NDLI: Early effects of smoke inhalation on alveolar macrophage functions.

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Early effects of smoke inhalation on alveolar macrophage functions.

Content Provider	Semantic Scholar
Author	Bidani, Akhil Wang, Cheng Zhang Heming, Thomas A.
Copyright Year	1996
Abstract	Alveolar macrophage (AM) dysfunctions have been implicated in the pathogenesis of smoke inhalation lung injury. We investigated the early (within 70 min) effects of smoke inhalation on AM. The cells were recovered by bronchoalveolar lavage from rabbits ventilated with cotton smoke for 5 min followed by O2/room air for 60 min (smoke-exposed) or with room air in place of smoke (control). Smoke injury caused arterial blood carboxyhaemoglobin levels to increase 11-fold and reduced arterial blood PO2 (measured approximately 1 h postinjury) by 25 per cent. Scanning electron micrographs revealed denudation of plasmalemmal pseudopods in smoke-exposed AM. Smoke exposure suppressed both AM adherence to plastic and phagocytosis of opsonized bacteria. Basal superoxide (O2-) production was elevated in smoke-exposed AM, compared with controls, whereas PMA-stimulated O2- production was unaffected. Smoke-exposed AM had reduced basal secretion of tumour necrosis factor-alpha (TNF-alpha), but displayed a greater TNF response to stimulation with LPS than did control cells. LPS-stimulated TNF-alpha releases from control and smoke-exposed AM were suppressed by phosphodiesterase inhibitors pentoxifylline and theophylline, and were enhanced by the lipoxygenase inhibitor, MK886. The early responses of AM to smoke inhalation lung injury are consistent with activation of O2- production and priming of TNF-alpha release, concurrent with a functional down regulation of phagocytosis.
Starting Page	198
Ending Page	201
Page Count	4
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://ehs.sph.berkeley.edu/krsmith/CRA/tb/BidaniA_1996.pdf
PubMed reference number	8634114v1
Volume Number	22
Issue Number	2
Journal	Burns : journal of the International Society for Burn Injuries
Language	English
Access Restriction	Open
Subject Keyword	Bacteria Carboxyhemoglobin Down-Regulation Inspiration function Irrigation Lipoxygenase Inhibitors Lung Injury Macrophages, Alveolar Neoplasms PO-2 Pentoxifylline Phagocytosis Priming Exercise Pseudopodia Pulmonary Alveolar Proteinosis Smoke Inhalation Injury Superoxides Tetradecanoylphorbol Acetate Theophylline Tumor Necrosis Factors
Content Type	Text
Resource Type	Article

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