Enterococcus faecalis-derived lactic acid suppresses macrophage activation to facilitate persistent and polymicrobial wound infections Macrophage activation is essential for innate immunity and antimicrobial defense. We show that Enterococcus faecalis suppresses macrophage activation …

Lactic acid lover? Check out @ronni.bsky.social 's new work in
@cp-cellhostmicrobe.bsky.social showing how Enterococcus faecalis-derived LA suppresses macrophage activation, in turn promoting bacterial persistence and polymicrobial wound infection in vivo.
www.sciencedirect.com/science/arti...

Fig. 1: Reversal of HFCS-induced metabolic dysfunctions by inulin supplementation.

A study in Nature Metabolism shows that the dietary fiber inulin modifies the gut #microbiome to better process fructose, helping prevent metabolic dysfunctions and emphasizing the role of dietary fiber. go.nature.com/4gKCvHe 🧪

The emerging view on the roles of butyrate in Clostridioides difficile pathogenesis | Infection and Immunity The Centers for Disease Control and Prevention classifies Clostridioides difficile as an urgent threat to the nation’s health, as it causes 450,000 infections, 15,000 deaths, and 1 billion dollars in excess healthcare costs per year in the United States (1, 2). Most C. difficile infections (CDIs) occur in healthcare settings, where CDI is the most common cause of infectious diarrhea (3). Known and suspected risk factors for CDI include antibiotics, proton pump inhibitors, impaired immune function, advanced age, and diet, all of which are associated with dysbiotic gastrointestinal (GI) microbiomes (4–6). Though most CDIs are associated with antibiotic treatment, 22% of individuals with community-acquired CDI have no recent history of antibiotic use. Factors affecting persistent and recurrent CDIs remain poorly defined (7, 8). Despite the morbidity and mortality caused by C. difficile, up to 15% of healthy adults are asymptomatic carriers of toxigenic C. difficile (9), highlighting the gaps in our understanding of C. difficile.

Thrilled to share @alex-dobrila.bsky.social’s new review in Infection & Immunity on how butyrate shapes C. difficile pathogenesis. A must-read for those interested in microbiome–pathogen interactions. 👉 journals.asm.org/doi/10.1128/...

🎉Congratulations to @maribyndloss.bsky.social @jenniferdoudna.bsky.social and Kim Orth—three HHMI scientists recently honored by The American Society for Microbiology @asm.org
asm.org/press-releas...

The short summary and behind-the-scenes of our paper in this Research Briefing article out today: www.nature.com/articles/d41...

Commensal yeast promotes Salmonella Typhimurium virulence - Nature Commensal Candida albicans enhances the virulence and dissemination of Salmonella enterica subsp. enterica serovar Typhimurium.

Nature research paper: Commensal yeast promotes Salmonella Typhimurium virulence

go.nature.com/4mTnRzG

That’s such a great news! Congratulations Rebecca!

How thoughtful experimental design can empower biologists in the omics era - Nature Communications Here, the authors discuss principles of experimental design that are relevant for all biology research, along with special considerations for projects using -omics approaches, highlighting common expe...

I am really excited to see this article on basic experimental design principles published. Definitely will be mandatory reading for incoming graduate students in my lab. Maggie Wagner who led this article did an amazing job with the illustrations of basic principles www.nature.com/articles/s41...

Commensal Yeast Boosts Salmonella Typhimurium Virulence In an unexpected twist to our understanding of host-pathogen interactions, recent research reveals that a common fungal commensal, Candida albicans, significantly shapes the virulence of the intestinal pathogen Salmonella Typhimurium. This surprising interplay sheds light on the nuanced metabolic crosstalk occurring within the gut environment, altering both microbial behavior and the host immune response in ways that challenge traditional paradigms.

Commensal Yeast Boosts Salmonella Typhimurium Virulence

In an unexpected twist to our understanding of host-pathogen interactions, recent research reveals that a common fungal commensal, Candida albicans, significantly shapes the virulence of the intestinal pathogen Salmonella Typhimurium. This…

Thank you, Rebecca!

Thank you!

This project was a true whole-lab effort. It was driven by @kanchanj.bsky.social (now on the job market for Assistant Professor positions) with substantial contributions by second author @oliviatodd.bsky.social. So proud of the whole lab!

My postdoc work is now online at Nature. Grateful to @judith-behnsen.bsky.social for her support and all the collaborators. #TeamBehnsenLab

Cholera toxin-induced disease generates epithelial cell-derived L-lactate that promotes Vibrio cholerae growth in the small intestine Cholera toxin (CT) promotes Vibrio cholerae colonization by altering gut metabolism to favor pathogen growth. We have previously found that CT-induced disease leads to increased concentrations of L-la...

1/ Excited to share the first preprint from my lab! 🎉

My postdoc Paz asked how cholera toxin (CT) helps Vibrio cholerae thrive in the gut.

Turns out, CT rewires epithelial metabolism toward L-lactate production—fueling pathogen growth in the small intestine during disease

Thank you Judith!

A Salmonella T3SS-2 mutant grows fine in spleen macrophages, contradicting tissue culture dogma (PMID: 23236281). This observation was largely ignored, but adding certain carbon sources rescues growth in cultured macrophages, hinting that T3SS-2 may be doing something entirely different in vivo.

Thank you Francis! It was a long wait 😀

Thank you Mason!

Thank you Stephen!

Thank you Lauren!

Thrilled to share that I’ve been awarded the NIH K99/R00 Pathway to Independence Award! Grateful to my mentor @judith-behnsen.bsky.social for her support. Can’t wait for the road ahead!

Super excited to share our paper online 🚨today🚨 in Cell Host & Microbe‬! Xiaomei Ren @xiaomeiren.bsky.social and Mason Clark @rmasonclark.bsky.social‬ co-led discovery of ecological factors for Acinetobacter baumannii carriage in the gut, a reservoir for pathogen spread. 🎉

tinyurl.com/443kfefk

NIH doesn’t just support infectious disease research—it drives breakthroughs in cancer, childhood diseases, heart disease, diabetes & more.

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💉 Cancer immunotherapy
❤️ Cholesterol-lowering statins
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Investing in NIH = investing in life-saving discoveries.