Dataset Information

Role of CXCL5 in leukocyte recruitment to the lungs during secondhand smoke exposure.

ABSTRACT: Chronic obstructive pulmonary disease (COPD) is the third leading cause of mortality in the United States. The major cause of COPD is cigarette smoking. Extensive leukocyte influx into the lungs, mediated by chemokines, is a critical event leading to COPD. Although both resident and myeloid cells secrete chemokines in response to inflammatory stimuli, little is known about the role of epithelial-derived chemokines, such as CXC chemokine ligand (CXCL)5, in the pathogenesis of cigarette smoke-induced inflammation. To explore the role of CXCL5, we generated CXCL5 gene-deficient mice and exposed them to secondhand smoke (SHS) for 5 hours/day for 5 days/week up to 3 weeks (subacute exposure). We observed a reduced recruitment of leukocytes to the lungs of CXCL5(-/-) mice compared with their wild-type (WT) counterparts, and noted that macrophages comprised the predominant leukocytes recruited to the lungs. Irradiation experiments performed on CXCL5(-/-) or WT mice transplanted with WT or CXCL5(-/-) bone marrow revealed that resident but not hematopoietic cell-driven CXCL5 is important for mediating SHS-induced lung inflammation. Interestingly, we observed a significant reduction of monocyte chemotactic protein-1 (MCP-1/CC chemokine ligand 2) concentrations in the lungs of CXCL5(-/-) mice. The instillation of recombinant MCP-1 in CXCL5(-/-) mice reversed macrophage recruitment. Our results also show the reduced activation of NF-?B/p65 in the lungs, as well as the attenuated activation of C-Jun N-terminal kinase, p42/44, and p38 mitogen-activated protein kinases and the expression of intercellular adhesion molecule-1 in the lungs of SHS-exposed CXCL5(-/-) mice. Our findings suggest an important role for CXCL5 in augmenting leukocyte recruitment in SHS-induced lung inflammation, and provide novel insights into CXCL5-driven pathogenesis.

SUBMITTER: Balamayooran G

PROVIDER: S-EPMC3402800 | biostudies-other | 2012 Jul

REPOSITORIES: biostudies-other

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Role of CXCL5 in leukocyte recruitment to the lungs during secondhand smoke exposure.

Balamayooran Gayathriy G Batra Sanjay S Cai Shanshan S Mei Junjie J Worthen G Scott GS Penn Arthur L AL Jeyaseelan Samithamby S

American journal of respiratory cell and molecular biology 20120223 1

Chronic obstructive pulmonary disease (COPD) is the third leading cause of mortality in the United States. The major cause of COPD is cigarette smoking. Extensive leukocyte influx into the lungs, mediated by chemokines, is a critical event leading to COPD. Although both resident and myeloid cells secrete chemokines in response to inflammatory stimuli, little is known about the role of epithelial-derived chemokines, such as CXC chemokine ligand (CXCL)5, in the pathogenesis of cigarette smoke-indu ...[more]

PMID: 22362385

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Project description:BackgroundAirports may represent significant sources of secondhand smoke (SHS) exposure for both travelers and employees. While previously common smoking rooms have largely disappeared from US airports, smoking continues to occur outdoors at terminal entrances. SHS may be especially high at arrival areas, since they oftentimes are partially enclosed by overhead departures, creating stagnant microenvironments. This study assessed particulate matter <2.5 microns in diameter (PM2.5), a common surrogate for SHS, at airport terminal locations to evaluate both outdoor exposure risk and possible indoor drift of SHS from outdoor sources.MethodsA convenience sample of nine airport terminal arrival areas in the US state of Florida was surveyed between February and July 2018. PM2.5 levels were assessed outdoors and indoors at terminal entrances and at control areas far into terminal interiors. We also examined the impact of smoking location on SHS exposure by correlating cigarette and passing vehicle counts with PM2.5 levels at terminals with contrasting proximity of designated smoking locations to terminal entrances.ResultsAlthough outdoor PM2.5 levels (mean 17.9, SD 6.1 µg/m3) were significantly higher than indoors (p < 0.001), there was no difference between indoor areas directly inside terminal entrances and areas much further interior (mean 8.8, SD 2.6 vs mean 8.5, SD 3.0 µg/m3, p=0.49). However, when smoking areas were in close proximity to terminal entrances, the number of lit cigarettes and vehicular traffic per minute predicted 70% of the variance of PM2.5 levels (p < 0.001), which was attributable mostly to the cigarette number (β = 0.83; 95% CI (0.55 to 1.11); p < 0.001). This effect was not observed at smoking areas further away.ConclusionPM2.5 data did not suggest indoor drift from outside smoking. Nevertheless, absolute exposure outdoors was high and correlated with the location of designated smoking areas. Further studies are needed to examine the effect of microclimate formation on exposure risk.

Project description:ImportanceSecondhand smoke is a substantial risk factor for youth health globally, including in Japan, where tobacco control policies should be reassessed.ObjectiveTo assess trends in the prevalence of secondhand smoke exposure among Japanese adolescents from 2008 to 2017 and to examine the association between its frequency and smoking during the study period.Design, setting, and participantsThis study comprised a nationally representative, self-administered, school-based, cross-sectional survey focusing on tobacco and alcohol use and related factors among students in grades 7 to 12 (ages 12-18 years) in Japan. This random sampling survey used single-stage cluster sampling. Using the national school directory, junior and senior high schools throughout Japan were randomly extracted from each regional block. All students enrolled in the sampled schools were included as participants, and school-based surveys were completed in 2008, 2012, and 2017. Data analysis was performed from January 1 to March 15, 2023.Main outcomes and measuresPrevalence of secondhand smoke exposure among adolescents in Japan from 2008 to 2017 and changes in the association between secondhand smoke exposure frequency and prevalence of smoking were examined using multiple logistic regression analysis.ResultsData were analyzed for 95 680 adolescents in 2008 (50.7% boys), 100 050 in 2012 (51.6% boys), and 64 152 in 2017 (53.9% boys). At baseline, 42.0%, 38.5%, and 34.6% of the participants were junior high school students in 2008, 2012, and 2017, respectively. Based on the 2008 surveys, 51.0% of adolescents in grades 7 to 12 were exposed to secondhand smoke in any place (≥1 day during the past 7 days), 37.2% were exposed at home, and 36.5% were exposed in public places. In 2017, 36.3% of participants were exposed to secondhand smoke in any place, 23.8% were exposed at home, and 27.0% were exposed in public places. An association between secondhand smoke exposure frequency and prevalence of smoking was observed consistently regardless of survey year, location, or pattern of exposure (adjusted odds ratios ranged from 2.29 [95% CI, 1.81-2.91] for 1-2 days at home to 11.15 [95% CI, 8.50-14.62] for 7 days in public places). Stratified analysis by higher education intention indicated that the prevalence of smoking and secondhand smoke exposure decreased but remained higher among adolescents who did not intend to pursue higher education. The association between secondhand smoke and smoking did not differ substantially between groups.Conclusions and relevanceIn this cross-sectional study, the prevalence of secondhand smoke exposure among adolescents in Japan decreased but remained at high levels overall. There may not be a hazard-free threshold for smoking. Enhancing comprehensive tobacco control strategies is Japan's first step toward achieving smoke-free environments to protect youths. Implementation and verification of the effectiveness of smoke-free legislation should be considered.

Dataset Information

Role of CXCL5 in leukocyte recruitment to the lungs during secondhand smoke exposure.

Publications

Role of CXCL5 in leukocyte recruitment to the lungs during secondhand smoke exposure.

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