PubMed · 1987 · 209 citations · 0 references
Veterinary MedicineImmunologyPathobiologyHost-pathogen InteractionsInflammationInnate ImmunityAcute InflammationCytokine BiologyInflammatory Cell ResponsesInflammatory MediatorsLeukocyte RecruitmentNeutrophil BiologyAcute Inflammatory InjuryAcute Inflammatory ResponseEndotoxin-mediated InflammationInflammatory Response To Bacterial InfectionNeutrophil Effector FunctionsNeutrophil Responses To BacteriaPhagocytosis Of Immune ComplexesPostcapillary Venule Interactions
Experimental bacterial infection of the dermis with gram‑negative microorganisms triggers an acute inflammatory reaction that serves as the primary local defense against infection spread, with kinetics similar to other inflammatory stimuli and involving neutrophil‑dependent vascular injury. Microorganisms release endotoxin, which induces interleukin‑1 and tumor necrosis factor secretion, and neutrophil phagocytosis of bacteria releases oxygen radicals and lysosomal proteases that damage microvasculature. In neutropenic animals neutrophil emigration fails and bacterial growth is unchecked; endotoxin is the most potent inducer of neutrophil influx, and the released radicals and proteases cause microvascular injury marked by increased permeability, hemorrhage, and thrombosis.
Experimental bacterial infection of the dermis induced with gram-negative microorganisms is associated with an acute inflammatory reaction, which represents the principal local defense against spread of the infection. When the inflammatory reaction is quantitated with radiolabeled cells and proteins, the kinetics resemble acute inflammation induced with other agents, such as immune complexes or chemotaxins. There is an interrelationship between the components or events of the inflammatory reaction; inasmuch as vascular injury is neutrophil-dependent, neutrophils must migrate to the site where the bacteria multiply. In neutropenic animals there is no such emigration and bacterial multiplication is not inhibited. The microorganisms shed endotoxin, which in turn induces secretion of interleukin 1 (IL 1) and probably tumor necrosis factor. Endotoxin is the most potent agent (10(-15) mol vs. 10(-12) mol of C5ades Arg) capable of inducing a neutrophil influx. Desensitization or tachyphylaxis of the tissues (probably of postcapillary venular endothelium) to IL 1 seems to control cessation of the neutrophil influx (also in vitro evidence). Phagocytosis of the bacteria by neutrophils is associated with release of oxygen radicals and lysosomal proteases from the neutrophils. These are instrumental in eliciting microvascular injury, which is characterized by enhanced vasopermeability, hemorrhage, and thrombosis.