Toll‐like receptor 4 mediates mitochondrial DNA damage and biogenic responses after heat‐inactivatedE. coli

Abstract
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 cytokine production in my...
Funding Information
  • National Institutes of Health (NIH PO1 HL‐42444)

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