The mechanism or mechanisms driving atopic asthma initiation: The infant respiratory microbiome moves to center stage

Holt, Patrick G.

doi:10.1016/j.jaci.2015.05.011

Cited by 44 publications

(30 citation statements)

References 94 publications

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“…The data obtained in this study supports the view of A.D. Ado et al [28][29][30] about the role of Neisseria perflata and Staph. аureus in the appearance and development of BA.…”

Section: Figuresupporting

confidence: 91%

“…3 The risk of developing severe bronchial asthma is particularly high when the child is exposed to airborne allergens and a viral infection. 4 Patients with atopic BA are also highly susceptible to viral infections, especially by the rhinovirus. 5 Patients with BA have an increased susceptibility to bacterial infections, particularly pneumococcal.…”

Section: The Susceptibility Of Patients With Allergies To Infectionmentioning

confidence: 99%

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Infectious and Non-Infectious Sensitisation of Patients with Bronchial Asthma and Chronic Obstructive Pulmonary Disease

Gb¹

2016

JLPRR

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The study involved 169 people, of which 33 were practically healthy, 69 had bronchial asthma, 24 had bronchial asthma combined with chronic obstructive pulmonary disease, 35 had COPD and 8 had community-acquired pneumonia. We assessed the presence of IgE to tick allergens, dust allergens, and the combined allergens of grass, trees, weeds and flower pollen. We determined the presence of IgE and IgG to the allergens Strept. рneumon., Haemofil. influenzae, Neisseria рerflava and Staph. аureus. We assessed the presence, multiplicity, severity and combination of sensitisation to the presence of specialised IgE towards infectious and atopic allergens. All study groups displayed sensitisation, including heaslthy people and patients with COPD and community-acquired pneumonia, who did not show clinical allergy symptoms. A statistically significant direct correlation was established between IgG and IgE to Strept. Pneumoniae and Haemofilus influenza in healthy subjects and those with pulmonary conditions. The IgE or IgG reaction to Neisseria perflava and Staph. аureus did not show a significant correlation in either healthy or affected subjects.Keywords: sensitization, allergy, mild bronchial asthma, immunoglobulin, allergen, food, industry, drug-related and other allergens, and every year new names are added to this list. The 15 most clinically common allergens are considered to be the main ones with diagnostic complexes being created for sensitisation diagnosis, which use specialised IgE. Using skin samples with airborne allergens, the rates of sensitisation in patients with BA varies between 51% and 81.9%. 16 The main fundamental mechanism of sensitisation is the formation of specialised IgE.17 There is a correlation between levels of specialised IgE, total IgE, the results of skin allergy testing, and BA severity.18 Patients with mild and moderate BA have a significant correlation between levels of specialised IgE to non-infectious allergens and the results of skin tests, the acetylcholine inhalation test, and the exhaled nitric oxide content. 19It is important to note that sensitisation and the related appearance of antigen-specific IgE antibodies is not necessarily accompanied by clinical allergy symptoms. 20 Therefore, sensitisation that manifests as an increased content of specialised class IgE antibodies can occur in people without allergy symptoms, including practically healthy people, as well as in people with allergies. An allergy is the combination of sensitisation (increased number of antigen-specific IgE antibodies) and clinical signs of an allergic condition. 21The sensitivity to airborne allergens does not decrease with time. 19 The biochemical properties of allergens and the sensitivity of respiratory epithelium to their active components can increase the permeability of the respiratory mucous membrane to respiratory allergens. Many allergens contain serine, cysteine and other proteases, which disrupt the barrier function of the respiratory epithelium and increase the allergenic effect of respirat...

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“…The data obtained in this study supports the view of A.D. Ado et al [28][29][30] about the role of Neisseria perflata and Staph. аureus in the appearance and development of BA.…”

Section: Figuresupporting

confidence: 91%

Section: The Susceptibility Of Patients With Allergies To Infectionmentioning

confidence: 99%

Infectious and Non-Infectious Sensitisation of Patients with Bronchial Asthma and Chronic Obstructive Pulmonary Disease

Gb¹

2016

JLPRR

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“…That bacteria colonizing the airways in the neonatancy and infancy might also shape the response to allergen exposure and to viral respiratory infection is also possible [56], but is beyond the scope of this review, especially since it is elegantly addressed by A. Beigelman in this edition.…”

Section: Early Life Environment Bronchial Microbiome and Asthma Devmentioning

confidence: 99%

The microbiome and development of allergic disease

Lynch

Boushey²

2016

Current Opinion in Allergy &Amp; Clinical Immunology

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Purposes of review First, to review how the global rise in prevalence of asthma prompted studies of the relationships between microbial exposure in early infancy, the rate and pattern of development of immune function, and the development of allergic sensitization and of wheezing in childhood. And, second, to review how those studies laid the groundwork for a possible strategy for primary prevention of asthma through manipulation of the microbiome of the gastrointestinal and/or respiratory tracts. Recent findings Atopy and asthma are complex diseases thought to result from a “gene-by-environment” interaction; the rapidity of their rise in prevalence points to a change in environment as most likely causal. Epidemiologic studies noting associations between events in infancy and later development of atopic diseases have suggested that their rise in prevalence is related to a deficiency in microbial exposure in early life. The findings from birth cohort studies of humans and from interventional studies of mice converge in suggesting that a deficiency in microbial colonization of the respiratory or gastrointestinal tract by certain commensal microbes results in skewed development of systemic and/or local immune function that increases susceptibility to allergic sensitization and to viral lower respiratory infection. Recent studies are now honing in on identifying the microbes, or collection of microbes, whose collective functions are necessary for induction of immune tolerance, and thus of reduced susceptibility. Summary Atopy and asthma appear to have their roots in an insufficiency of early life exposure to the diverse environmental microbiota necessary to ensure colonization of the gastrointestinal and/or respiratory tracts with the commensal microbes necessary for induction of balanced, toleragenic immune function. Identification of the commensal bacteria necessary, now ever closer at hand, will lay the groundwork for the development of strategies for primary prevention of atopic disease, especially of childhood asthma.

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“…A detailed description of mechanisms that may mediate the progression from severe RSV LRTI to asthma is beyond the scope of this review and are discussed elsewhere 12–14 .…”

Section: The Role Of Early Life Respiratory Viral Infections In Asthmmentioning

confidence: 99%

Early-life respiratory infections and asthma development

Beigelman

Bacharier

2016

Current Opinion in Allergy &Amp; Clinical Immunology

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Purpose of review To present recent findings and perspectives on the relationship between early life respiratory infections and asthma inception and to discuss emerging concepts on strategies that target these infectious agents for asthma prevention. Recent findings Cumulative evidence supports the role of early life viral infections, especially respiratory syncytial virus and human rhinovirus, as major antecedents of childhood asthma. These viruses may have different mechanistic roles in the pathogenesis of asthma. The airway microbiome and virus-bacteria interactions in early life have emerged as additional determinants of childhood asthma. Innovative strategies for the prevention of these early life infections, or for attenuation of acute infection severity, are being investigated and may identify effective strategies for the primary and secondary prevention of childhood asthma. Summary Early life infections are major determinants of asthma development. The pathway from early life infections to asthma is the result of complex interactions between the specific type of the virus, genetic and environmental factors. Novel intervention strategies that target these infectious agents have been investigated in proof-of-concepts trials, and further study is necessary to determine their capacity for asthma prevention.

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The mechanism or mechanisms driving atopic asthma initiation: The infant respiratory microbiome moves to center stage

Cited by 44 publications

References 94 publications

Infectious and Non-Infectious Sensitisation of Patients with Bronchial Asthma and Chronic Obstructive Pulmonary Disease

Infectious and Non-Infectious Sensitisation of Patients with Bronchial Asthma and Chronic Obstructive Pulmonary Disease

The microbiome and development of allergic disease

Early-life respiratory infections and asthma development

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