Cigarette smoke enhances Th-2 driven airway inflammation and delays inhalational tolerance

Hove, Chris L. Van; Moerloose, Katrien; Maes, Tania; Joos, Guy; Tournoy, Kurt G.

doi:10.1186/1465-9921-9-42

Cited by 49 publications

(43 citation statements)

References 47 publications

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“…[70][71][72] It will be important to determine in future studies if a similar relationship operates in healthy individuals, since it is conceivable that smoking will have distinct effects in the context of inflammation. 73 The functional significance of reduced TLR expression in smokers is unclear; it will be of interest to determine whether other intestinal cells, such as epithelial cells, also have reduced TLR expression in the context of smoking, as this may have significance for barrier integrity. 21 Blunted TLR2 and TLR4 expression on DC from smokers with CD may impair antimicrobial defenses in the intestinal tract.…”

Section: Discussionmentioning

confidence: 99%

Relationship between human intestinal dendritic cells, gut microbiota, and disease activity in Crohnʼs disease

Benjamin

McCarthy

et al. 2011

Inflammatory Bowel Diseases

101

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Section: Discussionmentioning

confidence: 99%

Relationship between human intestinal dendritic cells, gut microbiota, and disease activity in Crohnʼs disease

Benjamin

McCarthy

et al. 2011

Inflammatory Bowel Diseases

101

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“…The mechanisms mediating the adverse effects of smoking on asthma pathogenesis remain to be elucidated. Most murine models, designed to characterise the complex interaction between smoking and allergic airway inflammation, have relied on the sensitisation to the ''surrogate'' allergen ovalbumin (OVA) [13][14][15][16][17][18]. As OVA is an intrinsically inert protein, the role of cigarette smoke might have been overestimated in the past.…”

mentioning

confidence: 99%

Short cigarette smoke exposure facilitates sensitisation and asthma development in mice

et al. 2012

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Epidemiological studies indicate that cigarette smoke exposure is a risk factor for increased sensitisation and asthma development. The aim of this study was to examine the impact of cigarette smoke on sensitisation and allergic airway inflammation in response to a low dose of house dust mite (HDM), and to obtain potential mechanistic insights.Mice were exposed to low doses of HDM extract combined with air or cigarette smoke exposure, either during allergen sensitisation or during the development of allergic airway disease.Mice concomitantly exposed to low-dose HDM, combined with cigarette smoke for 3 weeks, demonstrated an asthmatic phenotype with significantly increased airway eosinophilia, goblet cell metaplasia, airway hyperresponsiveness and a rise in HDM-specific serum immunoglobulin G1, compared to sole HDM or cigarette smoke exposure. In addition, short cigarette smoke inhalation, during the initial contact with HDM allergens, was sufficient to facilitate sensitisation and development of a complete asthmatic phenotype after rechallenge with HDM. Mechanistically, short cigarette smoke exposure amplified dendritic cell-mediated transport of fluorescein isothiocyanate-labelled HDM allergens to the intrathoracic lymph nodes and generated a local T-helper cell type 2 response.Short cigarette smoke exposure is sufficient to facilitate allergic sensitisation and the development of low-dose HDM-induced allergic asthma, possibly by affecting dendritic cell function.

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“…Interestingly, in the cases where carbon dioxide is captured, inflammation is significantly decreased ( Figure 2B). We established an inflammatory score for each lung sample analyzed using a validated grading system (Curtis et al, 1991;Van Hove et al, 2008) and determined that the lungs exposed to cigarette smoke were highly inflamed. When carbon dioxide is partially trapped, the overall lung inflammation score dropped by two thirds ( Figure 2E).…”

Section: Resultsmentioning

confidence: 99%

“…The lungs were removed, treated with Hydrosafe solution, embedded in paraffin, and cut into 5-µm sections. Evaluation of overall histologic lung inflammation was performed using a semiquantitative and reproducible blinded scoring system (Curtis et al, 1991;Van Hove et al, 2008). For each animal, six lung sections stained with either hematoxylin, periodic acid-Schiff, or Massons trichrome were observed.…”

Section: Lung Histologymentioning

confidence: 99%

Carbon dioxide is largely responsible for the acute inflammatory effects of tobacco smoke

Schwartz¹,

Guais²,

Chaumet-Riffaud³

et al. 2010

Inhalation Toxicology

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Tobacco smoking is responsible for a vast array of diseases, particularly chronic bronchitis and lung cancer. It is still unclear which constituent(s) of the smoke is responsible for its toxicity. The authors decided to focus on carbon dioxide, since its level of concentration in mainstream cigarette smoke is about 200 times higher than in the atmosphere. The authors previously demonstrated that inhalation of carbon dioxide concentrations above 5% has a deleterious effect on lungs. In this study, the authors assessed the inflammatory potential of carbon dioxide contained in cigarette smoke. Mice were exposed to cigarette smoke containing a high or reduced CO(2) level by filtration through a potassium hydroxyde solution. The inflammatory response was evaluated by histological analysis, protein phosphatase 2 A (PP2A) and nuclear factor (NF)-kappaB activation, and proinflammatory cytokine secretion measurements. The data show that the toxicity of cigarette smoke may be largely due to its high level of CO(2). Pulmonary injuries consequent to tobacco smoke inhalation observed by histology were greatly diminished when CO(2) was removed. Cigarette smoke exposure causes an inflammatory response characterized by PP2A and NF-kappaB activation followed by proinflammatory cytokine secretion. This inflammatory response was reduced when the cigarette smoke was filtered through a potassium hydroxide column, and reestablished when CO(2) was injected downstream from the filtration column.Given that there is an extensive literature linking a chronic inflammatory response to the major smoking-related diseases, these data suggest that carbon dioxide may play a key role in the causation of these diseases by tobacco smoking.

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Cigarette smoke enhances Th-2 driven airway inflammation and delays inhalational tolerance

Abstract: Cigarette smoke enhances acute allergic inflammation and delays, but does not abrogate the development of tolerance due to prolonged challenge with inhaled antigen in experimental asthma.

Cited by 49 publications

References 47 publications

Relationship between human intestinal dendritic cells, gut microbiota, and disease activity in Crohnʼs disease

Relationship between human intestinal dendritic cells, gut microbiota, and disease activity in Crohnʼs disease

Short cigarette smoke exposure facilitates sensitisation and asthma development in mice

Carbon dioxide is largely responsible for the acute inflammatory effects of tobacco smoke

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