Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Herwald, H. et al.

Herwald, Cramer, Mörgelin, Russell, Sollenberg, Norrby-Teglund, Flodgaard, Lindbom, Björck,

M protein, a classical bacterial virulence determinant, forms complexes with fibrinogen that induce vascular leakage.

Increased vascular permeability is a key feature of inflammatory conditions. In severe infections, leakage of plasma from the vasculature induces a life-threatening hypotension. Streptococcus pyogenes, a major human bacterial pathogen, causes a toxic shock syndrome (STSS) characterized by excessive plasma leakage and multi-organ failure. Here we find that M protein, released from the streptococcal surface, forms complexes with fibrinogen, which by binding to beta2 integrins of neutrophils, activate these cells. As a result, neutrophils release heparin binding protein, an inflammatory mediator inducing vascular leakage. In mice, injection of M protein or subcutaneous infection with S. pyogenes causes severe pulmonary damage characterized by leakage of plasma and blood cells. These lesions were prevented by treatment with a beta2 integrin antagonist. In addition, M protein/fibrinogen complexes were identified in tissue biopsies from a patient with necrotizing fasciitis and STSS, further underlining the pathogenic significance of such complexes in severe streptococcal infections.[1]

References

M protein, a classical bacterial virulence determinant, forms complexes with fibrinogen that induce vascular leakage. Herwald, H., Cramer, H., Mörgelin, M., Russell, W., Sollenberg, U., Norrby-Teglund, A., Flodgaard, H., Lindbom, L., Björck, L. Cell (2004) [Pubmed]

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