Lung inflammation: role of endogenous chemotactic factors in attracting polymorphonuclear granulocytes.
The inflammatory reaction in the lungs can be considered a mechanism of host defense that augments local alveolar cellular and humoral defense against microorganisms and particulates which challenge the airways. As part of this reaction, the accumulation of blood inflammatory and phagocytic cells, primarily PMNs, and fluid components from plasma may be under control of chemoattractant factors and vasoactive mediators. From the air-side, chemotactic factors originating from alveolar macrophages or through activation of the complement system seem essential in initiating the influx of PMNs into the alveolar space. The kinetics of synthesis and release of chemotactic factors from alveolar macrophages of animals and humans and the status of their immunochemical analysis is the essence of this report. Coupling phagocytosis (afferent function) with its capacity to secrete several kinds of effector molecules (chemotactic factors, complement components, leukotrienes, and platelet activating factor), the alveolar macrophage is considered to have a pivotal role in overall regulation of the inflammatory reaction.
D000391:Air Microbiology; D000818:Animals; D002630:Chemotactic Factors / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000502:physiology*; D002631:Chemotactic Factors, Eosinophil / Q000502:physiology*; D006801:Humans; D008264:Macrophages / Q000166:cytology; D015846:Monokines; D010587:Phagocytosis; D011014:Pneumonia / Q000503:physiopathology*; D011506:Proteins / Q000378:metabolism; D011650:Pulmonary Alveoli / Q000166:cytology; D011817:Rabbits
D002630:Chemotactic Factors; D002631:Chemotactic Factors, Eosinophil; D015846:Monokines; D011506:Proteins