What is the role of host response to infection in the pathophysiology of multiple organ dysfunction syndrome (MODS) in sepsis?

Updated: Jan 27, 2020
  • Author: Ali H Al-Khafaji, MD, MPH, FACP, FCCP, FCCM; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, FAPS, MCCM  more...
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Clinical characteristics that relate to the severity of sepsis include the host response to infection, the site and type of infection, the timing and type of antimicrobial therapy, the offending organism, the development of shock, the underlying disease, the patient’s long-term health condition, and the number of failed organs. Factors that lead to sepsis and septic shock may not be essential in determining the ultimate outcome.

The host response to sepsis is characterized by both proinflammatory responses and anti-inflammatory immunosuppressive responses. The direction, extent, and duration of these reactions are determined by both host factors (eg, genetic characteristics, age, coexisting illnesses, medications) and pathogen factors (eg, microbial load, virulence). [10]

Inflammatory responses are initiated by interaction between pathogen-associated molecular patterns expressed by pathogens and pattern recognition receptors expressed by host cells at the cell surface (toll-like receptors [TLRs] and C-type lectin receptors [CLRs]), in the endosome (TLRs), or in the cytoplasm (retinoic acid inducible gene 1–like receptors [RLRs] and nucleotide-binding oligomerization domain–like receptors [NLRs]). [10]

The consequence of exaggerated inflammation is collateral tissue damage and necrotic cell death, which results in the release of damage-associated molecular patterns, so-called danger molecules that perpetuate inflammation at least in part by acting on the same pattern-recognition receptors triggered by pathogens. [10]

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