Immunopathology of Allergy and Asthma in Childhood

Jones, C. H. W.; Holt, Patrick G.

doi:10.1164/ajrccm.162.supplement_1.maic-10

Cited by 12 publications

(11 citation statements)

References 34 publications

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“…Allergic asthma is associated with elevated numbers of EOS and neutrophils in the lung (34, 35). To determine whether maternal exposure to SS promoted leukocytic infiltration in the lung before and after an allergen challenge, prenatally FA- and SS-exposed animals were challenged through i.t.…”

Section: Resultsmentioning

confidence: 99%

Maternal Exposure to Secondhand Cigarette Smoke Primes the Lung for Induction of Phosphodiesterase-4D5 Isozyme and Exacerbated Th2 Responses: Rolipram Attenuates the Airway Hyperreactivity and Muscarinic Receptor Expression but Not Lung Inflammation and Atopy

Singh

Mishra

Rir-sima-ah

et al. 2009

The Journal of Immunology

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Airway hyperreactivity (AHR), lung inflammation, and atopy are clinical signs of allergic asthma. Gestational exposure to cigarette smoke (CS) markedly increases the risk for childhood allergic asthma. Muscarinic receptors regulate airway smooth muscle tone, and asthmatics exhibit increased AHR to muscarinic agonists. We have previously reported that in a murine model of bronchopulmonary aspergillosis maternal exposure to mainstream CS increases AHR after acute intratracheal administration of Aspergillus fumigatus extract (Af). However, the mechanism by which gestational CS induces allergic asthma is unclear. We now show for the first time that, compared to controls, mice exposed prenatally to secondhand CS exhibit increased lung inflammation (predominant infiltration by eosinophils and polymorphs), atopy, and airway resistance, and produce proinflammatory cytokines (IL-4, IL-5, IL-6, and IL-13, but not IL-2 or IFN-γ). These changes, which occur only after an allergen (Af) treatment, are correlated with marked upregulated lung expression of M1, M2, and M3 muscarinic receptors and phosphodiesterase-4D5 (PDE4D5) isozyme. Interestingly, the PDE4-selective inhibitor rolipram attenuates the increase in AHR, muscarinic receptors, and PDE4D5, but fails to downregulate lung inflammation, Th2 cytokines, or serum IgE levels. Thus, the fetus is extraordinarily sensitive to CS, inducing allergic asthma after postnatal exposure to allergens. While the increased AHR might reflect increased PDE4D5 and muscarinic receptor expression, the mechanisms underlying atopy and lung inflammation are unrelated to the PDE4 activity. Thus, PDE4 inhibitors might ease AHR, but are unlikely to attenuate lung inflammation and atopy associated with childhood allergic asthma.

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Section: Resultsmentioning

confidence: 99%

Maternal Exposure to Secondhand Cigarette Smoke Primes the Lung for Induction of Phosphodiesterase-4D5 Isozyme and Exacerbated Th2 Responses: Rolipram Attenuates the Airway Hyperreactivity and Muscarinic Receptor Expression but Not Lung Inflammation and Atopy

Singh

Mishra

Rir-sima-ah

et al. 2009

The Journal of Immunology

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“…Only 25% of sensitized individuals sensitized to 1 or more allergens go on to develop asthma. 39 Linneberg et al 40 showed that sensitivity to perennial allergens significantly increases one's risk of developing asthma compared to those sensitized to seasonal allergens. Seasonal AR patients had a 10-fold greater risk of developing asthma, compared to a 50-fold increase in risk for those who have perennial allergies.…”

Section: Relationships Between Asthma and Upper Airway Diseasementioning

confidence: 99%

Comorbidities of asthma and the unified airway

Stachler

2015

Int Forum Allergy Rhinol

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“…AR is not only associated with, but is also a risk factor for, the development of asthma . Treatment of rhinitis has been shown to improve asthma control . In patients who do not have asthma, early and aggressive management of rhinitis may even prevent the development of asthma in later life …”

Section: Armentioning

confidence: 99%