Effect of cigarette smoking on the humoral immune response in pigeon fanciers

Carrillo, Teresa; Castro, Felipe Rodrı́guez de; Cuevas, M.; Díaz, Fernando; Cabrera, P.

doi:10.1111/j.1398-9995.1991.tb00580.x

Cited by 39 publications

(21 citation statements)

References 8 publications

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“…Hypersensitivity pneumonitis is known to contribute to 5−15% of ILD burden [10]. Cigarette smoke is believed to have an immunosuppressive effect on alveolar macrophages and thus hypersensitivity pneumonitis is less common in smokers [8]. This is consistent with our study, in which all the diagnosed subjects were non-smokers.…”

Section: Discussionsupporting

confidence: 92%

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Bird Fancier’s Lung: Clinical-Radiological Presentation in 15 Cases

Kumar

Singh²

2015

Advances in Respiratory Medicine

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Introduction: Bird fancier's lung (BFL) is a type of hypersensitivity pneumonitis occurring in response to avian antigens (usually inhaled proteins in bird feathers and droppings). The diagnosis is based on a combination of clinical, radiological, and biopsy characteristics. The present study was planned to highlight the clinico-radiological presentation in cases of BFL. Material and methods:The present study is a retrospective analysis of cases of bird fancier's lung diagnosed in a unit of Vallabhbhai Patel Chest Institute over a period of two years, from 2013−2014. The clinico-radiological features of the subjects were analysed. The diagnosis of BFL was made as per criteria laid down by Mark Schuyler and Yvon Cormier. Results: There were a total of fifteen cases diagnosed with BFL during the study period, comprising twelve females and three males with a mean age of 54.93 ± 14.21 years. All the studied subjects gave significant history of exposure to pigeons and were non-smokers. The period of symptoms prior to presentation varied from one to eight years. The main symptoms on presentation were exertional breathlessness and cough. Radiologically, diffuse centrilobular nodules, ground glassing -diffuse or patchy predominant in upper lobes, fibrosis with or without traction bronchiectasis, honeycombing, and mediastinal lymphadenopathy were seen. Bronchoscopy showed ill-defined granulomas and chronic interstitial inflammation. Conclusions: BFL can exhibit a wide range of radiological patterns, and a high index of suspicion must be maintained, with particular attention to detailed exposure history in every case of interstitial lung disease.

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Section: Discussionsupporting

confidence: 92%

“…The prevalence rates of pigeon-related hypersensitivity pneumonitis was found to be 1−10% in people highly exposed to pigeons [8,9]. In the present study all the diagnosed subjects gave significant history of exposure to pigeons.…”

Section: Discussionsupporting

confidence: 44%

Bird Fancier’s Lung: Clinical-Radiological Presentation in 15 Cases

Kumar

Singh²

2015

Advances in Respiratory Medicine

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“…In these experiments, after RW sensitization an i.t. allergen challenge was given either once (day 11) or on three consecutive days (days [11][12][13]. Although a single challenge with RW in RW-sensitized animals caused a robust increase in the expression of Th2 cytokines, the effects of NT treatment in these single RW-challenged animals was so strong that we were unable to detect any difference in the production of Th2 cytokines between CON and NRW rats (not shown).…”

Section: Nicotine Strongly Down-regulates Allergen-induced Th2 Cytokinesmentioning

confidence: 44%

“…Increasing evidence suggests that smokers have lower incidences of allergic and lung inflammatory diseases (3,4,10,11); however, the mechanism by which cigarette smoke modulates the allergic responses is not yet well understood. Allergic asthma is a Th2 disease and, in animal models of allergic asthma, airway inflammation is intimately associated with the increased production of Th2 cytokines and chemokines, particularly IL-13, IL-4, IL-5, and eotaxin (22,23,44).…”

Section: Discussionmentioning

confidence: 99%

Nicotine Primarily Suppresses Lung Th2 but Not Goblet Cell and Muscle Cell Responses to Allergens

Mishra

Rir-sima-ah

Langley

et al. 2008

The Journal of Immunology

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Allergic asthma, an inflammatory disease characterized by the infiltration and activation of various leukocytes, the production of Th2 cytokines and leukotrienes, and atopy, also affects the function of other cell types, causing goblet cell hyperplasia/hypertrophy, increased mucus production/secretion, and airway hyperreactivity. Eosinophilic inflammation is a characteristic feature of human asthma, and recent evidence suggests that eosinophils also play a critical role in T cell trafficking in animal models of asthma. Nicotine is an anti-inflammatory, but the association between smoking and asthma is highly contentious and some report that smoking cessation increases the risk of asthma in ex-smokers. To ascertain the effects of nicotine on allergy/asthma, Brown Norway rats were treated with nicotine and sensitized and challenged with allergens. The results unequivocally show that, even after multiple allergen sensitizations, nicotine dramatically suppresses inflammatory/allergic parameters in the lung including the following: eosinophilic/lymphocytic emigration; mRNA and/or protein expression of the Th2 cytokines/chemokines IL-4, IL-5, IL-13, IL-25, and eotaxin; leukotriene C4; and total as well as allergen-specific IgE. Although nicotine did not significantly affect hexosaminidase release, IgG, or methacholine-induced airway resistance, it significantly decreased mucus content in bronchoalveolar lavage; interestingly, however, despite the strong suppression of IL-4/IL-13, nicotine significantly increased the intraepithelial-stored mucosubstances and Muc5ac mRNA expression. These results suggest that nicotine modulates allergy/asthma primarily by suppressing eosinophil trafficking and suppressing Th2 cytokine/chemokine responses without reducing goblet cell metaplasia or mucous production and may explain the lower risk of allergic diseases in smokers. To our knowledge this is the first direct evidence that nicotine modulates allergic responses.

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“…Any hypothesis needs to account for the contrary situation in which airway inflammatory stimuli appear to protect against lung immunological injury. For example, the granulomatous inflammatory diseases sarcoidosis and extrinsic allergic alveolitis are less common in smokers [47,48]. Whether the interaction between particular inflammatory stimuli produces distinctive and readily recognisable pathological changes is another important area for further study.…”

Section: How Do Multiple Inflammatory Stimuli Results In More Severe Amentioning

confidence: 99%

Multiple inflammatory hits and the pathogenesis of severe airway disease: Fig. 1—

Pavord¹,

Birring²,

Berry³

et al. 2006

Eur Respir J

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Refractory or difficult-to-control asthma is associated with some clinical and pathological features normally associated with chronic obstructive pulmonary disease (COPD), raising the possibility that there are similarities in their pathogenesis. It is suggested that the coexistence of two or more inflammatory stimuli to the airway (multiple hits) is a key factor leading to the development of more severe airway disease. Airway inflammation in response to chronic inflammatory conditions elsewhere may be a particularly important additional inflammatory stimulus. The “multiple hit” hypothesis for the origins of severe airway disease has important implications for treatment and prevention, since identification and removal of additional inflammatory stimuli may delay progression of the underlying airway disease.

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Effect of cigarette smoking on the humoral immune response in pigeon fanciers

Cited by 39 publications

References 8 publications

Bird Fancier’s Lung: Clinical-Radiological Presentation in 15 Cases

Bird Fancier’s Lung: Clinical-Radiological Presentation in 15 Cases

Nicotine Primarily Suppresses Lung Th2 but Not Goblet Cell and Muscle Cell Responses to Allergens

Multiple inflammatory hits and the pathogenesis of severe airway disease: Fig. 1—

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