Toll-like receptor 4 mediates mitochondrial DNA damage and biogenic responses after heat-inactivated E. coli Hagir B. Suliman, Karen E. Welty-Wolf, Martha Sue Carraway, David A. Schwartz, John W. Hollingsworth and Claude A. Piantadosi 1 Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA 1 Correspondence: Box 3315, Room 0590, CR2 Building, Duke University Medical Center Durham, NC 27710, USA. E-mail: piant001@mc.duke.edu The body’s innate immune system closely monitors and contains bacterial products, but in pathological states the host response damages tissues by releasing inflammatory mediators that contribute to cell damage and cell death. In systemic infection by enteric bacteria, the liver’s immune role is to clear circulating microbes and their products and to produce the acute-phase response. Resident hepatic macrophages, Kuppfer cells (KC), are activated by lipopolysaccharide (LPS) and generate cytokines, especially tumor necrosis factor-α (TNF-α) and interleukins (IL), which induce reactive oxygen species (ROS) and nitric oxide (NO) production, as well as chemokines that recruit leukocytes. Elaborated factors activate receptor and nonreceptor pathways that involve mitochondria in hepatocyte necrosis and apoptosis. Mammalian cells recognize conserved microbial motifs by means of at least 10 transmembrane Toll-like receptors (TLR). TLR activation leads to immediate antimicrobial peptide and
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Toll-like receptor 4 mediates mitochondrial DNA damage and biogenic responses after heat-inactivated E. coli
Suliman, Hagir B.; Welty-Wolf, Karen E.; Carraway, Martha Sue; Schwartz, David A.; Hollingsworth, John W.; Piantadosi, Claude A.
Follow The FASEB Journal
, Volume 19 (11): 1531
Fed of American Socs for Experimental Biology – Sep 1, 2005
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