The immunopathogenesis of sepsis

Abstract

Sepsis is a condition that results from a harmful or damaging host response to infection. Many of the components of the innate immune response that are normally concerned with host defences against infection can, under some circumstances, cause cell and tissue damage and hence multiple organ failure, the clinical hallmark of sepsis. Because of the high mortality of sepsis in the face of standard treatment, many efforts have been made to improve understanding of the dysregulation of the host response in sepsis. As a result, much has been learnt of the basic principles governing bacterial-host interactions, and new opportunities for therapeutic intervention have been revealed.

Morphometric analysis of proinflammatory cytokines in mammary glands of sows suggests an association between clinical mastitis and local production of IL-1beta, IL-6 and TNF-alpha

“…The earliest and most potent proinflammatory cytokine released by the host in response to infection, has an essential role in the development of infectious disease [15,16,39,40]. Here we show that proinflammatory cytokines can be constitutively produced in mammary glands of healthy sows at parturition.…”

“…the production of these proinflammatory cytokines in inoculated mammary glands did not differ between the two groups. Possible explanation for this discrepancy between systemic and local proinflammatory cytokine levels might be that proinflammatory cytokines could also be produced elsewhere but the site of bacterial inoculation [1,8,12,15]. Alternatively, there might be a larger diffusion of cytokines into the blood in the sows with clinical signs of mastitis attributable to the inflammatory damage of mammary glands.…”

Genomic variations within DEFB1 are associated with the susceptibility to and the fatal outcome of severe sepsis in Chinese Han population

“…1,2 Studies confirmed that single nucleotide polymorphisms (SNPs) in some particular genes, such as tumor necrosis factor locus, interleukin-1 receptor antagonist, plasminogen activator inhibitor-1 and so on, play a critical role in sepsis. 3,4 Defensins are cysteine-rich cationic antimicrobial polypeptides with three disulfide bridges and are expressed in plants, insects and mammals.…”

The immunomodulator ginsan induces resistance to experimental sepsis by inhibiting Toll‐like receptor‐mediated inflammatory signals

“…In Gram-positive bacteria, peptidoglycan and lipoteichoic acid in the cell wall are possible sepsis-inducing molecules [4]. Staphylococcus aureus, a Gram-positive bacterium, often causes toxic shock syndrome by producing toxic shock syndrome toxin-1 (TSST-1) [5] or by inducing proinflammatory cytokines, such as TNF-a, IL-1b, and IL-6 in infected animals. Therefore, S. aureus is considered an appropriate Gram-positive bacterium for the study of sepsis [6].…”