Page 702 - Veterinary Immunology, 10th Edition

throughout the small intestine and colon. Bovine defensins are
VetBooks.ir secreted as active molecules, as opposed to the human and mouse

molecules that are secreted as inactive precursors and subsequently
activated by trypsin within the intestine. Parasitic or other intestinal

infections may increase production of α- and β-defensins.
Enterocytes possess a complete set of PRRs and can sense signals
coming from the microbiota. They can then pass on these signals to
the immune cells in the lamina propria and are actively involved in

shaping the intestinal immune environment. They help maintain
balance between antiinflammatory and proinflammatory signals.
They also block access of intact antigens to the lamina propria.
Tight junctions between enterocytes help maintain this barrier.

(Molecules larger than about 2 kDa are excluded.) Thus they keep
the intestinal microbes away from the intestinal immune system.
Enterocytes secrete or respond to regulatory cytokines. Thus they
produce thymic stromal lymphopoietin (TSLP) that is required for

the generation of Tregs. They also produce TGF-β and the B cell
stimulating molecules, BAFF and APRIL (see Box 15.2). The
enterocytes form a major barrier against microbial invasion. If an
enterocyte becomes infected, it can respond by releasing

antimicrobial peptides and increasing mucin and cytokine
production. It can also respond by undergoing inflammasome-
mediated cell death. This mechanism is used by enterocytes to
block invasion of Salmonella enterica serovar Typhimurium.

Inflammasomes are protein activation complexes, some of which
can trigger a form of cell death called pyroptosis. When S.
Typhimurium invades enterocytes, the number of intracellular
bacterial colonies increases for the first 12 hours and then begins to

decline at 18 hours. This decline is correlated with the extrusion of
infected enterocytes into the lumen. At the same time,
inflammasome activation also results in cytokine secretion that in
turn activates Th17 cells and promotes local inflammation.

The gastrointestinal mucus layer is also critical to the exclusion of
both commensals and pathogens. The layer consists of a gel made
of mucins, glycoproteins, and lipids that prevents bacteria from
contacting the epithelium. This mucus acts as a lubricant, blocks
chemical insults, and can capture and then expel pathogens. The

mucus forms an inner and outer layer. The inner layer next to the

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