Abstract
Sepsis is one of the most challenging health problems worldwide. In the USA alone, around three-quarters of a million cases occur every year, and the fatality rate remains between 30% and 50% [1]. A recent report indicates that between 1999 and 2005, sepsis contributed to 6% of all deaths in the United States [2]. Treating sepsis remains problematic, as no effective anti-sepsis drug is currently available.
Highlights
This is generated by massive activation of an inflammatory cascade mediated by various pro-inflammatory mediators of the innate immune system that contribute to fulminant sepsis and death
In line with this hypothesis, it’s feasible to assume that a host intracellular component predominantly regulates the early proinflammatory response and that this intracellular component would be a potential target for therapeutic intervention
Recent results from our laboratory demonstrate that Myeloid Differentiation primary response protein 88 (MyD88)-mediated pro-inflammatory signaling is activated after staphylococcal enterotoxin (SEB) binding to MHC class II [10] and that MyD88-/- mice are resistant to SEB intoxication [11,12]
Summary
Innate Immunity and Sepsis: MyD88 as a Target for Therapeutics Host responses to bacterial infections are mediated by the innate immune system, which recognizes pathogens or pathogen-associated molecular patterns (PAMPs). Excessive production of inflammatory mediators or other pathogen-derived factors cause dys-regulation of the innate immune responses.
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