Sepsis: avoiding its deadly toll

Abstract

Systemic bacterial infection may culminate in a frequently fatal septic shock syndrome. The underlying pathology is the result of an uncontrolled inflammatory response, stimulated by the pathogen and its products. Toll-like receptors (TLRs) are critically involved in sensing bacteria and, in the case of sepsis, stimulate a pathogenic response by the innate immune system. A new study reports a successful attempt to inhibit systemic inflammation in mice by disrupting the formation of complexes between Gram-positive bacteria and their cognate receptor, TLR2.

Figure 1

Potential targets of treatments of septic shock. Interaction of bacteria with receptors recognizing PAMPs like the TLRs stimulates cells of the innate immune system to produce proinflammatory molecules, which, together with components of the activated complement and coagulation systems, promote the development of septic shock syndrome. Some prominent examples of molecules involved in the inflammatory cascade are shown in parentheses.