Paediatric allergy and asthma

Warner, John O.; Boner, Attilio

doi:10.1016/b978-0-7234-3658-4.00022-6

Cited by 2 publications

(1 citation statement)

References 10 publications

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“…There is also hypertrophy of smooth muscle and associated bronchial hyper-responsiveness (BHR). Many of these features sometimes manifest independent of allergy [2].…”

Section: Introductionmentioning

confidence: 99%

Asthma/Rhinitis (The United Airway) and Allergy: Chicken or Egg; Which Comes First?

Warner

2020

JCM

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While allergy, asthma and rhinitis do not inevitably co-exist, there are strong associations. Not all those with asthma are allergic, rhinitis may exist without asthma, and allergy commonly exists in the absence of asthma and/or rhinitis. This is likely due to the separate gene/environment interactions which influence susceptibility to allergic sensitization and allergic airway diseases. Allergic sensitization, particularly to foods, and eczema commonly manifest early in infancy, and not infrequently are followed by the development of allergic rhinitis and ultimately asthma. This has become known as the “allergic march”. However, many infants with eczema never develop asthma or rhinitis, and both the latter conditions can evolve without prior eczema or food allergy. Understanding the mechanisms underlying the ontogeny of allergic sensitization and allergic disease will facilitate rational approaches to the prevention and management of asthma and allergic rhinitis. Furthermore, a range of new, so-called biological, therapeutic approaches, targeting specific allergy-promoting and pro-inflammatory molecules, are now in clinical trials or have been recently approved for use by regulatory authorities and could have a major impact on disease prevention and control in the future. Understanding basic mechanisms will be essential to the employment of such medications. This review will explain the concept of the united airway (rhinitis/asthma) and associations with allergy. It will incorporate understanding of the role of genes and environment in relation to the distinct but interacting origins of allergy and rhinitis/asthma. Understanding the patho-physiological differences and varying therapeutic requirements in patients with asthma, with or without rhinitis, and with or without associated allergy, will aid the planning of a personalized evidence-based management strategy.

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“…There is also hypertrophy of smooth muscle and associated bronchial hyper-responsiveness (BHR). Many of these features sometimes manifest independent of allergy [2].…”

Section: Introductionmentioning

confidence: 99%

Asthma/Rhinitis (The United Airway) and Allergy: Chicken or Egg; Which Comes First?

Warner

2020

JCM

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Childhood asthma: causes, risks, and protective factors; a role of innate immunity

Noutsios¹,

Floros²

2014

Swiss Med Wkly

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Childhood asthma is an umbrella of multifactorial diseases with similar clinical features such as mast cell and eosinophil infiltration causing airway hyper responsiveness, inflammation, and airway obstruction. There are various factors that are implicated in childhood asthma pathogenesis. A combined contribution of genetic predisposition, environmental insults, and epigenetic changes account for polarisation of the immune system towards T helper (Th) type 2 cell responses that include production of pro-inflammatory cytokines, IgE, and eosinophil infiltrates, shown to associate with asthma. Environmental cues in prenatal, perinatal, and early childhood seem to determine development of asthma incidence or protection against it. Mode of birth delivery, use of antibiotics, oxidative stress, exposure to tobacco smoke and an industrialised lifestyle are significant contributors to childhood asthma exacerbation. Environmental stimuli such as exposure to maternal antibodies through breast milk, and certain early infections favour Th1 cell responses, leading to the production of anti-inflammatory cytokines that protect from asthma. Aside from the Th cell responses the role of innate immunity in the context of alveolar macrophages, dendritic cells, and surfactant protein A (SP-A) and SP-D is discussed. SP-A and SP-D enhance pathogen phagocytosis and cytokine production by alveolar macrophages, bind and clear pathogens, and interact with dendritic cells to mediate adaptive immunity responses. Further study of the interactions between genetic variants of genes of interest (SP-A and SP-D) and the environment may provide valuable knowledge about the underlying mechanisms of various interactions that differentially affect asthma susceptibility, disease severity, and reveal potential points for therapeutic interventions.

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Paediatric allergy and asthma

Cited by 2 publications

References 10 publications

Asthma/Rhinitis (The United Airway) and Allergy: Chicken or Egg; Which Comes First?

Asthma/Rhinitis (The United Airway) and Allergy: Chicken or Egg; Which Comes First?

Childhood asthma: causes, risks, and protective factors; a role of innate immunity

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