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The human MAIT cell response to controlled ETEC challenge

ABSTRACT: Mucosa-associated invariant T (MAIT) cells recognize conserved microbial antigens presented by the non-polymorphic MR1 molecules and play important roles in barrier immunity. Enterotoxigenic E. coli (ETEC) is a major cause of diarrheal disease especially among children in lower-income countries. Here we investigate the potential role of MAIT cells in ETEC infection using samples from a human experimental ETEC challenge study. MAIT cells were activated with elevated function and proliferation in blood on day 7 after challenge, reflected both at protein and transcript levels, a pattern most evident among individuals who developed mild to severe diarrhea (MSD). The MSD-positive group had elevated expression of CCR9 and α4β7 on MAIT cells and experienced expansion of the peripheral MAIT cell pool at day 28 after challenge. Finally, the size of the MAIT cell pool correlated with MSD disease severity score. These findings indicate that MAIT cells respond to ETEC infection in a way associated with the development of symptomatic disease.

ORGANISM(S): Homo sapiens

PROVIDER: GSE276378 | GEO | 2025/05/20

REPOSITORIES: GEO

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Project description:Enterotoxigenic Escherichia coli (ETEC) strains that produce both heat-stable (ST) and heat-labile (LT) enterotoxins cause severe post-weaning diarrhea in piglets. However, the relative importance of the individual enterotoxins to the pathogenesis of ETEC infection is poorly understood. In this study, we investigated the effect on virulence of an F4+ ETEC strain when removing some or all of its enterotoxins. Several isogenic mutant strains were constructed that lack the expression of LT in combination with one or both types of ST enterotoxins (STa and/or STb). Host early immune responses induced by these mutant strains 4h after infection were compared to the wild type strain GIS26 Â (O149:F4ac+, Â LT+ Â STa+ Â STb+). At the same time, the immune response of this wild type ETEC strain was compared to the mock-infected control, demonstrating the expression of porcine inflammatory response genes. For these purposes, the small intestinal segment perfusion (SISP) technique and microarray analysis were used and results were validated by qRT-PCR. We also measured net fluid absorption of pig small intestinal mucosa 4h after infection with wild type ETEC, the mutant strains and PBS (mock-infected). These data indicate an important role for STb in inducing small intestinal secretion early after infection. The microarray analysis of the different mutant strains also revealed an important role for STb in ETEC-induced immune response by the significant differential regulation of immune mediators like matrix metalloproteinase 3, interleukin 1 and interleukin 17. We conclude that STb can play a prominent role in ETEC-induced secretion and early immune response. In three pigs, 6 different treatments were performed. These treatments consisted of 4 mutant enterotoxigenic Escherichia coli GIS26 strains, GIS26 wild type strain, or PBS control. Per pig, the small intestine was divided into 6 loops with an interloop in between to avoid cross-contamination. In conclusion, every pig received each of the 6 treatments ad random.

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The human MAIT cell response to controlled ETEC challenge

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