Deposition of Inhaled Pollen and Pollen Extract in Human Airways

Wilson, Archie F.; Novey, Harold S.; Berke, Raymond A.; Surprenant, Edgar L.

doi:10.1056/nejm197305172882006

Cited by 118 publications

(55 citation statements)

References 5 publications

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“…Similar increases in airway hyperresponsiveness and airway inflammation have been described by several other groups who have studied these indices during natural pollen exposure [7,33]. The experimental approach of using conventional allergen challenge to study pathophysiology of asthma has been criticized [34]. The main reason for this criticism is the fact that allergen challenge involved brief single exposure to a high dose of allergen, which would not often occur in the everyday life of the majority of asthmatics.…”

Section: Discussionmentioning

confidence: 87%

Increases in airway eosinophils and interleukin-5 with minimal bronchoconstriction during repeated low-dose allergen challenge in atopic asthmatics

Sulakvelidze¹,

Inman²,

Rerecich³

et al. 1998

Eur Respir J

100

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Asthma induced by the inhalation of various allergens in the clinical research laboratory, has been a model for studying pathophysiology and pathogenesis of this disease for many years [1][2][3][4]. The inhalation of a specific allergen by asthmatic subjects can cause three types of airway responses [5]: the isolated response, that develops within 10-30 min after allergen challenge; the isolated late response that develops 3-8 h after the challenge; and the dual response, where subjects develop both early and late airway responses. The late response is associated with allergeninduced increases in airway responsiveness [6] and with eosinophilic airway inflammation [7].The doses of allergen usually used to study experimentally induced asthma are of a magnitude that causes an early response of at least a 15% reduction in forced expiratory volume in one second (FEV1) and a late response of at least 20% [5]. A shortcoming of this method is that these doses of allergen may be much higher than those to which patients with asthma are exposed in their natural environments. This shortcoming has been addressed by IHRE and co-workers [8,9], who used airway challenge with a low-dose of allergen. At first, these investigators studied early and late responses after a single challenge with low-dose allergen [8]. Later, they used repeated lowdose allergen challenge and demonstrated a significant increase in airway hyperresponsiveness [9]. However, the role of airway inflammation in causing these changes, as well as the time course of these events, has not been studied previously.The purposes of the present study were: 1) to determine the effects of repeated low-dose allergen challenge on airway inflammation as measured by numbers of eosinophils and metachromatic cells in induced sputum, as well as markers of eosinophil activation and level of the eosinopoietic cytokine IL-5; 2) to evaluate the effects of repeated low-dose allergen challenge on the development of late responses and methacholine airway hyperresponsiveness and to examine the time course of the changes; and 3) to evaluate the effects of repeated low-dose challenge on asthma symptoms and β 2 -agonist use. Increases in airway eosinophils and interleukin-5 with minimal bronchoconstriction during repeated low-dose allergen challenge in atopic asthmatics. I. Sulakvelidze, M.D. Inman, T. Rerecich, P.M. O'Byrne. ©ERS Journals Ltd 1998.ABSTRACT: Repeated low-dose allergen challenge increases airway hyperresponsiveness in atopic asthmatics. However, it is not known whether low-dose allergen challenge increases airway inflammation.Eight atopic asthmatics were enrolled in a controlled, cross-over study to evaluate the effect and time course of repeated low-dose allergen challenge on airway inflammation and hyperresponsiveness. The dose of allergen to reduce forced expiratory volume in one second (FEV1) by approximately 5% was selected in a screening allergen challenge. The subjects then were challenged for five consecutive days with either diluent or the selected low-dose of a...

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Section: Discussionmentioning

confidence: 87%

Increases in airway eosinophils and interleukin-5 with minimal bronchoconstriction during repeated low-dose allergen challenge in atopic asthmatics

Sulakvelidze¹,

Inman²,

Rerecich³

et al. 1998

Eur Respir J

100

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“…Pollen grains are the primary carriers of pollen allergens, which explains why the symptoms typical of hay fever are located in the eyes, nose and nasopharynx. Differently, allergic asthma in pollen-sensitive patients is an enigma because intact pollen grains, measuringw10 mm in diameter, are too large to enter the lower airways [32,122,123]. Moreover, in many instances peak asthma symptom scores differ temporally from peak pollen counts, and early morning symptoms sometimes precede later peaks in the daily pollen cycle.…”

Section: Plant-derived Allergensmentioning

confidence: 99%

Outdoor air pollution, climatic changes and allergic bronchial asthma

D’Amato¹,

Liccardi²,

D’Amato³

et al. 2002

European Respiratory Journal

221

158

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Both the prevalence and severity of respiratory allergic diseases such as bronchial asthma have increased in recent years. Among the factors implicated in this "epidemic" are indoor and outdoor airborne pollutants. Urbanisation with its high levels of vehicle emissions and Westernised lifestyle parallels the increase in respiratory allergy in most industrialised countries, and people who live in urban areas tend to be more affected by the disease than those of rural areas. In atopic subjects, exposure to air pollution increases airway responsiveness to aeroallergens. Pollen is a good model with which to study the interrelationship between air pollution and respiratory allergic diseases. Biological aerosols carrying antigenic proteins, such as pollen grains or plantderived paucimicronic components, can produce allergic symptoms. By adhering to the surface of these airborne allergenic agents, air pollutants could modify their antigenic properties. Several factors influence this interaction, i.e., type of air pollutant, plant species, nutrient balance, climatic factors, degree of airway sensitisation and hyperresponsiveness of exposed subjects. However, the airway mucosal damage and the impaired mucociliary clearance induced by air pollution may facilitate the penetration and the access of inhaled allergens to the cells of the immune system, and so promote airway sensitisation. As a consequence, an enhanced immunoglobulin E-mediated response to aeroallergens and enhanced airway inflammation favoured by air pollution could account for the increasing prevalence of allergic respiratory diseases in urban areas.

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“…Whole pollen grains are too large to penetrate the small airways [6]. However, episodes of wet weather during the pollen season can trigger pollen grains to emit respirable particles that can penetrate into the lower airways where they may trigger asthmatic responses [7,8,9,10].…”

Section: Introductionmentioning

confidence: 99%

Links between Pollen, Atopy and the Asthma Epidemic

Taylor

Jacobson²,

House

et al. 2007

Int Arch Allergy Immunol

101

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Pollen allergy has been found in 80–90% of childhood asthmatics and 40–50% of adult-onset asthmatics. Despite the high prevalence of atopy in asthmatics, a causal relationship between the allergic response and asthma has not been clearly established. Pollen grains are too large to penetrate the small airways where asthma occurs. Yet pollen cytoplasmic fragments are respirable and are likely correlated with the asthmatic response in allergic asthmatics. In this review, we outline the mechanism of pollen fragmentation and possible pathophysiology of pollen fragment-induced asthma. Pollen grains rupture within the male flowers and emit cytoplasmic debris when winds or other disturbances disperse the pollen. Peak levels of grass and birch pollen allergens in the atmosphere correlated with the occurrence of moist weather conditions during the flowering period. Thunderstorm asthma epidemics may be triggered by grass pollen rupture in the atmosphere and the entrainment of respirable-sized particles in the outflows of air masses at ground level. Pollen contains nicotinamide adenine dinucleotide phosphate (reduced) oxidases and bioactive lipid mediators which likely contribute to the inflammatory response. Several studies have examined synergistic effects and enhanced immune response from interaction in the atmosphere, or from co-deposition in the airways, of pollen allergens, endogenous pro-inflammatory agents, and the particulate and gaseous fraction of combustion products. Pollen and fungal fragments also contain compounds that can suppress reactive oxidants and quench free radicals. It is important to know more about how these substances interact to potentially enhance, or even ameliorate, allergic asthma.

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Deposition of Inhaled Pollen and Pollen Extract in Human Airways

Cited by 118 publications

References 5 publications

Increases in airway eosinophils and interleukin-5 with minimal bronchoconstriction during repeated low-dose allergen challenge in atopic asthmatics

Increases in airway eosinophils and interleukin-5 with minimal bronchoconstriction during repeated low-dose allergen challenge in atopic asthmatics

Outdoor air pollution, climatic changes and allergic bronchial asthma

Links between Pollen, Atopy and the Asthma Epidemic

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