Interleukin 1 Production by Alveolar Macrophages Is Decreased in Smokers

Yamaguchi, Etsuro; Okazaki, Nozomu; Itoh, Akichika; Abe, Shosaku; Kawakami, Yoshikazu; Okuyama, Harue

doi:10.1164/ajrccm/140.2.397

Cited by 56 publications

(23 citation statements)

References 13 publications

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“…Smoking-related differences in the proinflammatory cytokine release (IL-1β and TNF-α) shown in the studies reported so far may reflect different culture conditions or different populations [21, 22, 23, 24, 25]. In our Japanese study, the stimulation with a low concentration of LPS (1 µg/ml), the absence of serum factors, and the relatively short culture time (24 h) all partly differed from the conditions in previous studies.…”

Section: Discussionmentioning

confidence: 99%

Proinflammatory or Regulatory Cytokines Released from BALF Macrophages of Healthy Smokers

Mikuniya

Nagai²,

Tsutsumi³

et al. 1999

Respiration

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Background: Chronic smoking influences bronchoalveolar lavage fluid (BALF) cell profiles in healthy subjects, which may alter profiles of inflammatory and regulatory cytokines. Objective: We focused on the evaluation of smoking-related changes in the amounts of cytokines released from BALF macrophages. Methods: We measured the amounts of immunoreactive culture supernatants by using ELISA. Results: The amounts of IL-1 receptor antagonist (IL-1ra) were lower in smokers [n = 10, median 22.1 ng/ml, 25th and 75th percentiles (18.7–39.1)] than in nonsmokers [n = 10, 48.6 (39.2–66.1), p = 0.010]. In smokers, lipopolysaccharide stimulation revealed decreases in the amounts of interleukin-6 (IL-6) [nonsmokers: 2.1 ng/ml (0.68–5.4 vs. smokers: 0.5 (0.03–0.87), p = 0.049] as well as IL-1ra [nonsmokers: 69.2 ng/ml (48.3– 83.8) vs. smokers: 27.3 (17.2–56.7), p = 0.028]. A delay in release from intracellular storage was not the cause of the reduced amounts of IL-1ra. In addition, interleukin-1β (IL-1β) was positively correlated with IL-6 and granulocyte macrophage colony-stimulating factor in nonsmokers, but not in smokers. Furthermore, the decreases in IL-1ra and interleukin-8 were correlated with the increase in the number of BALF macrophages in smokers, but not in nonsmokers. Conclusions: Chronic smoking caused changes in the profiles of cytokines released from BALF macrophages in healthy subjects. Decreases in the amounts of regulatory cytokines, but not prominent changes in the amounts of inflammatory ones, were characteristic.

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Section: Discussionmentioning

confidence: 99%

Proinflammatory or Regulatory Cytokines Released from BALF Macrophages of Healthy Smokers

Mikuniya

Nagai²,

Tsutsumi³

et al. 1999

Respiration

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“…The studies included healthy subjects, including smokers, and non-smokers (N = 19) [69-77, 79-83, 85, 86, 88, 90, 91]. Also studied were smokers with inflammatory lung disease (e.g., COPD) (N = 6) [68,78,84,87,89,90].…”

Section: Comparative Studies Of Lung Macrophages Of Current Smokers Amentioning

confidence: 99%

“…Yamaguchi [90] Cigarettes not defined MU from smokers & non-smokers TNF-a measured by ELISA The study explored the mechanisms underlying lung diseases by measuring TNF-a release by LPS-stimulated MU from smokers, non-smokers and sarcoid patients. In several reported studies, the tissue culture medium containing the smoke was passed through a micropore filter to remove tobacco smoke particulates (''tar'', N = 6) [24,41,47,49,52,54].…”

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confidence: 99%

Inflammatory response of lung macrophages and epithelial cells to tobacco smoke: a literature review of ex vivo investigations

et al. 2010

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Chronic inflammation contributes to the initiation and progression of tumors and tobacco smoke-associated inflammation is associated with malignant and certain non-neoplastic lung diseases. Reported herein are the results of an interpretative synthesis review of the literature assessing the inflammatory response of lung macrophages (MPhi) and epithelial cells to tobacco smoke as measured ex vivo. Papers were retrieved using Boolean operations from PubMed and Scopus. Many writings reported the results of assays of human MPhi from fresh surgically excised human lung tissue, bronchoalveolar lavage, activated blood monocytes, long-term cell lines and MPhi from different laboratory animals. Some publications reported the findings of comparative studies of lung MPhi freshly isolated from the lungs of smokers and non-smokers. Other papers described the effect of tobacco smoke on lung epithelial cells. Most investigators quantified the response of the target cells to tobacco smoke by measuring the production of pro-inflammatory mediators; these included chemokines, cytokines, reactive oxygen species and enzymes. Investigators have reported conflicting observations of the response of human and animal MPhi and epithelial cells to tobacco smoke. The spectrum included papers describing robust production of various inflammatory mediators, significant reduction of a pro-inflammatory response to a known stimulant and overt cytotoxicity. This literature review documents that there exists no consensus, and no emerging trend line, of the reproducible effect(s) of cigarette smoke. This discrepancy reflects the absence of standardized protocols for collecting, processing and bioassaying the smoke, a highly complex aerosol, and identifies the need for establishing collaborative research schemes.

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“…17 Smoking has been shown to significantly decrease the immune response, leading to poor wound healing. In particular, smoking decreases interleukin-1 production, 18 inhibits the early signals for B-cell transduction pathways, 19 decreases cytotoxicity of natural killer cells, and causes T-cell anergy. 20 By decreasing blood flow to damaged skin, smoking increases postsurgical infections, the result of effects on the normal pathways of repair and the response to foreign contamination.…”

Section: Cutaneous Effects Of Smokingmentioning

confidence: 99%