Journal
TRENDS IN MOLECULAR MEDICINE
Volume 12, Issue 1, Pages 10-16Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.molmed.2005.11.002
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Funding
- NHLBI NIH HHS [HL46810, R01 HL046810-13] Funding Source: Medline
- NIAID NIH HHS [R01 AI053733-03, AI53733] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL046810] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI053733] Funding Source: NIH RePORTER
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The sepsis syndrome is thought to occur when microbial products activate Toll-like receptors stimulating widespread inflammation, in turn causing organ failure, shock and death. However, recent discoveries reveal that: (i) not only microbial substances but also endogenous molecules can trigger Toll-like receptors; (ii) Toll-like receptor-4, the endotoxin receptor, is constitutively suppressed; and (iii) the first step in sepsis could be the release of Toll-like receptor-4 from suppression. These discoveries suggest that endotoxin might not always initiate the sepsis syndrome and they explain why anti-endotoxin therapies fail. The discoveries also suggest new therapeutic targets - endogenous agonists and Toll-like receptor regulators - for treatment of sepsis.
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