Cigarette Smoking Increases Neutrophil Formyl Methionyl Leucyl Phenylalanine Receptor Numbers

Matheson, Melissa; Rynell, Ann-Christine; McClean, Melissa; Berend, Norbert

doi:10.1378/chest.123.5.1642

Cited by 24 publications

(13 citation statements)

References 11 publications

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“…These data are in line with a previous study showing enhanced migration of PMN to formyl-methionyl-leucyl phenylalanine (fMLP) in patients with stable COPD [4]. Whereas that observation could be explained by increased expression of fMLP-receptors on PMN from smokers with and without COPD [23], in this study, with CXCL-8 being used as chemotactic stimulus, no correlation between the expression of CXC receptors and the chemotactic index was demonstrable in vitro. Previous authors studying patients with sepsis found significant decreases in the surface expression of CXCR-2 [24] in association with a marked deficit in the chemotactic response to CXC chemokines.…”

Section: Discussionsupporting

confidence: 92%

Enhanced PMN response in chronic bronchitis and community-acquired pneumonia

Strassburg¹

2004

Eur Respir J

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Chronic bronchitis is a frequent underlying disease in communityacquired pneumonia (CAP). It is unclear to what extent an impaired or exaggerated innate immune response contributes to disease manifestations and severity.To assess the role of neutrophil activation and recruitment during acute pneumonic episodes, peripheral polymorphonulcear neutrophil (PMN) activation, chemotactic activity, interleukin-8 (CXCL-8) and CXCL-8 receptor (CXCR) expression and apoptosis rate were evaluated in CAP patients with and without chronic bronchitis. In addition, the expression of CXCRs and CXCL-8 was assessed on pulmonary neutrophils in chronic bronchitis patients to compare the activation of the chemokine system in different compartments. CAP severity was assessed by the simplified acute physiology score II and the prognosis of disease was assessed by the pneumonia severity index (PSI).An increased chemotactic activity of PMN from chronic bronchitis patients with CAP was found, which was not related to the expression of CXCRs. In addition, a decreased apoptosis rate of PMN was observed. Chemotactic activity was related to the PSI. Comparison of peripheral and pulmonary PMN revealed enhanced CXCL-8 levels and a decreased CXCR expression in the lung.In conclusion, neutrophil function in patients with chronic bronchitis and communityacquired pneumonia is characterised by an increased chemotactic activity combined with a decreased apoptosis rate. The downregulation of interleukin-8 receptors in the pulmonary compartment deserves further investigation. Eur Respir J 2004; 24: 772-778.

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Section: Discussionsupporting

confidence: 92%

Enhanced PMN response in chronic bronchitis and community-acquired pneumonia

Strassburg¹

2004

Eur Respir J

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“…Tobacco‐induced increases in fMLP receptor numbers have been noted by others (Matheson et al 2003). In the periodontal environment, where there is a plentiful source of fMLP, priming of gingival neutrophils by tobacco smoke components could lead to an increase in the local burden of potentially degradative elastase and superoxide in response to the plaque bacteria – a hyperinflammatory response.…”

Section: Smoking and Neutrophil Functionsupporting

confidence: 64%

Mechanisms of action of environmental factors – tobacco smoking

Palmer

Wilson

Hasan

et al. 2005

J Clinic Periodontology

433

470

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“…FPR1 has been shown to be involved on the lung migration of neutrophil and macrophage and pro-inflammatory responses after cigarette smoke exposure in a mouse model [ 7 ]. In line with our findings that FPR1 expression on neutrophil was increased in COPD patients with a high MMRC dyspnea scale and reversed to normal after 1-year treatment, previous studies reported that cigarette smoking increased FPR1 numbers on blood neutrophils in emphysema patients, and that its expression was not correlated with the severity of airflow limitation [ 24 , 25 ].…”

Section: Discussionsupporting

confidence: 91%

Defective formyl peptide receptor 2/3 and annexin A1 expressions associated with M2a polarization of blood immune cells in patients with chronic obstructive pulmonary disease

et al. 2018

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BackgroundControversy exists in previous studies on macrophage M1/M2 polarization in chronic obstructive pulmonary disease (COPD). We hypothesized that formyl peptide receptor (FPR), a marker of efferocytosis and mediator of M1/M2 polarization, may be involved in the development of COPD.MethodsWe examined FPR 1/2/3 expressions of blood M1/M2a monocyte, neutrophil, natural killer (NK) cell, NK T cell, T helper (Th) cell, and T cytotoxic (Tc) cell by flowcytometry method in 40 patients with cigarette smoking-related COPD and 16 healthy non-smokers. Serum levels of five FPR ligands were measured by ELISA method.ResultsThe COPD patients had lower M2a percentage and higher percentages of NK, NK T, Th, and Tc cells than the healthy non-smokers. FPR2 expressions on Th/Tc cells, FPR3 expressions of M1, M2a, NK, NK T, Th, and Tc cells, and serum annexin A1 (an endogenous FPR2 ligand) levels were all decreased in the COPD patients as compared with that in the healthy non-smokers. FPR1 expression on neutrophil was increased in the COPD patient with a high MMRC dyspnea scale, while FPR2 expression on neutrophil and annexin A1 were both decreased in the COPD patients with a history of frequent moderate exacerbation (≥ 2 events in the past 1 year). In 10 COPD patients whose blood samples were collected again after 1-year treatment, M2a percentage, FPR3 expressions of M1/NK/Th cells, FPR2 expression on Th cell, and FPR1 expression on neutrophil were all reversed to normal, in parallel with partial improvement in small airway dysfunction.ConclusionsOur findings provide evidence for defective FPR2/3 and annexin A1 expressions that, associated with decreased M2a polarization, might be involved in the development of cigarette smoking induced persistent airflow limitation in COPD.

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Cigarette Smoking Increases Neutrophil Formyl Methionyl Leucyl Phenylalanine Receptor Numbers

Cited by 24 publications

References 11 publications

Enhanced PMN response in chronic bronchitis and community-acquired pneumonia

Enhanced PMN response in chronic bronchitis and community-acquired pneumonia

Mechanisms of action of environmental factors – tobacco smoking

Defective formyl peptide receptor 2/3 and annexin A1 expressions associated with M2a polarization of blood immune cells in patients with chronic obstructive pulmonary disease

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