Skip to main content

Advertisement

Springer Nature is making SARS-CoV-2 and COVID-19 research free. View research | View latest news | Sign up for updates

Fig. 2 | Gut Pathogens

Fig. 2

From: Animal models to study acute and chronic intestinal inflammation in mammals

Fig. 2

Small intestine mucosal immunity. Intestinal epithelial cells (IEC) make up the epithelial lining. The IEC are covered by mucus which serves as an important component of the innate immune system. In the large intestine mucus is divided into two distinct layers that vary in thickness ; the thicker outer layer being bacteria-rich and the thinner inner layer containing no or few bacteria  (not shown in image). The epithelium is composed of enterocytes and M cells, and these cells are held together by tight junction proteins. Of note, these cells and structures are also areas where bacteria can enter the host to induce inflammation and activate underlying immune cells. Cells important in immuno-surveillance, such as dendritic cells within the lamina propria can move through M cells or tight junctions in the IECs to sample luminal contents [28]. This information is presented to T-cell populations through the secretion of cytokines to facilitate cell maturation and proliferation [294]. Th1 (IFN-γ, IL-6, TNF-α) cytokines and Th17 (IL-17A, IL-22) cytokines activate pro-inflammatory responses, Treg (IL-10, TGF-β) cytokines are anti-inflammatory and Th2 (IL-4, IL-5, IL-13) cytokines have both anti-inflammatory and pro-inflammatory potential. Immunoglobulin A (IgA) is released from plasma cells at intestinal crypts while antimicrobial peptides (AMP) and defensins are released from Paneth cells (not shown) [28]. M cell microfold cell, TLR toll-like receptor, Th helper T-cell. Transcription factors; Foxp3 (Treg), T bet (Th1), Rorγt (Th17), Gata3 (Th2)

Back to article page