Effects of Nicotine on the Functions of Human Polymorphonuclear Leukocytes In Vitro

Sasagawa, Sumiko; Suzuki, Kazuo; Sakatani, Tatsuichiro; Fujikura, Toshio

doi:10.1002/jlb.37.5.493

Cited by 49 publications

(41 citation statements)

References 25 publications

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“…The non-volatile component did not inhibit migration. Nicotine had no effect on PMN migration and chemotaxis (Sasagawa et al, 1985). Macrophages from the lungs of smokers have a greater inhibitory effect on lymphocyte proliferation than macrophages from the lungs of nonsmokers.…”

Section: Cell-mediated Immune Responsesmentioning

confidence: 81%

Cigarette Smoking and Lower Respiratory Tract Infection

Saldías¹,

Díaz²

2011

Bronchitis

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Section: Cell-mediated Immune Responsesmentioning

confidence: 81%

Cigarette Smoking and Lower Respiratory Tract Infection

Saldías¹,

Díaz²

2011

Bronchitis

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“…The importance of nAChR-coupled signaling pathways for the physiologic regulation of the subcellular machinery of crawling locomotion has been underscored by the results of the studies involving different cell types. Interestingly, both stimulatory (Dwivedi and Long, 1989;Grando et al, 1995;Yong et al, 1997) and inhibitory ( Owen and Bird, 1995;Thomas et al, 1981;Zia et al, 2000) effects have been reported, as have lack of effects (Drell et al, 2003;Grando et al, 1993a;Sasagawa et al, 1985), suggesting that either different cells express different combinations of cell surface receptors to ACh and/or in different cells the same types of ACh receptors are coupled to different signaling pathways. The reports of lack of effects of ACh and its congeners on migration suggested that one type of ACh receptors stimulates and another inhibits migration and that simultaneous activation of both groups of the receptors in a single cells results in a zero net effect on motility.…”

Section: Discussionmentioning

confidence: 99%

Differential regulation of keratinocyte chemokinesis and chemotaxis through distinct nicotinic receptor subtypes

Chernyavsky

Arredondo

Marubio

et al. 2004

Journal of Cell Science

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Nicotinergic agents can act as both chemokines and chemoattractants for cell migration. Epidermal keratinocytes both synthesize acetylcholine and use it as a paracrine and autocrine regulator of cell motility. To gain a mechanistic insight into nicotinergic control of keratinocyte motility, we determined types of nicotinic acetylcholine receptors and signaling pathways regulating keratinocyte chemokinesis and chemotaxis, using respective modifications of the agarose gel keratinocyte outgrowth assay. Random migration of keratinocytes was significantly (P<0.05) inhibited by hemicholinum-3, a metabolic inhibitor of acetylcholine synthesis, as well as by the α-conotoxins MII and AuIB, preferentially blocking α3-containing nicotinic acetylcholine receptors. The use of antisense oligonucleotides specific for nicotinic-acetylcholine-receptor subunits and knockout mice demonstrated pivotal role for the α3β2 channel in mediating acetylcholine-dependent chemokinesis. Signaling pathways downstream of α3β2 included activation of the protein-kinase-C isoform δ and RhoA-dependent events. The nicotinergic chemotaxis of keratinocytes was most pronounced towards the concentration gradient of choline, a potent agonist of α7 nicotinic acetylcholine receptor. The α7-preferring antagonist α-bungarotoxin significantly (P<0.05) diminished keratinocyte chemotaxis, further suggesting a central role for the α7 nicotinic acetylcholine receptor. This hypothesis was confirmed in experiments with anti-α7 antisense oligonucleotides and α7-knockout mice. The signaling pathway mediating α7-dependent keratinocyte chemotaxis included intracellular calcium, activation of calcium/calmodulin-dependent protein-kinase II, conventional isoforms of protein-kinase C, phosphatidylinositol-3-kinase and engagement of Rac/Cdc42. Redistribution of α7 immunoreactivity to the leading edge of keratinocytes upon exposure to a chemoattractant preceded crescent shape formation and directional migration. Application of high-resolution deconvolution microscopy demonstrated that, on the cell membrane of keratinocytes, the nicotinic acetylcholine receptor subunits localize with the integrin β1. The obtained results demonstrate for the first time that α3 and α7 nicotinic acetylcholine receptors regulate keratinocyte chemokinesis and chemotaxis, respectively, and identify signaling pathways mediating these functions, which has clinical implications for wound healing and control of cancer metastases.

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“…This factor is mainly produced by haematopoietic cells, and influences the proliferation, survival, maturation and functional activation of cells of the neutrophilic granulocyte lineage (19). Chronic cigarette smoking is associated with functional depression (20) and an increased blood count (21) of neutrophils. Tobacco smoking also causes an increased production of TNF-a (22) and high serum G-CSF levels (23).…”

mentioning

confidence: 99%

Evaluation of Tumor Necrosis Factor-Alphaand Granulocyte Colony-Stimulating Factor Serum Levels in Lead-Exposed Smoker Workers

Lorenzo

Vacca

Corfiati³

et al. 2007

Int J Immunopathol Pharmacol

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Inorganic lead (Pb) is able to modulate the immune response even at low to moderate exposure levels. It inhibits in vitro and in vivo activities of neutrophilleucocytes and influences their blood count in humans. Neutrophil functions are governed by a number of cytokines. Pb has been shown to affect leukocyte production of some ofthese cytokines in vitro. The objective ofthis study is to assess serum tumor necrosis factor-alpha (TNF-a) and granulocyte colony-stimulating factor (G-CSF) levels of thirty-three male lead-exposed (E) workers at a lead recycling plant as compared with twenty-eight male non-exposed (NE) workers at a food processing plant, whose current smoking habit was known. Serum TNF-a and G-CSF levels were measured by a quantitative sandwich enzyme immunoassay. Blood lead levels (Pb-B) were significantly higher in E (geometric mean (GM) 30.7 pg/dl, GSD 1.7; min-max: 9.1-81.6 pg/ dl) workers than controls (GM 3.6 pg/dl, GSD 1.7; min-max: 1.0-11.0pg/dl). E workers had significantly higher serum TNF-a (median: 107.1; min-max: 11.1-623.0 pg/ml) and G-CSF levels (median: 53.0, min-max: 31.1-197.0 pg/ml) than NE workers (TNF-a: median: 12.0; min-max: 9.4-18.8 pg/ml; G-CSF: median: 34.3, min-max: 25.1-52.2 pg/ml). In particular, the TNF-a level was shown to be significantly influenced by lead exposure and smoking habit, as well as by interaction between these two factors. Both serum TNF-a and G-CSF levels were correlated with Pb-B and absolute neutrophil count. This study is the first to detect higher serum levels of G-CSF in E over NE workers. Our data confirm that exposure to low to medium doses of lead may interfere in the complex cytokine network involved in inflammation, especially in workers who are current smokers.

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Effects of Nicotine on the Functions of Human Polymorphonuclear Leukocytes In Vitro

Cited by 49 publications

References 25 publications

Cigarette Smoking and Lower Respiratory Tract Infection

Cigarette Smoking and Lower Respiratory Tract Infection

Differential regulation of keratinocyte chemokinesis and chemotaxis through distinct nicotinic receptor subtypes

Evaluation of Tumor Necrosis Factor-Alphaand Granulocyte Colony-Stimulating Factor Serum Levels in Lead-Exposed Smoker Workers

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