Cigarette smoke exposure facilitates allergic sensitization in mice

Moerloose, Katrien; Robays, Lander; Maes, Tania; Brusselle, Guy; Tournoy, Kurt G.; Joos, Guy

doi:10.1186/1465-9921-7-49

Cited by 74 publications

(64 citation statements)

References 30 publications

(38 reference statements)

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“…1B), and marked airway goblet cell hyperplasia on histological airway sections (Fig. 1C), fully consistent with earlier observations in this model (17). In line with the goblet cell hyperplasia, we observed a strong induction of pulmonary IL-13 mRNA expression in mice concomitantly exposed to OVA and cigarette smoke compared with OVA alone (Fig.…”

Section: Simultaneous Exposure To Cigarette Smoke and Ova Induces Allsupporting

confidence: 80%

“…Blood was collected by cardiac puncture for measurement of total and OVA-specific IgE with a homemade ELISA as described before (17).…”

Section: Measurement Of Ova-specific Igementioning

confidence: 99%

“…We and others recently established a mouse model in which concomitant inhalation of aerosolized OVA along with mainstream cigarette smoke, without prior immunization, induces features of allergic airway inflammation (16,17). This allergic response was absent after exposure to OVA alone, suggesting a prominent role for cigarette smoking in the establishment of an OVA-specific Th2 immune response.…”

mentioning

confidence: 99%

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Concomitant Inhalation of Cigarette Smoke and Aerosolized Protein Activates Airway Dendritic Cells and Induces Allergic Airway Inflammation in a TLR-Independent Way

Robays

Lanckacker

Moerloose

et al. 2009

The Journal of Immunology

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Cigarette smoking is associated with the development of allergic asthma. In mice, exposure to cigarette smoke sensitizes the airways toward coinhaled OVA, leading to OVA-specific allergic inflammation. Pulmonary dendritic cells (DCs) are professional APCs involved in immunosurveillance and implicated in the induction of allergic responses in lung. We investigated the effects of smoking on some of the key features of pulmonary DC biology, including trafficking dynamics and cellular activation status in different lung compartments. We found that cigarette smoke inhalation greatly amplified DC-mediated transport of inhaled Ags to mediastinal lymph nodes, a finding supported by the up-regulation of CCR7 on airway DCs. Pulmonary plasmacytoid DCs, which have been involved in inhalational tolerance, were reduced in number after smoke exposure. In addition, combined exposure to cigarette smoke and OVA aerosol increased surface expression of MHC class II, CD86, and PDL2 on airway DCs, while ICOSL was strongly down-regulated. Although inhaled endotoxins, which are also present in cigarette smoke, have been shown to act as DC activators and Th2-skewing sensitizers, TLR4-deficient and MyD88 knockout mice did not show impaired eosinophilic airway inflammation after concomitant exposure to cigarette smoke and OVA. From these data, we conclude that cigarette smoke activates the pulmonary DC network in a pattern that favors allergic airway sensitization toward coinhaled inert protein. The TLR independency of this phenomenon suggests that alternative immunological adjuvants are present in cigarette smoke.

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Section: Simultaneous Exposure To Cigarette Smoke and Ova Induces Allsupporting

confidence: 80%

“…Blood was collected by cardiac puncture for measurement of total and OVA-specific IgE with a homemade ELISA as described before (17).…”

Section: Measurement Of Ova-specific Igementioning

confidence: 99%

mentioning

confidence: 99%

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Concomitant Inhalation of Cigarette Smoke and Aerosolized Protein Activates Airway Dendritic Cells and Induces Allergic Airway Inflammation in a TLR-Independent Way

Robays

Lanckacker

Moerloose

et al. 2009

The Journal of Immunology

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“…As smoke has adjuvant property [5,7,8], these cells play important roles in the exacerbation of asthmatic airway inflammation [4,5]. And, IL-4 plays an important role in B cell growth, differentiation, and secretion of IgE and IL-13 [40,41].…”

Section: Discussionmentioning

confidence: 99%

Cigarette smoke exacerbates mouse allergic asthma through Smad proteins expressed in mast cells

et al. 2011

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BackgroundMany studies have found that smoking reduces lung function, but the relationship between cigarette smoke and allergic asthma has not been clearly elucidated, particularly the role of mast cells. This study aimed to investigate the effects of smoke exposure on allergic asthma and its association with mast cells.MethodsBALB/c mice were sensitized and challenged by OVA to induce asthma, and bone marrow-derived mast cells (BMMCs) were stimulated with antigen/antibody reaction. Mice or BMMCs were exposed to cigarette smoke or CSE solution for 1 mo or 6 h, respectively. The recruitment of inflammatory cells into BAL fluid or lung tissues was determined by Diff-Quik or H&E staining, collagen deposition by Sircol assay, penh values by a whole-body plethysmography, co-localization of tryptase and Smad3 by immunohistochemistry, IgE and TGF-β level by ELISA, expressions of Smads proteins, activities of signaling molecules, or TGF-β mRNA by immunoblotting and RT-PCR.ResultsCigarette smoke enhanced OVA-specific IgE levels, penh values, recruitment of inflammatory cells including mast cells, expressions of smad family, TGF-β mRNA and proteins, and cytokines, phosphorylations of Smad2 and 3, and MAP kinases, co-localization of tryptase and Smad3, and collagen deposition more than those of BAL cells and lung tissues of OVA-induced allergic mice. CSE solution pretreatment enhanced expressions of TGF-β, Smad3, activities of MAP kinases, NF-κB/AP-1 or PAI-1 more than those of activated-BMMCs.ConclusionsThe data suggest that smoke exposure enhances antigen-induced mast cell activation via TGF-β/Smad signaling pathways in mouse allergic asthma, and that it exacerbates airway inflammation and remodeling.

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“…However, other studies in asthmatic patients have failed to find any relationship between MTS and asthma (Siroux, 2000;Vidal, 2004). Even in experimental animal models, the impact of MTS on OVA-induced asthmatic responses in mice is controversial (Robbins, 2005;Moerloose, 2005Moerloose, , 2006Thatcher, 2008). Thus, the difference between the effects of ETS and MTS on asthma should be further analyzed in experimental studies.…”

mentioning

confidence: 99%

Aggravation of Allergic Rhinitis by Air Pollution: Demonstration by an Animal Model of Pollenosis

Nabe¹,

Mizutani²

2011

Advanced Topics in Environmental Health and Air Pollution Case Studies

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Cigarette smoke exposure facilitates allergic sensitization in mice

Abstract: Background: Active and passive smoking are considered as risk factors for asthma development. The mechanisms involved are currently unexplained.

Cited by 74 publications

References 30 publications

Concomitant Inhalation of Cigarette Smoke and Aerosolized Protein Activates Airway Dendritic Cells and Induces Allergic Airway Inflammation in a TLR-Independent Way

Concomitant Inhalation of Cigarette Smoke and Aerosolized Protein Activates Airway Dendritic Cells and Induces Allergic Airway Inflammation in a TLR-Independent Way

Cigarette smoke exacerbates mouse allergic asthma through Smad proteins expressed in mast cells

Aggravation of Allergic Rhinitis by Air Pollution: Demonstration by an Animal Model of Pollenosis

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