Morphology of Rectal Mucosa of Patients with Shigellosis

Polymorphonuclear leukocyte transmigration promotes invasion of colonic epithelial monolayer by Shigella flexneri.

“…In the case of Salmonella and Yersinia, M cells seem to be the privileged site ofentry (32). These cells also appear important in the development of shigellosis, since shigellae have been shown in M cells ofrabbit Peyer's patches ( 1 1; and Perdomo, J., personal observations) during the first 8 h of infection and in human biopsies (33). In addition, when macaque monkeys are infected intragastrically with a S. flexneri icsA mutant that has lost the capacity to spread from cell to cell, they do not develop dysentery, but nevertheless have small colonic and rectal lesions that correspond to the solitary lymphoid nodules ( 12) that lie beneath M cells.…”

Apoptosis of human intestinal epithelial cells after bacterial invasion.

“…We further suggest a major role for apoptosis after bacterial infection may be to delete populations of epithelial cells from the intestinal mucosa to restore normal epithelial cell growth regulation. Thus, mucosal infection can result in increased crypt mitotic activity (48,49), crypt hyperplasia and branching, and increased epithelial cell proliferation with heaping up of epithelial cells (50,51). Consistent with altered epithelial cell growth, prostaglandin H synthase-2, which inhibits apoptosis in bacteria-infected intestinal epithelial cells (data not shown) as well as noninfected cells (52), is upregulated for more than 24 h after bacterial infection in both infected and uninfected neighboring epithelial cells (26).…”

Cell death in the host response to infection

“…39 A facultative intracellular pathogen, Shigella invades eukaryotic cells and evades the phagosome to enter the cytosol. 40 Shigella was the first invasive bacterial pathogen reported to induce programmed cell death in host macrophages.…”