New Publication: Neutrophil-mediated innate immune resistance to bacterial pneumonia is dependent on Tet2 function

https://bsky.app/profile/msmacrophage.bsky.social/post/3kubwknbcts2e
Click here for the full thread from Bluesky highlighting the major findings of the paper.
To see the full paper click here:
To see the commentary click here:

Bluesky thread:

Let me tell you about the #BowdishLab & friend’s most recent paper “Neutrophil-mediated innate immune resistance to bacterial pneumonia is dependent on Tet2 function”, led by Dr. C. Quin (now at @uniofaberdeen.bsky.social) @jclinical-invest.bsky.social https://www.jci.org/articles/view/171002
Tet2 is gene that is involved with methylating genes and therefore changing gene expression. Sometimes spontaneous mutations of Tet2 in hematopoetic stem cells (HSC) occur. These mutants tend to produce more myeloid cells (monocytes/neutrophils).
These myeloid producing HSCs tend to be more fit in the aging bone marrow (Darwinian survival of the fittest) and overtime, more and more of your myeloid cells are made from these Tet2 mutant clones.
In extreme cases this can lead to myelodysplastic disorders or cancer, but sub-clinical CHIP or clonal hematopoeisis of indeterminant potential occurs in many older adults.
People with CHIP (i.e., too many of their myeloid cells are made from Tet2 mutant progenitors) are prone to all sorts of conditions (e.g., heart disease) and pneumonia. We hypothesized that pneumonia risk might be due to changes in innate immune/myeloid cell function.
Mice defective in Tet2 did very poorly during Streptococcus pneumoniae infection (the most common cause of community acquired pneumonia in older adults), because their neutrophils were less able to kill bacteria.
We are excited about this @jclinical-invest.bsky.social publication because it is the first mechanistic explanation for the increased risk of pneumonia in CHIP. Generally CHIP is thought to affect macrophage function, but it clearly affects neutrophil gene expression & function as well.
Many thanks to Dr. Elsa Bou Ghahem for her most excellent Commentary https://www.jci.org/articles/view/181064 and for the great editorial & reviewer experience @jclinical-invest.bsky.social
Research Team:Candice Quin, Erica N. DeJong, Elina K. Cook, Yi Zhen Luo, Caitlyn Vlasschaert, Sanathan Sadh, Amy J.M. McNaughton, Marco M. Buttigieg, Jessica A. Breznik, Allison E. Kennedy, Kevin Zhao, Jeffrey Mewburn, Kimberly J. Dunham-Snary, Charles C.T. Hindmarch, Alexander G. Bick, Stephen L. Archer, Michael J. Rauh, Dawn M.E. Bowdish

Dr. Bowdish discusses the lab’s research on microbiota and healthy/unhealthy aging on the Agora Health Podcast

Or listen on

Apple podcasts https://podcasts.apple.com/co/podcast/how-the-microbiome-can-affect-your-overall-health-and/id1712499485?i=1000642050180&l=en-GB

Spotify: https://open.spotify.com/episode/0flH90zGfa5bXAVoy1ZiiF?si=f3680075df4b4a2a

Amazon Music: https://music.amazon.com/podcasts/2e2f7513-9491-40e9-a9dc-a31859560d1d/episodes/fce86aa3-0d05-4245-ab87-08be6b86323b/decoding-healthcare-research-how-the-microbiome-can-affect-your-overall-health-and-its-effects-on-aging-ep-15

The Bowdish lab is no longer taking thesis or project students for the 2024/25 academic year, but click here for an opportunity for students interested in aging research.

Unfortunately the Bowdish lab is at capacity for undergraduate students for next year; however, if you are looking to meet supervisors doing research in aging MIRA (McMaster Institute for Research on Aging) is partnering with McMaster’s Association for Undergraduate Research on Aging (AURA) to host Meet Your Supervisor – an in-person, networking and informational session aimed at connecting undergraduate students seeking research experience with MIRA Researchers. MIRA will also share information about the MIRA Undergraduate Summer Research Fellowships.

RSVP to attend.

Event details:

WHEN: Monday January 22nd ,  4 – 5:30 PM

WHERE: Farncombe Atrium, HSC 3N4

Please RSVP by January 15, 2022

Publication: Age-associated Inflammation alters the aging trajectory.

This article is written for lay/broad audiences and describes what age-associated inflammation is and why it may be key to healthy/unhealthy aging.