Humoral Mediators in Sepsis

Local infection may develop into a systemic inflammatory response syndrome that encompasses a complex mosaic of interconnected events, including the so-called compensatory antiinflammatory response syndrome. A 2002 hypothesis holds that a defective host innate response may render bacteria resistant to host recognition and defense mechanisms, leading to systemic infection and sepsis. In higher organisms, a variety of host defense mechanisms control the resident microflora and, in most cases, effectively prevent invasive microbial disease. Many microbial pathogens avoid host recognition or dampen the subsequent immune activation through sophisticated interactions with host responses, but some pathogens even benefit from the inflammatory reaction. The defective response of the host may depend on a unique genetic makeup of a pathogen that can render it more resistant to antibiotics or on disturbances in the integrated response of the innate arm and the adaptive arm of the immune system. Differences in reactivity of dendritic cells to microbial molecules through Toll-like receptors are associated with susceptibility and resistance to microbes.