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The immune response to sepsis can be seen as a pattern recognition receptor-mediated dysregulation of the immune system following pathogen invasion in which a careful balance between inflammatory and anti-inflammatory responses is vital. Invasive infection triggers both pro-inflammatory and anti-inflammatory host responses, the magnitude of which depends on multiple factors, including pathogen virulence, site of infection, host genetics, and comorbidities. Toll-like receptors, the inflammasomes, and other pattern recognition receptors initiate the immune response after recognition of danger signals derived from microorganisms, so-called pathogen-associated molecular patterns or derived from the host, so-called danger-associated molecular patterns. Further dissection of the role of host-pathogen interactions, the cytokine response, the coagulation cascade, and their multidirectional interactions in sepsis should lead toward the development of new therapeutic strategies in sepsis.

Original publication

DOI

10.4161/viru.25436

Type

Journal article

Journal

Virulence

Publication Date

01/2014

Volume

5

Pages

36 - 44

Addresses

Center for Infection and Immunity Amsterdam (CINIMA); Center for Experimental and Molecular Medicine (CEMM); Division of Infectious Diseases; Academic Medical Center; University of Amsterdam; Amsterdam, The Netherlands.

Keywords

Humans, Sepsis, Inflammation, Cytokines, Signal Transduction, Receptors, Pattern Recognition, Toll-Like Receptors, Host-Pathogen Interactions, Immunity, Innate