Respiratory epithelial cell innate immunity against <i>Mycobacterium tuberculosis</i> is deregulated by air pollution particulate matter (PM) (INC7P.417)

Schwander, Stephan; Cantarella, Pasquale; Sarkar, Srijata; Rockafellow, Megan; Rivas‐Santiago, César

doi:10.4049/jimmunol.192.supp.186.18

The Journal of Immunology

2014

DOI: 10.4049/jimmunol.192.supp.186.18

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Respiratory epithelial cell innate immunity against Mycobacterium tuberculosis is deregulated by air pollution particulate matter (PM) (INC7P.417)

Stephan Schwander

Pasquale Cantarella

Srijata Sarkar

et al.

Abstract: Epidemiological studies demonstrate a link between exposure to indoor air pollution and cigarette smoke and risk of development of Tuberculosis (TB). The role of ambient air pollution PM in human antimycobacterial immunity has not been studied. We examined the effects of PM (<2.5 and <10 μm diameter, from Mexico City) on Mycobacterium tuberculosis (M.tb)-induced expression of mRNA and protein of human β-defensin 2 and 3 (HBD-2,3, antimicrobial peptides), IL-8 and MCP-1 by qRT-PCR and ELISA, respe… Show more

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Association of air pollution with the risk of initial outpatient visits for tuberculosis in Wuhan, China

Liao

Yin

et al. 2019

Occup Environ Med

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ObjectivesPrevious studies suggested the association of air pollution with initial Mycobacterium tuberculosis infection and the disease development. However, few studies have been conducted on air pollution and initial tuberculosis (TB) consults using short-interval data. We investigated the weekly association between air pollution and initial TB outpatient visits.MethodsWe used a Poisson regression model combined with a distributed lag non-linear model to conduct a time-series study with weekly air pollution data and TB cases during 2014–2017 in Wuhan, China.ResultsA 10 µg/m3 increase in NO2 (nitrogen dioxide) was associated with 11.74% (95% CI: 0.70 to 23.98, lag 0–1 weeks), 21.45% (95% CI: 1.44 to 45.41, lag 0–2 weeks) and 12.8% (95% CI: 0.97 to 26.02, lag 0–1 weeks) increase in initial TB consults among all patients with TB, old patients (≥60 years old) and male ones, respectively. A 10 µg/m3 increase in SO2 (sulfur dioxide) was associated with −22.23% (95% CI: −39.23 to −0.49, lag 0–16 weeks), −28.65% (95% CI: −44.3 to −8.58, lag 0–16 weeks), −23.85 (95% CI: −41.79 to −0.37, lag 0–8 weeks) and −23.82% (95% CI: −41.31 to −1.11, lag 0–16 weeks) increase in initial TB consults among the total, young (aged 15–59 years old), old and male patients, respectively. In old patients, a 0.1 mg/m3 increase in CO (carbon monoxide) and a 10 µg/m3 increase in PM2.5 (particulate matter) were separately associated with 42.32% (95% CI: 1.16 to 100.22, lag 0–16 weeks) and 17.38% (95% CI: 0.28 to 37.38, lag 0–16 weeks) increases in TB consults.ConclusionOur study first highlighted the importance of weekly association between air pollution and the risk of initial TB consults, which is helpful for the arrangements of TB screening and medical assistance.

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Association of air pollution with the risk of initial outpatient visits for tuberculosis in Wuhan, China

Liao

Yin

et al. 2019

Occup Environ Med

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Water-pipe smoke condensate increases the internalization of Mycobacterium Bovis of type II alveolar epithelial cells (A549)

et al. 2017

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BackgroundTuberculosis (TB) is a major global health problem, and there is an association between tobacco smoke and TB. Water pipe smoking has become an increasing problem not only in Middle Eastern countries but also globally because users consider it as safer than cigarettes. The presence of high levels of toxic substances in water-pipe smoke may be a predisposing factor that enhances the incidence of pulmonary disorders. For example, uncontrolled macropinocytosis in alveolar epithelial cells following exposure to water-pipe smoke may predispose subjects to pulmonary infection. Here, we studied the effects of water-pipe condense (WPC) on the internalization of Mycobacterium Bovis BCG by macropinocytosis in the alveolar epithelial cell line A549.MethodsA549 cells were exposed to WPC (4 mg/ml) for 24, 48, 72 and 96 h. Cell viability was studied using the methyl thiazolyldipenyl-tetrazolium bromide (MTT) reduction assay and proliferation by bromodeoxyUridine (BrdU) incorporation. Cells were exposed to FITC-Dextran (1 mg/ml) (as a control) and FITC-BCG (MOI = 10) for 20 min at 37 °C before cells were collected and the uptake of BCG-FITC determined by flow cytometry. Similar experiments were performed at 4 °C as a control. The Rho-associated protein kinase (ROCK) inhibitor Y-27632 (1 μM) was used to assess the mechanism by which WPC enhanced BCG uptake.ResultsWPC (4 mg/ml) increased the uptake of BCG-FITC after 72 (1.3 ± 0.1 fold, p < 0.05) and 96 (1.4 ± 0.05 fold, p < 0.05) hours. No effect on BCG-FITC uptake was observed at 24 or 48 h. WPC also significantly increased the uptake of FITC-Dextran (2.9 ± 0.3 fold, p < 0.05) after 24 h. WPC significantly decreased cell viability after 24 (84 ± 2%, p < 0.05), 48 (78±, 3%, p < 0.05), 72 (64 ± 2%, p < 0.05) and 96 h (45 ± 2%, p < 0.05). Y-27632 completely attenuated the increased uptake of BCG by WPC. Cell proliferation showed a decreasing trend in a time-dependent manner with WPC exposure.ConclusionWPC exposure increased epithelial cell endocytosis activity and death as well as enhancing their capacity for macropinocytosis. Our in vitro data indicates possible harmful effects of WPC on the ability of lung epithelial cells to phagocytose mycobacterium.

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Respiratory epithelial cell innate immunity against Mycobacterium tuberculosis is deregulated by air pollution particulate matter (PM) (INC7P.417)

Cited by 2 publications

References 0 publications

Association of air pollution with the risk of initial outpatient visits for tuberculosis in Wuhan, China

Association of air pollution with the risk of initial outpatient visits for tuberculosis in Wuhan, China

Water-pipe smoke condensate increases the internalization of Mycobacterium Bovis of type II alveolar epithelial cells (A549)

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