Secondhand Smoke Induces Allergic Sensitization in Mice

Rumold, Robert; Jyrala, Minna; Díaz-Sánchez, David

doi:10.4049/jimmunol.167.8.4765

Cited by 75 publications

(54 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The increased numbers of peribronchial eosinophils in mice exposed to chronic ETS and chronic OVA was associated with a trend to increased levels of eosinophil active cytokines and chemokines such as IL-5 and eotaxin-1. Increased expression of Th2 cytokines such as IL-5 have previously been noted in studies of mice exposed to ETS and acute OVA allergen (17,18). Increased expression of eotaxin-1 in mice coexposed to ETS and OVA has not been previously reported.…”

Section: Discussionmentioning

confidence: 99%

Coexposure to Environmental Tobacco Smoke Increases Levels of Allergen-Induced Airway Remodeling in Mice

Min

Song

Miller

et al. 2007

The Journal of Immunology

View full text Add to dashboard Cite

Environmental tobacco smoke (ETS) can increase asthma symptoms and the frequency of asthma attacks. However, the contribution of ETS to airway remodeling in asthma is at present unknown. In this study, we have used a mouse model of allergen-induced airway remodeling to determine whether the combination of chronic exposure to ETS and chronic exposure to OVA allergen induces greater levels of airway remodeling than exposure to either chronic ETS or chronic OVA allergen alone. Mice exposed to chronic ETS alone did not develop significant eosinophilic airway inflammation, airway remodeling, or increased airway hyperreactivity to methacholine. In contrast, mice exposed to chronic OVA allergen had significantly increased levels of peribronchial fibrosis, increased thickening of the smooth muscle layer, increased mucus, and increased airway hyperreactivity which was significantly enhanced by coexposure to the combination of chronic ETS and chronic OVA allergen. Mice coexposed to chronic ETS and chronic OVA allergen had significantly increased levels of eotaxin-1 expression in airway epithelium which was associated with increased numbers of peribronchial eosinophils, as well as increased numbers of peribronchial cells expressing TGF-β1. These studies suggest that chronic coexposure to ETS significantly increases levels of allergen-induced airway remodeling (in particular smooth muscle thickness) and airway responsiveness by up-regulating expression of chemokines such as eotaxin-1 in airway epithelium with resultant recruitment of cells expressing TGF-β1 to the airway and enhanced airway remodeling.

show abstract

Section: Discussionmentioning

confidence: 99%

Coexposure to Environmental Tobacco Smoke Increases Levels of Allergen-Induced Airway Remodeling in Mice

Min

Song

Miller

et al. 2007

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…In mice, SHS exposure has an adjuvant effect, characterized by an increase in antigen-specific IgE, elevated Th2 responses, and influx of eosinophils into the lungs (7,8). It is unclear which of the more than 6,000 compounds in sidestream tobacco smoke act as adjuvants; however, other particulate pollutants resulting from incomplete combustion of organic materials, such as ambient particulate matter and diesel exhaust, contain many of the constituents of SHS, such as polyaromatic hydrocarbons, suggesting that a spectrum of xenobiotics in the environment can contribute to enhancement of responses to allergens (9,17,(39)(40)(41).…”

Section: Table 5 Correlation Of Differences In Nasal Allergic Endpoimentioning

confidence: 99%

“…The explanation for the heightened sensitivity among those with allergic airway diseases is likely multifactorial, but involves synergistic effects of SHS and allergens in initiating and exacerbating allergic airway diseases (6)(7)(8). In conjunction with allergen, SHS can act to enhance IgE antibody responses, T-helper cell (Th) 2 cytokine production, and histamine release in vivo (6).…”

Section: What This Study Adds To the Fieldmentioning

confidence: 99%

GlutathioneS-Transferases M1 and P1 Prevent Aggravation of Allergic Responses by Secondhand Smoke

Gilliland

Gong

et al. 2006

Am J Respir Crit Care Med

Self Cite

View full text Add to dashboard Cite

Rationale: Secondhand tobacco smoke (SHS) and traffic-related air pollutants are associated with asthma and allergy. Diesel exhaust particles (DEPs) and SHS can interact with allergens in exacerbating allergic airway diseases through generation of reactive oxygen species. Glutathione S-transferases (GSTs) metabolize reactive oxygen species and detoxify electrophilic xenobiotics present in SHS and DEPs. Objectives: We tested the hypotheses that functional GSTM1-null genotype and GSTP1 codon 105 variants (Ile105 and Val105) are determinants of allergic responses to SHS, and that responses to SHS and DEPs are correlated. Methods and Measurements: In a randomized, placebo-controlled crossover trial, 19 ragweed allergen-sensitive subjects who had previously participated in a DEP trial were challenged intranasally with allergen after having been exposed to either clean air or SHS at separate visits. Nasal allergen-specific IgE, histamine, IL-4, and IFN-␥ levels were measured before and after allergen challenge. Main Results: Individuals with GSTM1-null or GSTP1 Ile105 genotypes showed larger nasal responses to allergens with SHS compared with clean air. GSTM1-null subjects had a larger increase in IgE than GSTM1-present subjects (median, 173.3 vs. 46.7 U/ml; p ϭ 0.03), and the Ile105 GSTP1 genotype subjects had increased histamine (median, 10.2 vs. 4.6 nM; p ϭ 0.01) after SHS plus allergen challenge. Responses to SHS and DEPs were correlated. Enhancement of IgE and histamine was greatest in the subjects with both the GSTM1-null and GSTP1 Ile/Ile genotypes. Conclusions: GSTM1 and GSTP1 are important cytoprotective factors that reduce SHS and DEP exacerbation of allergic responses.

show abstract

“…We (Seymour et al, 1998) and others (McMenamin et al, 1994) have shown that repeated exposure of naive adult mice to aerosolized OVA resulted in IgE unresponsiveness. However Rumold et al (2001) have demonstrated that exposure of naïve adult mice to aerosolized OVA along with ETS resulted in elevated levels of serum IgE and eosinophils in the BAL. These observations prompted an interest in further investigating the effects of ETS on exposure to a clinically relevant and more complex antigen.…”

Section: Introductionmentioning

confidence: 99%

Second‐Hand Smoke Increases Bronchial Hyperreactivity and Eosinophilia in a Murine Model of Allergic Aspergillosis

Seymour

Schelegle

Pinkerton

et al. 2003

Journal of Immunology Research

View full text Add to dashboard Cite

Involuntary inhalation of tobacco smoke has been shown to aggravate the allergic response. Antibodies to fungal antigens such as Aspergillus fumigatus (Af) cause an allergic lung disease in humans. This study was carried out to determine the effect of environmental tobacco smoke (ETS) on a murine model of allergic bronchopulmonary aspergillosis (ABPA). BALB/c mice were exposed to aged and diluted sidestream cigarette smoke to simulate 'second-hand smoke'. The concentration was consistent with that achieved in enclosed public areas or households where multiple people smoke. During exposure, mice were sensitized to Af antigen intranasally. Mice that were sensitized to Af antigen and exposed to ETS developed significantly greater airway hyperreactivity than did mice similarly sensitized to Af but housed in ambient air. The effective concentration of aerosolized acetylcholine needed to double pulmonary flow resistance was significantly lower in Af þ ETS mice compared to the Af þ AIR mice. Immunological data that supports this exacerbation of airway hyperresponsiveness being mediated by an enhanced type 1 hypersensitivity response include: eosinophilia in peripheral blood and lung sections. All Af sensitized mice produced elevated levels of IL4, IL5 and IL10 but no IFN-g indicating a polarized Th2 response. Thus, ETS can cause exacerbation of asthma in ABPA as demonstrated by functional airway hyperresponsiveness and elevated levels of blood eosinophilia.

show abstract

Secondhand Smoke Induces Allergic Sensitization in Mice

Cited by 75 publications

References 33 publications

Coexposure to Environmental Tobacco Smoke Increases Levels of Allergen-Induced Airway Remodeling in Mice

Coexposure to Environmental Tobacco Smoke Increases Levels of Allergen-Induced Airway Remodeling in Mice

GlutathioneS-Transferases M1 and P1 Prevent Aggravation of Allergic Responses by Secondhand Smoke

Second‐Hand Smoke Increases Bronchial Hyperreactivity and Eosinophilia in a Murine Model of Allergic Aspergillosis

Contact Info

Product

Resources

About