Is the increase in asthma prevalence linked to increase in allergen load?

Woolcock, Ann J.; Peat, Jennifer K.; Trevillion, Louise

doi:10.1111/j.1398-9995.1995.tb02504.x

Cited by 69 publications

(36 citation statements)

References 55 publications

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“…Despite this limitation, the presence of Th2-associated biomarkers has been confirmed as a characteristic feature of the human asthmatic airway (1,2), but beyond that qualitative conclusion little is known regarding precisely how Th2 immunity functions in the human airway to drive acute asthma symptoms. Understanding the pathogenesis of the human disease is also complicated by the evidence indicating that while Th2-associated atopy is a major risk factor for asthma, only a small proportion of humans sensitized to aeroallergens develop significant airway symptoms (6). This contrasts with the reproducible respiratory response profiles of sensitized/aerosol-challenged animals, and suggests that additional cofactors are operative in the human disease that are not accounted for in current experimental models.…”

mentioning

confidence: 53%

Interactions between Innate Antiviral and Atopic Immunoinflammatory Pathways Precipitate and Sustain Asthma Exacerbations in Children

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Bizzintino

Mamessier

et al. 2009

The Journal of Immunology

188

172

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Severe asthma exacerbations in children requiring hospitalization are typically associated with viral infection and occur almost exclusively among atopics, but the significance of these comorbidities is unknown. We hypothesized that underlying interactions between immunoinflammatory pathways related to responses to aeroallergen and virus are involved, and that evidence of these interactions is detectable in circulating cells during exacerbations. To address this hypothesis we used a genomics-based approach involving profiling of PBMC subpopulations collected during exacerbation vs convalescence by microarray and flow cytometry. We demonstrate that circulating T cells manifest the postactivated “exhausted” phenotype during exacerbations, whereas monocyte/dendritic cell populations display up-regulated CCR2 expression accompanied by phenotypic changes that have strong potential for enhancing local inflammation after their recruitment to the atopic lung. Notably, up-regulation of FcεR1, which is known to markedly amplify capacity for allergen uptake/presentation to Th2 effector cells via IgE-mediated allergen capture, and secondarily programming of IL-4/IL-13-dependent IL-13R+ alternatively activated macrophages that have been demonstrated in experimental settings to be a potent source of autocrine IL-13 production. We additionally show that this disease-associated activation profile can be reproduced in vitro by cytokine exposure of atopic monocytes, and furthermore that IFN-α can exert both positive and negative roles in the process. Our findings suggest that respiratory viral infection in atopic children may initiate an atopy-dependent cascade that amplifies and sustains airway inflammation initiated by innate antiviral immunity via harnessing underlying atopy-associated mechanisms. These interactions may account for the unique susceptibility of atopics to severe viral-induced asthma exacerbations.

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mentioning

confidence: 53%

Interactions between Innate Antiviral and Atopic Immunoinflammatory Pathways Precipitate and Sustain Asthma Exacerbations in Children

Subrata

Bizzintino

Mamessier

et al. 2009

The Journal of Immunology

188

172

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“…Among these are increased indoor allergen load, changes in immune response with increasing antibiotic use and increased rate of vaccinations, changes in air pollution and diet, improved survival of premature infants, increase in smoking rate of mothers, and increase in sedentary lifestyle with associated decreased lung expansion. 2,5,21,22 Although the cause of the seasonal increases found in this study is not established, the fall and spring asthma peaks correlate with both environmental allergen levels and rhinovirus seasons. Tree pollen levels in the Charleston area are highest in April, weed pollen levels are highest in October, and peak rhinovirus activity is highest in the fall and spring in nearby areas.…”

Section: Discussionmentioning

confidence: 89%

“…It is unlikely, however, that the Charleston black population has seen a steady increase in indoor allergen load since 1970 to explain the increase in asthma. 21,22,28 Another theory deserves consideration. It is known that among urban black populations there is an association between obesity and asthma.…”

Section: Discussionmentioning

confidence: 99%

Asthma Hospitalization Trends in Charleston, South Carolina, 1956 to 1997: Twenty-fold Increase Among Black Children During a 30-Year Period

et al. 2001

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ABSTRACT. Objective. The increase in asthma prevalence has been documented worldwide, affecting many races living in many different climates. Multiple studies have demonstrated that the most striking prevalence and morbidity of asthma in the United States has been in black children, but little research has determined the scale of the increase, or specifically when the disease became severe in this group. This study sought to determine exactly when the rise in asthma hospitalizations among black patients began and what the pattern of asthma hospitalizations has been in different races and age groups over a 40-year period in 1 urban area.Methods. A retrospective chart review of discharges from the Medical University of South Carolina was conducted from 1956 to 1997. Charts with the primary discharge diagnosis of asthma were examined for discharge date, race, and age group (0-to 4-year-olds, 5-to 18-yearolds, 19-to 50-year-olds, >51-year-olds). The diagnostic codes used were based on the International Classification of Diseases (ICD)-6, 1956 -1957; ICD-7, 1958 -1967; ICD-8, 1968 -1978; and ICD-9, 1979 -1997. Over the period studied, this hospital was the primary inpatient provider for children in this area, and the only provider for uninsured children. Between 1960 and 1990, the racial makeup of the area remained stable, as did the percentage of blacks living at the poverty level. The raw number of asthma discharges, rate per 10 000 discharges of the same race, and rate per 100 000 population in Charleston County were tabulated for each age group and racial category.Results. Over the time period examined, there has been a progressive increase in asthma hospitalizations in black individuals of all age groups and in whites under 18 years. The most striking increase has been in black children 0 to 18 years old (Figure). The increase either as raw values or as a rate per 100 000 began around 1970, and was linear. This increase in black children discharged with asthma as a rate per 100 000 population was 20-fold: the rate increased from 18 in 1970 to 370 in 1997. Asthma discharges as a rate per 10 000 black children discharged increased by 24-fold from 1960 to 1997. Total discharges from the hospital increased from 49 000 to 128 000 per year over this period. Blacks made up only 28% of discharges in 1957, but that proportion increased to 56% in 1960 and remained relatively stable over the following 35 years. The increase seen in white children 0 to 18 years of age as a rate per 100 000 population was 5-fold and began around 1980. Both increases seem to be consistent over the time period studied, and continued to 1997.Conclusions. Among a predominantly poor black population living in a southern US city, there has been a steady increase in childhood asthma hospitalizations over the past 30 years. A significant although less dramatic rise has occurred in white children. Over this time period, although there have been many changes in lifestyle that could have contributed to this rise, there have been no major changes in hou...

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“…This Th memory generation process in many individuals appears to be complete by the end of the preschool or early school years, potentially locking individuals into lifelong patterns of allergen responsiveness. However, as discussed later, this memory generation process is not the sole determinant of clinical responder phenotype, in particular in relation to asthma, as only a subset of children sensitized to inhalant allergens go on to develop persistent wheeze [19].…”

Section: T-cell Immunity To Inhalant Allergens: the Basis Of Variatiomentioning

confidence: 99%

“…2) The symptomatology associated with the sensitization to inhalants during childhood does not usually progress beyond intermittent wheeze, and severe long-term sequelae appear restricted to a subset of atopics [19] manifesting high levels of Th2-mediated inflammation [56][57][58] and subsequent airway remodelling [57,58].…”

Section: The Apparent Dualistic Effects Of Respiratory Tract Infectiomentioning

confidence: 99%

Interactions between respiratory tract infections and atopy in the aetiology of asthma: Fig. 1.—

Holt

Sly²

2002

Eur Respir J

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The prevalence of asthma, in particular atopic asthma, has markedly increased in recent years. Accumulating evidence suggests that environmental factors associated with allergic sensitization and exposure to microbial stimuli during infancy and early childhood, are associated with these changes in prevalence. However, considerable controversy surrounds the role of microbial agents, as evidence has been presented for both positive and negative effects in this context.The review below focuses upon interactions between immune competence during infancy, the development of T-helper (Th)1-polarized versus Th2-polarized memory against inhalant allergens, and susceptibility to virus infection. In particular, recent finding are highlighted which suggest that delayed postnatal maturation of Th1 function is associated with increased risk for early postnatal sensitization to inhalant allergens, and also with risk for viral bronchiolitis during infancy.Variations in the kinetics of postnatal maturation of T-helper 1 function may in part be attributable to polymorphisms in the CD14 gene, which influence host responsiveness both to bacterial as well as viral stimuli. It is evident from a wide range of studies carried out in different geographical areas, that the prevalence of allergic diseases, and in particular atopic asthma, has increased markedly over the last 2-3 decades. Moreover, the increases become evident in successive birth cohorts during early childhood. It is also generally accepted that "diagnostic shift" is not a significant factor in these changes. Accordingly, given the timeframe over which the changes have occurred, the responsible factor(s) must be environmental, presumably interacting with one or more susceptibility genes.The search for the relevant genetic and environmental factors continues, and a variety of potential candidates have been identified. Prominent amongst these are factors related to respiratory infections, particularly those occurring in childhood. Paradoxically, these infections have been invoked both as potential protective factors in relation to asthma/ allergy development, and as triggers of asthma exacerbations in atopic asthmatics. The mechanisms by which these effects may be mediated are incompletely understood; however, recent findings suggest some intriguing new possibilities, which are discussed in this review. T-cell immunity to inhalant allergens: the basis of variations in responder phenotype within the adult populationThe epithelial surface of the upper and lower respiratory tract are continuously exposed to an array of pathogenic and nonpathogenic airborne antigens, and the induction and local expression of local T-cell immunity must accordingly be tightly controlled, in order to avoid the pathological consequences of chronic T-cell-driven inflammation. While it is highly plausible that resistance to airborne pathogens is a direct function of the speed of mobilization and the intensity of expression of local innate and adaptive immune mechanisms in the lung, the conve...

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Is the increase in asthma prevalence linked to increase in allergen load?

Cited by 69 publications

References 55 publications

Interactions between Innate Antiviral and Atopic Immunoinflammatory Pathways Precipitate and Sustain Asthma Exacerbations in Children

Interactions between Innate Antiviral and Atopic Immunoinflammatory Pathways Precipitate and Sustain Asthma Exacerbations in Children

Asthma Hospitalization Trends in Charleston, South Carolina, 1956 to 1997: Twenty-fold Increase Among Black Children During a 30-Year Period

Interactions between respiratory tract infections and atopy in the aetiology of asthma: Fig. 1.—

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