To the modern mind, the term ‘sepsis’ conjures up images of microbes. It is easy to forget that the word predates any understanding of the microbial origins of infectious disease. Derived from the Greek ‘sepsios’ (rotten), sepsis denotes decay: a phenomenon that humans once regarded as a mysterious though inevitable natural process. A living organism does not accept decay passively. Virtually all multicellular life forms are capable of resisting infection through the generation of a vigorous immune response. In mammals, the response is so stereotypic that it has come to define sepsis itself: it is often called the ‘septic syndrome’. Our current understanding of the innate immune system is deeply rooted in the study of sepsis. The chain of events linking infection to tissue injury and cardiovascular collapse is not obvious, and affirmation of the concept required three major discoveries. First, the septic syndrome was found to be caused by toxic products of microbes. Secondly, these toxic substances were found to be toxic because of their propensity to activate cells of the innate immune system, prompting cytokine production. Thirdly, the activating events initiated by microbial toxins were traced to members of an ancient family of defensive molecules, versions of which operate in virtually all multicellular life forms. In mammals, proteins of this family are now known as Toll-like receptors. They represent a point of direct contact, and first contact, between a pathogen and the host immune system.
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Conference Article|
November 01 2001
Sepsis begins at the interface of pathogen and host
B. Beutler
B. Beutler
1
1Department of Immunology, The Scripps Research Institute, 10550 N. Torrey Pines Road, La Jolla, CA 92037, U.S.A.
1e-mail bruce@scripps.edu
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Publisher: Portland Press Ltd
Received:
July 13 2001
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© 2001 Biochemical Society
2001
Biochem Soc Trans (2001) 29 (6): 853–859.
Article history
Received:
July 13 2001
Citation
B. Beutler; Sepsis begins at the interface of pathogen and host. Biochem Soc Trans 1 November 2001; 29 (6): 853–859. doi: https://doi.org/10.1042/bst0290853
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