Journal
SHOCK
Volume 32, Issue 4, Pages 348-357Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/SHK.0b013e3181a551bd
Keywords
Innate immune cells; phagocytes; inflammation; cytokines; sepsis; antibodies; HMGB1; tanshinones
Funding
- National Institutes of Health
- National Institute of General Medical Science [R01GM063075, R01GM070817]
- National Center for Complementary & Integrative Health [R01AT005076] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM070817, R01GM063075] Funding Source: NIH RePORTER
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Sepsis refers to a systemic inflammatory response syndrome resulting from a microbial infection. The inflammatory response is partly mediated by innate immune cells (such as macrophages, monocytes, and neutrophils), which not only ingest and eliminate invading pathogens but also initiate an inflammatory response by producing early (e.g., TNF and IFN-gamma and late (e.g., high-mobility group box [HMGB1]) proinflammatory cytokines. Here, we briefly review emerging evidence that support extracellular HMGB1 as a late mediator of experimental sepsis and discuss therapeutic potential of several HMGB1-inhibiting agents (including neutralizing antibodies and steroid-like tanshinones) in experimental sepsis.
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