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نوتروفیل
Local endo- thelial interactions with neutrophils mediate some of the local inflammatory responses associated with the zone of stasis.
However, interleukins 1 and 6, platelet-activating factor, tumor necrosis factor, endotoxin, neutrophil adherence complexes, reactive oxygen species, nitric oxide, and coagulation as well as complement cascades have also been implicated in regulating this response to burn injury.13 Once these cascades are initiated, their mediators and byproducts appear to stimulate the persistent and increased metabolic rate associated with altered glucose metabolism seen after severe burn injury.13
Total neutrophil counts are initially increased after burn injury, a phenomenon that is related to a decrease in cell death by apoptosis.
However, neutrophils that are present are dysfunctional in terms of diapedesis, chemotaxis, and phagocytosis. ftese effects are explained, in part, by a deficiency in CD11b/CD18 expression after inflammatory stimuli, decreased respiratory burst activity associated with a deficiency in p47phox activity, and impaired actin mechanics related to neutrophil motile responses.
After 48 to 72 hours, neutrophil counts decrease somewhat, like macrophages, with similar causes.
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