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Category: Clinical Microbiology
Biomarkers of Gastrointestinal Host Responses to Microbial Infections, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555819071/9781555819088.ch46-1.gif /docserver/preview/fulltext/10.1128/9781555819071/9781555819088.ch46-2.gifAbstract:
The gastrointestinal (GI) environment is a complex ecosystem, where the host lives in complete homeostasis with its microbiota, with the two generally maintaining a delicate balance (1, 2). An immune tolerance exists between the host and its microflora and is acquired soon after birth, preventing harmful inflammation in the setting of a normal microbiota (3–5). When an infection disturbs this stability, the host response is targeted towards rebuilding the equilibrium as quickly as possible. The initial barrier between this internal environment and the outside is the intestinal epithelial cell, which not only plays a role as a physical barrier and nutrient provider, but also protects its local milieu by initiating the immune response sequence (6, 7). The microbiota is also thought to play an important role in the immune response and regulation; this has been referred to as “host-commensal mutualism” (2, 3, 8, 9). The innate response, depending on the infection, may lead to activation of pro- or anti-inflammatory signaling pathways, producing cytokines and chemokines that protect the host from this invasion. However, in some instances, this response may become deleterious to the host and exacerbate the damage.
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Antibacterial inflammatory responses against S. Typhimurium infection. Inflammatory cytokine production was triggered upon detection of S. Typhimurium by mononuclear cells, epithelial cells, and complements which leads to production of antibacterial responses by macrophage activation, neutrophil recruitment, and epithelial release of antimicrobials. (Adapted from reference 140 .)
Antibacterial inflammatory responses against S. Typhimurium infection. Inflammatory cytokine production was triggered upon detection of S. Typhimurium by mononuclear cells, epithelial cells, and complements which leads to production of antibacterial responses by macrophage activation, neutrophil recruitment, and epithelial release of antimicrobials. (Adapted from reference 140 .)
Innate immune responses during C. parvum infection. Parasite infection to intestinal epithelial cells (IEC) leads to production of various antiparasite molecules which help to maintain epithelial integrity. Infected IECs increased production of inflammatory cytokines such as IL-15, IL-18, and INF-α/β which help in establishing immune effector mechanisms, such as IFN-γ production by NK cells and macrophages and cytotoxic NK cell activity. Dendritic cells produce cytokines (e.g., type I IFN and IL-12) that activate NK cells and IL-4 from an unknown cell may promote dendritic cell maturation. (Adapted from reference 254 .)
Innate immune responses during C. parvum infection. Parasite infection to intestinal epithelial cells (IEC) leads to production of various antiparasite molecules which help to maintain epithelial integrity. Infected IECs increased production of inflammatory cytokines such as IL-15, IL-18, and INF-α/β which help in establishing immune effector mechanisms, such as IFN-γ production by NK cells and macrophages and cytotoxic NK cell activity. Dendritic cells produce cytokines (e.g., type I IFN and IL-12) that activate NK cells and IL-4 from an unknown cell may promote dendritic cell maturation. (Adapted from reference 254 .)