10/ Our work demonstrates how a single virulence factor—cholera toxin—remodels epithelial metabolism to generate L-lactate in the small intestine, highlighting how cAMP-modulating toxins may have co-evolved with pathogens to reshape host metabolic landscapes to promote pathogen growth during disease

9/ L-lactate is an emerging gut metabolite that supports the growth of enteric pathogens, including Salmonella (Gillis et al., 2018) and C. jejuni (Sinha, 2024) in the large intestine. Epithelial-derived lactate also fuels Enterobacteriaceae expansion in the cecum (Taylor et al., 2022)

8/ This work reveals how a bacterial toxin reprograms epithelial cell metabolism to generate a novel growth substrate in the small intestine. We show that V. cholerae leverages this host-derived metabolite to expand during CT-induced disease

7/ Where’s the L-lactate coming from? Using mice lacking LDHA specifically in intestinal epithelial cells, we show the epithelium is the main source. In these mice, V. cholerae's LldD-dependent fitness is significantly reduced—revealing that CT rewires epithelial metabolism to fuel pathogen growth

6/ Strains lacking CT did not show this advantage — but adding exogenous CT rescued the fitness defect, confirming that CT itself is responsible for generating the L-lactate–rich environment that V. cholerae exploits via LldD to grow during infection

5/ To test if V. cholerae exploits host-derived L-lactate, we turned to the suckling mouse model. Consistent with our hypothesis, CT-producing wild-type bacteria had a fitness advantage over the lldD mutant in the small intestine

4/ We show that V. cholerae’s previously uncharacterized L-lactate dehydrogenase (LldD) — upregulated in a CT-dependent manner during infection — functions to metabolize L-lactate during both in the presence of oxygen and nitrate

3/ We found that CT increases expression of host lactate dehydrogenase A (LDHA) in small intestinal epithelial cells. 🧪 LDHA converts pyruvate → L-lactate, pointing to epithelial-derived L-lactate as a key metabolite generated during cholera disease

2/ We previously found CT creates a unique gut niche—iron-starved but rich in long-chain fatty acids and L-lactate (PMID: 31367037, 2019). But how CT manipulates host metabolism to generate this niche was still a mystery.

All brought to you by the good people at OMICS International who own and operate“more than 500 peer-reviewed journals”

So do I

(A) just ignore this?
(B) do something?

If you chose the latter, what do you suggest I do?

Any replies with some guidance or cynical humor welcome

Nothing is better than your past trainees successes

Congrats!