Airway inflammatory responses to diesel exhaust in allergic rhinitics

Larsson, Nirina; Brown, Joanna; Stenfors, Nikolai; Wilson, Susan J.; Mudway, Ian; Pourazar, Jamshid; Behndig, Annelie F.

doi:10.3109/08958378.2013.765932

Cited by 14 publications

(19 citation statements)

References 43 publications

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“…MPO, produced by neutrophils, serves as a surrogate marker for this inflammation [19]. Previous reports have shown that DE can increase neutrophil counts and MPO concentration in bronchial samples [41,43]. The concentration of MPO is also responsive to allergen; MPO increases in BWs from asthmatics after segmental allergen [44], and in NLF after nasal challenge in patients with allergic rhinitis [45].…”

Section: Discussionmentioning

confidence: 99%

Effect of controlled human exposure to diesel exhaust and allergen on airway surfactant protein D, myeloperoxidase and club (Clara) cell secretory protein 16

Biagioni

Tam

Chen

et al. 2016

Clin Experimental Allergy

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These findings suggest that allergen and DE variably influence different aspects of the innate immune response of the lung. SPD and MPO, known markers of allergic inflammation in the lung, are strongly increased by allergen while DE has a minor effect therein. DE induces a loss of CC16, a protective protein, while allergen has a minor effect therein. Results support site- and exposure-specific responses in the human lung upon multiple exposures.

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Section: Discussionmentioning

confidence: 99%

Effect of controlled human exposure to diesel exhaust and allergen on airway surfactant protein D, myeloperoxidase and club (Clara) cell secretory protein 16

Biagioni

Tam

Chen

et al. 2016

Clin Experimental Allergy

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“…The prevalence of NAEB varied from country to country, it was hard to provide a convincing explanation for the high prevalence of NAEB in our study. It is possible that the high air pollution in Guangzhou could be a factor contributing to the high prevalence of NAEB in our study because air pollution has been shown to have an effect on airway inflammation . However, because we did not measure exposure or air pollution, this is only a speculation.…”

Section: Discussionmentioning

confidence: 90%

“…It is possible that the high air pollution in Guangzhou could be a factor contributing to the high prevalence of NAEB in our study because air pollution has been shown to have an effect on airway inflammation. [28][29][30] However, because we did not measure exposure or air pollution, this is only a speculation.…”

Section: Discussionmentioning

confidence: 99%

Eosinophilic airway inflammation is common in subacute cough following acute upper respiratory tract infection

et al. 2016

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Background and objective: Patients presenting with refractory postinfectious cough may respond to glucocorticosteroids but it is unclear whether airway eosinophilic inflammation exists in those patients. We aimed to determine the airway inflammation and causes of subacute cough following acute upper respiratory tract infection (AURTI). Methods: One hundred and sixteen patients with persistent cough lasting 3-8 weeks after upper respiratory tract infection were evaluated with differential cell count in induced sputum, spirometry and methacholine bronchial challenge testing. Results: In patients with subacute cough, sputum eosinophilia (median 8.5%,3.0-73.0%) was identified in 35 (33.6%) patients, 22 (18.5%) without bronchial hyperresponsiveness (BHR) were diagnosed as nonasthmatic eosinophilic bronchitis (NAEB), 13 (14.3%) of whom with BHR were diagnosed as cough variant asthma (CVA). Cough in patients with sputum eosinophilia improved after treatment with corticosteroids. Compared with postinfectious cough (PIC) and NAEB, CVA had significantly higher median eosinophil count in induced sputum (0.5% vs 7.5% vs 20.0%, P < 0.01). MMEF in CVA was significantly lower than PIC and NAEB (P < 0.05). The common causes of subacute cough following acute upper respiratory tract infection (AURTI) were PIC (37.8%), NAEB (18.5%), CVA (14.3%) and upper airway cough syndrome (UACS) (10.1%). Atopic cough (AC) (5.2%) and gastroesophageal refluxrelated cough (GERC) (3.4%) were less common in subacute cough following AURTI, while 9 (7.8%) patients had unexplained cough. Conclusion: Subacute cough following AURTI can be attributed to different entities, eosinophilic airway inflammation is common. Induced sputum should be considered when evaluating patients with subacute cough following acute upper respiratory tract infection.

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“…Many studies have reported associations between short-term exposure to air pollution and acute changes in inflammatory markers, such as increase in pulmonary interleukin (IL-6) measured in exhaled breath condensate (Behndig et al 2006;Kongerud et al 2006;Thompson et al 2010), as well as systemic IL-6 and TNFa levels in adult populations (Tsai et al 2012), including subgroups with preexisting chronic inflammatory conditions (Rückerl et al 2007). However, others failed to demonstrate associations with IL-6 (Bräuner et al 2008;Panasevich et al 2009;Zuurbier et al 2011) or TNF-a (Bräuner et al 2008;Larsson et al 2013). Studies of long-term exposure to air pollution demonstrate mixed effects on blood markers of systemic inflammation (Chuang et al 2011;Forbes et al 2009;Mostafavi et al 2015;Panasevich et al 2009).…”

Section: Introductionmentioning

confidence: 99%

Exposure to traffic-related air pollution and serum inflammatory cytokines in children

Gruzieva¹,

Merid²,

Gref³

et al. 2016

ISEE Conference Abstracts

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BACKGROUND: Long-term exposure to ambient air pollution can lead to adverse health effects in children; however, underlying biological mechanisms are not fully understood. OBJECTIVES: We evaluated the effect of air pollution exposure during different time periods on mRNA expression as well as circulating levels of inflammatory cytokines in children. METHODS:We measured a panel of 10 inflammatory markers in peripheral blood samples from 670 8-y-old children in the Barn/Child, Allergy, Milieu, Stockholm, Epidemiology (BAMSE) birth cohort. Outdoor concentrations of nitrogen dioxide (NO 2 ) and particulate matter (PM) with aerodynamic diameter <10 lm (PM 10 ) from road traffic were estimated for residential, daycare, and school addresses using dispersion modeling. Timeweighted average exposures during infancy and at biosampling were linked to serum cytokine levels using linear regression analysis. Furthermore, gene expression data from 16-year-olds in BAMSE (n = 238) were used to evaluate links between air pollution exposure and expression of genes coding for the studied inflammatory markers. RESULTS: A 10 lg=m 3 increase of NO 2 exposure during infancy was associated with a 13.6% (95% confidence interval (CI): 0.8; 28.1%) increase in interleukin-6 (IL-6) levels, as well as with a 27.8% (95% CI: 4.6, 56.2%) increase in IL-10 levels, the latter limited to children with asthma. However, no clear associations were observed for current exposure. Results were similar using PM 10 , which showed a high correlation with NO 2 . The functional analysis identified several differentially expressed genes in response to air pollution exposure during infancy, including IL10, IL13, and TNF. CONCLUSION: Our results indicate alterations in systemic inflammatory markers in 8-y-old children in relation to early-life exposure to traffic-related air pollution. https://doi.

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Airway inflammatory responses to diesel exhaust in allergic rhinitics

Cited by 14 publications

References 43 publications

Effect of controlled human exposure to diesel exhaust and allergen on airway surfactant protein D, myeloperoxidase and club (Clara) cell secretory protein 16

Effect of controlled human exposure to diesel exhaust and allergen on airway surfactant protein D, myeloperoxidase and club (Clara) cell secretory protein 16

Eosinophilic airway inflammation is common in subacute cough following acute upper respiratory tract infection

Exposure to traffic-related air pollution and serum inflammatory cytokines in children

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