An immunofluorescence microscopy image depicts the intestinal lumen of a mouse lacking claudin-2, a diarrhea-inducing tight junction protein. In these deficient mice, C. rodentium bacteria (red) infiltrate the intestines. DNA stained in blue; F-actin (denoting cells' external-facing surfaces) in green.
TURNER LABORATORY AT BRIGHAM AND WOMEN’S HOSPITAL
Scientists investigating the functional role of diarrhea found that bacterial pathogens stimulate the immune signaling protein IL-22, which increases claudin-2 expression and facilitates the outflow of water and subsequently, diarrhea. According to a news release, this “play[s] a critical role in pathogen clearance in the early stages of infection.”
See P.-Y. Tsai et al., “IL-22 upregulates epithelial claudin-2 to drive diarrhea and enteric pathogen clearance,” Cell Host & Microbe, doi:10.1016/j.chom.2017.05.
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