Endotoxin shock is intiated by -
Cells of the innate immune system express receptors (e.g., Toll-like receptors ) that recognize a host of microbe-derived substances containing so-called pathogen-associated molecular patterns (PAMPs). Activation of pathogen recognition receptors by PAMPs triggers the innate immune responses that drive sepsis. Upon activation, the inflammatory cells produce TNF and IL-1 (and other cytokines), plus cytokine-like mediators such as high-mobility group box 1 (HMGB1). Reactive oxygen species and lipid mediators such as prostaglandins and plateletactivating factor (PAF) also are elaborated (Chapter 2). These effector molecules activate endothelial cells, resulting in expression of adhesion molecules. ( Robbins Basic Pathology, 9 th edition, page 95 )
endothelial injury
Peripheral vasodilation
Increased vascular permeability
Cytokines action
General pathology