only be true in females! (also – always investigate sex in your research) 9/n

Why? Well the female gut changes dramatically during pregnancy to increase nutrient absorption – perhaps that is why women seem to have more permeability over the life-course. We are doing some cool ongoing studies in vitro looking at male vs female monocytes ability to break the gut barrier. 10/n

Caveats: This was a non-frail, mostly white population – aging & immunology studies show tremendous differences by location so needs to be reproduced. Gut permeability measures were done by looking at serum markers – easy on the participant but indirect at best. 11/n

Thanks to the whole (unfortunately not on Bluesky team)! This was an incredibly fun and challenging project to work on but has cemented my commitment to considering sex in all the research we do. 👩‍🔬🧪🦠🚨 12/12