Environmental and lifestyle factors may act in concert to increase the prevalence of respiratory allergy including asthma

Steerenberg,; Amsterdam, Van; Vandebriel,; VOS, $$$; Bree, van Pj Patrick; Loveren, Van

doi:10.1046/j.1365-2222.1999.00658.x

Cited by 22 publications

(11 citation statements)

References 44 publications

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“…Thus, the timing of allergen exposure during one's lifetime, along with the frequency and intensity of exposure, play a crucial role in the establishment of tolerance or sensitization and the development of asthma. 22,23 The presumed impact on atopy of immune conditioning by prior microbial exposures is translated in the hygiene hypothesis postulating that reduced exposure to bacteria, viruses, and parasites in early childhood facilitates atopic sensitization, 1,24 probably because of a diminished induction of regulatory T cells. 25 Inversely, frequent stimulation of the innate immune system by environmental PAMPs such as lipopolysaccharide or by contact with livestock may diminish the risk of developing allergic sensitization.…”

Section: Role Of Danger-associated Signaling In Allergic Sensitizationmentioning

confidence: 99%

Where Asthma and Hypersensitivity Pneumonitis Meet and Differ

Bogaert

Tournoy

Naessens

et al. 2009

The American Journal of Pathology

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Asthma is a type-I allergic airway disease characterized by Th 2 cells and IgE. Episodes of bronchial inflammation, eosinophilic in nature and promoting bronchoconstriction, may become chronic and lead to persistent respiratory symptoms and irreversible structural airway changes. Representative mostly of mild to moderate asthma, this clinical definition fails to account for the atypical and often more severe phenotype found in a considerable proportion of asthmatics who have increased neutrophil cell counts in the airways as a distinguishing trait. Neutrophilic inflammation is a hallmark of another type of allergic airway pathology , hypersensitivity pneumonitis. Considered as an immune counterpart of asthma, hypersensitivity pneumonitis is a prototypical type-III allergic inflammatory reaction involving the alveoli and lung interstitium, steered by Th 1 cells and IgG and, in its chronic form, accompanied by fibrosis. Although pathologically very different and commonly approached as separate disorders, as discussed in this review, clinical studies as well as data from animal models reveal undeniable parallels between both airway diseases. Danger signaling elicited by the allergenic agent or by accompanying microbial patterns emerges as critical in enabling immune sensitization and in determining the type of sensitization and ensuing allergic disease. On this basis , we propose that asthma allergens cause severe noneosinophilic asthma because of sensitization in the presence of hypersensitivity pneumonitis-promoting danger signaling.

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Section: Role Of Danger-associated Signaling In Allergic Sensitizationmentioning

confidence: 99%

Where Asthma and Hypersensitivity Pneumonitis Meet and Differ

Bogaert

Tournoy

Naessens

et al. 2009

The American Journal of Pathology

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“…The introduction of vaccinations and antibiotics, smaller family sizes and better hygiene are associated with atopy. The common denominator to these factors is decreased microbial stimulation [8,[12][13][14][15][16][17]. Also, altered patterns of food consumption [18,19] and increased exposure and sensitization to indoor allergens [20][21][22][23] are considered important cofactors for the development of atopic disease in westernized societies.…”

Section: Introductionmentioning

confidence: 99%

Do parents with an atopic family history adopt a ‘prudent’ lifestyle for their infant? (KOALA Study)

Kummeling

Thijs

Stelma

et al. 2006

Clin Experimental Allergy

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SummaryBackground Atopic parents may adopt lifestyle characteristics that allegedly protect against atopic disease. If this is true, infants from atopic parents will be characterized by low-risk behaviour. Consequently, aetiologic studies on lifestyle factors and allergic disease in childhood may be biased by confounding by indication. Objective We explored whether the prevalence of 'prudent' lifestyle characteristics differs between atopic and non-atopic families. Methods Information about a family history of atopic manifestations and lifestyle characteristics was collected by repeated questionnaires in the Dutch KOALA Birth Cohort Study in 2469 infants from families with divergent lifestyle practices (conventional vs. alternative). Results In conventional lifestyle families, infants were less often exposed to environmental tobacco smoke when parents were atopic than when they were non-atopic (10.0% vs. 14.7%, P = 0.001). In alternative lifestyle families, exposure to smoking was very rare in both groups (1.7% vs. 2.6%). Pets were less often present in families with than without parental atopy (38.8% vs. 51.1%, P = 0.008 for conventional lifestyle families; 43.0% vs. 48.4%, P = 0.014 for alternative lifestyle families). Infants with atopic siblings had less often been vaccinated according to the standard scheme than infants with non-atopic siblings in conventional lifestyle families (76.6% vs. 85.5%, P o 0.001). In alternative lifestyle families, the difference was in the same direction but not statistically significant (30.1% vs. 40.5%, P = 0.143). Antibiotic use, breastfeeding and consumption of organic foods were unrelated to a family history of atopic manifestations. Conclusion Some 'prudent' lifestyle characteristics differed between atopic and non-atopic families, depending on whether atopic manifestations were present in parents or older siblings. This has important consequences for the validity in epidemiological studies on the aetiology of allergy in children. Confounding by indication because of a family history of atopic manifestations can best be controlled for by considering atopy in parents and siblings as separate confounders.

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“…Thus, the temporal arrangement of matter exposure throughout one's lifespan, at the side of the frequency and intensity of exposure, play an important role within the institution of tolerance or sensitization and therefore the development of asthma [22,23]. The likely impact on type I allergic reaction of immune learning by previous microbic exposures is translated within the hygiene hypothesis postulating that reduced exposure to microorganism, viruses, and parasites in time of life facilitates atopic sensitization, in all probability attributable to a diminished induction of restrictive T cells [25]. Inversely, frequent stimulation of the innate system by environmental PAMPs like lipopolysaccharide or by contact with placental could diminish the chance of developing allergic sensitization.…”

Section: Role Of Danger-associated Signal In Allergic Sensitizationmentioning

confidence: 99%

Noneosinophilic Severe Asthma

Peter¹,

Kirey²,

Naessens³

et al. 2017

J Blood Lymph

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Asthma could be a type-I allergic airway illness characterized by Th2 cells and immunoglobulin. Episodes of cartilaginous tube inflammation, white corpuscle in nature and promoting bronchoconstriction, could become chronic and result in persistent metabolism symptoms and irreversible structural airway changes. Representative largely of delicate to moderate bronchial asthma, this clinical definition fails to account for the atypical and infrequently additional severe makeup found during a tidy proportion of asthmatics United Nations agency have augmented white blood cell counts within the airways as a characteristic attribute. Neutrophilic inflammation could be a hallmark of another sort of allergic airway pathology, hypersensitivity redness. Thought-about as associate degree immune counterpart of bronchial asthma, hypersensitivity redness could be a prototypic type-III allergic inflammatory reaction involving the alveoli and respiratory organ interstitium, steered by Th1 cells and immune serum globulin and, in its chronic type, among pathology. Though pathologically terribly completely different and ordinarily approached as separate disorders, as mentioned during this review, clinical studies also as information from animal models reveal simple parallels between each airway diseases. Danger communication induced by the matter agent or by incidental to microorganism patterns emerges as vital in facultative immune sensitization and in deciding the sort of sensitization and succeeding allergic illness. On this basis, we have a tendency to propose that allergens cause severe noneosinophilic asthma attributable to sensitization within the presence of hypersensitivity pneumonitispromoting danger communication.

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Environmental and lifestyle factors may act in concert to increase the prevalence of respiratory allergy including asthma

Cited by 22 publications

References 44 publications

Where Asthma and Hypersensitivity Pneumonitis Meet and Differ

Where Asthma and Hypersensitivity Pneumonitis Meet and Differ

Do parents with an atopic family history adopt a ‘prudent’ lifestyle for their infant? (KOALA Study)

Noneosinophilic Severe Asthma

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