Neutrophilic airways inflammation in lung cancer: the role of exhaled LTB-4 and IL-8

Carpagnano, Giovanna Elisiana; Palladino, Grazia Pia; Lacedonia, Donato; Koutelou, Anna; Orlando, Silvio; Barbaro, Maria Pia Foschino

doi:10.1186/1471-2407-11-226

Cited by 49 publications

(49 citation statements)

References 43 publications

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“…2B). Our data are consistent with recent studies, which have shown increased levels of IL-8 in lung epithelia as a potent chemoattractant for recruiting inflammatory cells (30,31).…”

Section: Cse Triggers Il-8 Release In Pulmonary Epithelial Cellssupporting

confidence: 93%

Shp2 Plays an Important Role in Acute Cigarette Smoke-Mediated Lung Inflammation

Shen

et al. 2012

The Journal of Immunology

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Cigarette smoke (CS), the major cause of chronic obstructive pulmonary disease, contains a variety of oxidative components that were implicated in the regulation of Src homology domain 2-containing protein tyrosine phosphatase 2 (Shp2) activity. However, the contribution of Shp2 enzyme to chronic obstructive pulmonary disease pathogenesis remains unclear. We investigated the role of Shp2 enzyme in blockading CS-induced pulmonary inflammation. Shp2 levels were assessed in vivo and in vitro. Mice (C57BL/6) or pulmonary epithelial cells (NCI-H292) were exposed to CS or cigarette smoke extract (CSE) to induce acute injury and inflammation. Lungs of smoking mice showed increased levels of Shp2, compared with those of controls. Treatment of lung epithelial cells with CSE showed elevated levels of Shp2 associated with the increased release of IL-8. Selective inhibition or knockdown of Shp2 resulted in decreased IL-8 release in response to CSE treatment in pulmonary epithelial cells. In comparison with CS-exposed wild-type mice, selective inhibition or conditional knockout of Shp2 in lung epithelia reduced IL-8 release and pulmonary inflammation in CS-exposed mice. In vitro biochemical data correlate CSE-mediated IL-8 release with Shp2-regulated epidermal growth factor receptor/Grb-2–associated binders/MAPK signaling. Our data suggest an important role for Shp2 in the pathological alteration associated with CS-mediated inflammation. Shp2 may be a potential target for therapeutic intervention for inflammation in CS-induced pulmonary diseases.

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“…2B). Our data are consistent with recent studies, which have shown increased levels of IL-8 in lung epithelia as a potent chemoattractant for recruiting inflammatory cells (30,31).…”

Section: Cse Triggers Il-8 Release In Pulmonary Epithelial Cellssupporting

confidence: 93%

Shp2 Plays an Important Role in Acute Cigarette Smoke-Mediated Lung Inflammation

Shen

et al. 2012

The Journal of Immunology

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“…There are several non-invasive biomarkers measurable in exhaled breath condensate, such as ferritin and superoxide dismutase [130], LTB-4 and IL-8 [131], microsatellite alterations (MAs) at the long arm of chromosome 19 [132], cyclooxygenase (COX-2) and survivin [133], IL-2, TNF-alpha and leptin [134], which, if deemed feasible, have clinical implications in the monitoring of lung cancer and as an religious outcome predictor.…”

Section: Cancermentioning

confidence: 99%

Religious and Spiritual Biomarkers in Both Health and Disease

Kharitonov¹

2012

Religions

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Religious thought and spirituality can be considered as a part of natural human capacities. There is an exponential rise in clinical research in the relationship between religion, spirituality and positive health outcomes. Most of these studies, however, have been primarily descriptive, rather than explanatory, focusing on identifying their underlying mechanisms. Almost no attempts have been made to find novel methods to mirror and monitor positive, and possibly negative, reactions related to the local and general effects of religion and spirituality in healthy subjects and patients. As this area of interest is rather new, we propose to put forward a new hypothesis that effects of religion and spirituality can be objectively studied by various exhaled biomarkers, some of which have already been developed and tested in health and disease. The lungs are particularly well suited for this purpose, as we have easy access to exhaled air and thereby a possibility to develop methods that measure compounds directly released from them. This work is the first step in the convergence of medical and theological research by linking various biomarkers and physiological measures with indicators of individual belief systems, religiosity and spirituality.

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“…16,19 There are vast evidence about the harmful effects of tobacco-derived carcinogen in a variety of ....................................................................................................................... tumor developments, especially in lung cancer. 14,15 However, little is known about the roles of tobacco-derived carcinogen on lung cancer metastasis and invasion.…”

Section: Discussionmentioning

confidence: 99%

Benzopyrene promotes lung cancer A549 cell migration and invasion through up-regulating cytokine IL8 and chemokines CCL2 and CCL3 expression

Zhang

Jin

et al. 2016

Exp Biol Med (Maywood)

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Tobacco-sourced carcinogen including benzopyrene (B[a]P) in lung cancer metastasis has not been fully reported. In this study, lung carcinoma A549 cell line was used to investigate the potential roles of tobacco-sourced B[a]P on cell metastasis and invasion and to assess its underlying mechanism. Effects of tobacco-sourced carcinogen on A549 cell proliferation, metastasis, and invasion were analyzed using MTT assay, Transwell assay, and scratch method, respectively. The effects of tobacco-sourced carcinogen on cytokines and chemokines secretion were detected using enzyme-linked immunosorbent assay. Moreover, correlation between inflammatory factor expression and cancer cell migration and invasion was assessed using siRNA-mediated gene silencing. Data showed that both B[a]P and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone either at high or low dose performed no significant difference on A549 cell proliferation with time increasing. 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone performed no significant difference on A549 cell migration and invasion while B[a]P significantly increased A549 cell migration and invasion compared to the control group (P < 0.05). Consequently, except for IL-6, IL-8, CCL-2, and CCL-3, secretions were significantly increased by B[a]P treatment compared to the control (P < 0.05). Furthermore, when CCL-2 and CCL-3 were silenced, the migrated and invasive A549 cells were significantly decreased compared to the control, respectively (P < 0.05), while silenced IL-8 drastically decreased the migrated and invasive cells compared to the control (P < 0.01). Taken together, this study illustrated that there may be significant correlation between smoking and lung cancer metastasis. B[a]P maybe an excellent contributor for lung cancer metastasis through up-regulating IL-8, CCL-2, and CCL-3 expression.

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Neutrophilic airways inflammation in lung cancer: the role of exhaled LTB-4 and IL-8

Cited by 49 publications

References 43 publications

Shp2 Plays an Important Role in Acute Cigarette Smoke-Mediated Lung Inflammation

Shp2 Plays an Important Role in Acute Cigarette Smoke-Mediated Lung Inflammation

Religious and Spiritual Biomarkers in Both Health and Disease

Benzopyrene promotes lung cancer A549 cell migration and invasion through up-regulating cytokine IL8 and chemokines CCL2 and CCL3 expression

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