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Pathogenic bacteria adhering to the human vascular wall triggers vascular damage during meningococcal sepsis

Researchers at the Paris Cardiovascular Research Center (PARCC) have shown how adhesion of Neisseria (N.) meningitidis to human microvessels in a humanized mouse model leads to the characteristic cutaneous lesions of meningococcal sepsis. This work, published on January 24 in the Open Access journal PLOS Pathogens, is an important demonstration of the direct role of adhesion, specifically Type IV pili mediated adhesion, plays in the development of the disease.

Meningococcal sepsis is a rapidly developing and often fatal infection. Cutaneous lesions, often presenting clinically as purpuric or petechial skin rashes, are a hallmark feature of the infection hence the term purpura fulminans to describe this severe form of sepsis. Understanding the mechanisms behind the development of these lesions is important to understand disease progression because it reveals the underlying mechanisms of the pathological process. From the experimental point of view the strict human specificity of N. meningitidis has long been a limiting factor in the development of relevant in vivo models of this infection and for understanding how the bacteria interact with the blood vessels. It was previously thought that that the large number of circulating bacteria was responsible for the vascular damage through the release of LPS in particular.

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