Cigarette smoking and respiratory infections in a class of student nurses

Parnell, John L.; Anderson, Donald O.; Kinnis, S; Blackwell, Martin

doi:10.1097/00006199-196701610-00076

Cited by 11 publications

(13 citation statements)

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“…The suggestion has been made that smokers suffer an increased susceptibility to infections (29)(30)(31). Previous studies of human alveolar macrophages have, to our knowledge, revealed no substantial depression of phagocytosis in the cells from smokers (5,10).…”

Section: Resultsmentioning

confidence: 81%

Pinocytosis by Human Alveolar Macrophages COMPARISON OF SMOKERS AND NONSMOKERS

Yeager¹,

Zimmet²,

Schwartz³

1974

J. Clin. Invest.

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Section: Resultsmentioning

confidence: 81%

Pinocytosis by Human Alveolar Macrophages COMPARISON OF SMOKERS AND NONSMOKERS

Yeager¹,

Zimmet²,

Schwartz³

1974

J. Clin. Invest.

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“…However, there is a considerable amount of epidemiologic data that have shown an association between human respiratory symptoms indicative of viral infection and exposure to various airborne chemicals (163)(164)(165)(166)(167)(168). Because of this relationship, it is important to continue to investigate how noxious agents can affect the macrophages interaction with viruses of the human respiratory tract.…”

Section: Macrophage Defense Against Viral Agentsmentioning

confidence: 99%

Alterations in Macrophage Functions by Environmental Chemicals

Gardner¹

1984

Environmental Health Perspectives

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“…Because cigarette smoking inhibits the cyclooxygenase-related metabolism of arachidonic acid in the AM (21,22) and is associated with an increased incidence of infectious diseases in the lung (23,24), we undertook a comparative study of LTB4 production by AM in smokers and nonsmokers. For comparison, we also studied the 5-lipoxygenase products synthesis in blood PMNL from smokers and nonsmokers.…”

Section: Introductionmentioning

confidence: 99%

Decreased leukotriene B4 synthesis in smokers' alveolar macrophages in vitro.

Laviolette¹,

Coulombe²,

Picard³

et al. 1986

J. Clin. Invest.

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Recent studies have shown that alveolar macrophages (AM) are able to release leukotrienes (LTs). Since cigarette smoking inhibits the cyclooxygenase pathway of arachidonic acid metabolism in the AM, we evaluated the LT production by AM from smokers and nonsmokers. AM from nonsmokers, those from smokers showed a 80-90% reduction of 5-HETE and LTB4 synthesis (P < 0.05 to P < 0.001 according to stimulatory conditions). This defective lipoxygenase metabolite production in AM from smokers was observed over a wide range of stimuli concentrations and incubation times; AM from smokers also had lower levels of intracellular (esterified) 5-HETE than nonsmokers' AM. We also studied blood polymorphonuclear leukocytes (PMNL) and no difference in the synthesis of 5-lipoxygenase products in these cells was noticed between smokers and nonsmokers. These data show that cigarette smoking causes a profound inhibition of the 5-lipoxygenase pathway in AM but not in blood PMNL.

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Cigarette smoking and respiratory infections in a class of student nurses

Cited by 11 publications

References 0 publications

Pinocytosis by Human Alveolar Macrophages COMPARISON OF SMOKERS AND NONSMOKERS

Pinocytosis by Human Alveolar Macrophages COMPARISON OF SMOKERS AND NONSMOKERS

Alterations in Macrophage Functions by Environmental Chemicals

Decreased leukotriene B4 synthesis in smokers' alveolar macrophages in vitro.

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