Synergism between rhinovirus infection and oxidant pollutant exposure enhances airway epithelial cell cytokine production.

Spannhake, E. W.; Reddy, Sekhar P.; Jacoby, David B.; Yu, Xiao; Saatian, Bahman; Tian, Jingyan

doi:10.1289/ehp.02110665

Cited by 104 publications

(83 citation statements)

References 38 publications

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“…Studies indicate that virus-induced inflammation in the upper and lower respiratory tract may be exacerbated by concurrent exposure to low levels of diesel exhaust particulate matter, nitrogen dioxide and ozone commonly encountered in indoor and outdoor environments [51,52].…”

Section: Discussionmentioning

confidence: 99%

Household Conditions, Eczema Symptoms and Rhinitis Symptoms: Relationship with Wheeze and Severe Wheeze in Children Living in the Polokwane Area, South Africa

Wichmann

Wolvaardt

Maritz

et al. 2008

Matern Child Health J

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Background This is the fifth study that applied the International Study of Asthma and Allergies in Childhood (ISAAC) methodology in the Southern African Development Community (SADC region). However, it is the first ISAAC study that focused on 6-to 7-year-old children living in South Africa and that also investigated the association between potential risk factors and asthma symptoms. Objective To assess the 12-month prevalence of wheeze and severe wheeze along with their potential risk factors. Setting Within a 60-km radius from the Polokwane city centre, Limpopo Province. Methods The survey was conducted during August 2004 and February 2005. Parents/guardians of 6-to 7-year-old children completed the questionnaires in English, Afrikaans or North-Sotho. However, the statistical analyses were restricted to the North-Sotho group (n = 2,437). Results The 12-month prevalence rates of wheeze and severe wheeze were 11.2% and 5.7%, respectively. The 12-month prevalence rates of eczema symptoms and rhinoconjunctivitis symptoms were 8.0% and 7.3%, respectively. Living in a rural area significantly decreased the likelihood of wheeze by 31%. Exposure to environmental tobacco smoke at home and the presence of eczema symptoms and rhinoconjunctivitis symptoms increased the likelihood of wheeze by 77%, 104% and 226%, respectively. Only the presence of rhinoconjunctivitis symptoms increased the likelihood of severe wheeze by 107%. Conclusion Wheeze appears to be an emerging public health problem in the Polokwane area. Hopefully, detailed analytical intervention studies will further explicate these results in the near future.

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Section: Discussionmentioning

confidence: 99%

Household Conditions, Eczema Symptoms and Rhinitis Symptoms: Relationship with Wheeze and Severe Wheeze in Children Living in the Polokwane Area, South Africa

Wichmann

Wolvaardt

Maritz

et al. 2008

Matern Child Health J

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“…Human nasal epithelial (HNE) cells were isolated following typical procedures, as previously described (35). After overnight digestion of the tissues at 4°C in 0.01% protease Sigma type XIV (Sigma, St. Louis, MO) in Ham's F-12 medium containing penicillin (100 U/ml; GIBCO, Gaithersburg, MD), streptomycin (100 g/ml, GIBCO), amphotericin B (2.5 g/ml, GIBCO), and gentamicin (50 g/ml, GIBCO), the protease was neutralized by the addition of 10% fetal calf serum (Invitrogen), and the epithelial cells were freed from the tissue by agitation and isolated by centrifugation.…”

Section: Methodsmentioning

confidence: 99%

Expression of genes for B7-H3 and other T cell ligands by nasal epithelial cells during differentiation and activation

Saatian¹,

Yu²,

Lane³

et al. 2004

American Journal of Physiology-Lung Cellular and Molecular Phys

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Epithelial cells of the human respiratory tract express human leukocyte antigen (HLA) and the costimulatory molecules B7-1 and B7-2. Little is known, however, about the constitutive expression of genes encoding for the more recently identified members of the B7 homolog family of costimulatory molecules or about the influence of cellular differentiation and cytokines on their activity or on that of HLA or B7-1 and B7-2. Human nasal epithelial (HNE) cells were grown at the air-liquid interface (ALI) for 2 or 21 days to model in vivo conditions. Expression of genes for HLA-B and HLA-DR1 increased during mucociliary differentiation during this period and became more similar to HNE cells obtained fresh by brush biopsy from nasal turbinates. Gene transcripts for B7-H3 and B7-H2 were abundantly expressed in cells cultured at the ALI, but neither their activities nor that of B7-2 was significantly altered during differentiation. IFN-gamma and TNF-alpha upregulated mRNA encoding for both HLA molecules, but not for the B7 molecules. This study describes, for the first time, the expression of B7-H3 and B7-H2 by HNE cells and thus expands the range of potential costimulatory signals through which these cells may interact with activated mucosal T lymphocytes. In addition, the results suggest that the extent of mucociliary differentiation of cultured cells may influence this capability

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“…Asthma and COPD are commonly exacerbated by bacterial and viral infections (3,24) that can often coexist and synergize with pollutant exposure (8,46). Inhalation of small particulate matter is also a major cause of airway inflammation, and rising air pollution levels are associated with elevated mortality and increased hospital admissions in individuals with respiratory diseases such as asthma and COPD (2,10,45).…”

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confidence: 99%

Diesel exhaust particles override natural injury-limiting pathways in the lung

Chaudhuri

Paiva

Donaldson³

et al. 2010

American Journal of Physiology-Lung Cellular and Molecular Phys

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tion of effective inflammation in the lung in response to environmental and microbial stimuli is dependent on cooperative signaling between leukocytes and lung tissue cells. We explored how these inflammatory networks are modulated by diesel exhaust particles (DEP) using cocultures of human monocytes with epithelial cells. Cocultures, or monoculture controls, were treated with DEP in the presence or absence of LPS or flagellin. Production of cytokines was explored by Western blotting and ELISA; cell signaling was analyzed by Western blotting. Here, we show that responses of epithelial cells to DEP are amplified by the presence of monocytes. DEP amplified the responses of cellular cocultures to very low doses of TLR agonists. In addition, in the presence of DEP, the responses induced by LPS or flagellin were less amenable to antagonism by the physiological IL-1 antagonist, IL-1ra. This was paralleled by the uncoupling of IL-1 production and release from monocytes, potentially attributable to an ability of DEP to sequester or degrade extracellular ATP. These data describe a model of inflammation where DEP amplifies responses to low concentrations of microbial agonists and alters the nature of the inflammatory milieu induced by TLR agonists.cocultures; inflammation; interleukin-1; Toll-like receptors ENVIRONMENTAL EXPOSURE to microbial products through the inhalation of bacterial fragments, such as LPS, has long been associated with exacerbations of airway disease, and levels of LPS within the environment can correlate with severity of asthma (30,38). Asthma and COPD are commonly exacerbated by bacterial and viral infections (3, 24) that can often coexist and synergize with pollutant exposure (8, 46). Inhalation of small particulate matter is also a major cause of airway inflammation, and rising air pollution levels are associated with elevated mortality and increased hospital admissions in individuals with respiratory diseases such as asthma and COPD (2, 10, 45).Diesel exhaust particles (DEP) are the major particulate matter of air pollution and comprise a nanoparticular carbonaceous core, multiple organic components such as polyaromatic hydrocarbons (PAH), transition metals, and adsorbed materials such as pollen and dust. Their small size (5-20 nm; 100-nm aggregates) means that they are often denoted nanoparticles and favors their deposition in the lung (7, 11). Acute and chronic inhalation of DEP in healthy individuals, and those with preexisting respiratory disease, results in respiratory toxicity with consequent development of lung edema, infiltration of polymorphonuclear leukocytes, and the production of proinflammatory cytokines and reactive oxygen species (ROS) (5,36,44,47).The active inflammation that occurs in asthma and COPD leads to the recruitment of monocytes to the alveolar wall (28). Furthermore, urban particulate matter has been shown to cause the release of monocytes from the bone marrow (17, 23). We have previously shown that effective inflammatory responses to bacterial-derived stimuli are media...

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Synergism between rhinovirus infection and oxidant pollutant exposure enhances airway epithelial cell cytokine production.

Cited by 104 publications

References 38 publications

Household Conditions, Eczema Symptoms and Rhinitis Symptoms: Relationship with Wheeze and Severe Wheeze in Children Living in the Polokwane Area, South Africa

Household Conditions, Eczema Symptoms and Rhinitis Symptoms: Relationship with Wheeze and Severe Wheeze in Children Living in the Polokwane Area, South Africa

Expression of genes for B7-H3 and other T cell ligands by nasal epithelial cells during differentiation and activation

Diesel exhaust particles override natural injury-limiting pathways in the lung

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