Allergic inflammatory mediators and bronchial hyperresponsiveness
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Allergic inflammatory mediators and bronchial hyperresponsiveness

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Published by Saunders in Philadelphia, London .
Written in English

Book details:

Edition Notes

StatementC. Warren Bierman and Tak H. Lee, guest editors. 1.
SeriesImmunology and allergy clinics of North America -- 10/2
ContributionsBierman, C. Warren 1924-, Lee, T. H.
ID Numbers
Open LibraryOL14338647M

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Q. Gu, L.-Y. Lee, in Encyclopedia of Respiratory Medicine, Effect of Airway Inflammation. Bronchial hyperresponsiveness is known to occur during acute airway inflammation/injury caused by ozone exposure, viral infection, etc., and the involvement of an augmented reflex bronchoconstriction in these pathophysiological conditions has been clearly documented. is reduced under the allergic reactions, probably due to release of many inflammatory mediators or reactive oxygen species. Any inflammatory process within the respiratory system may lead to the imbalance at the level of nervous system, thus leading to the bronchial hyper-reactivity [2]. Inflammatory Cells, Mediators and NuclearFile Size: KB. The complex pathophysiology of lung allergic inflammation and bronchial hyperresponsiveness (BHR) that characterize asthma is achieved by the regulated accumulation and activation of different leukocyte subsets in the lung. The development and maintenance of these processes correlate with the coordinated production of chemokines. This review is written to summarize and critically analyze pathogenesis of bronchial hyperreactivity (BHR) as an underlying outcome for suitable treatment options. It describes and discusses the role of genetic predisposition, inflammatory mediators and other endogenous factors (growth factors, nuclear transcription factors), neural regulation and proinflammatory neurotransmitter in the.

Over the last decade there has been an intense interest in the potential role of cytokines and chemokines as important mediators in various atopic diseases, including asthma and the mechanisms by which these mediators regulate airway inflammation and bronchial hyperresponsiveness. This research effo .   Bronchial hyperresponsiveness (BHR) is defined as excessive bronchial narrowing and manifests itself as an exaggerated bronchoconstrictor response of the airways to various inhaled stimuli ().It is considered to be a hallmark of inflammation in asthma, is related to the severity of the disease, and is increasingly being recognized as a clinical endpoint for therapeutic intervention. The immunological characterization of lung eosinophilia implicates chemokines in the initiation of lung allergic inflammation and the subsequent development of BHR (5, 13–17).Chemokines are a group of cytokines that promote leukocyte recruitment to inflammatory sites, stimulate leukocyte exocytosis, and induce hematopoiesis (18–20).Chemokine expression is high and readily modulated in the. Allergic inflammation of the lining of the nose produces symptoms of rhinitis including rhinorrhoea, nasal obstruction, sneezing and itching. These result from increased glandular secretions and afferent nerve stimulation. The allergic response makes individuals more susceptible to the nasal irritant effects of other, nonallergenic stimuli, such as tobacco smoke and changes in temperature.

  Inflammatory Cells and Mediators in Bronchial Asthma provides reviews and summaries regarding state-of-the-art articles that examine the role of various. Inflammatory Cells and Mediators in Bronchial Asthma book. By Devendra K. Agrawal, Robert G. Townley. Edition 1st Edition. First Published eBook Published 28 October Inflammation has assumed a more central role in the pathogenesis of the disease, as it contributes not only to airflow obstruction, but also to bronchial hyperresponsiveness. The inciting trigger, or inhaled allergen, in asthma induces the activation of mast cells and macrophages with the subsequent release of several proinflammatory mediators. Bronchial hyperresponsiveness (BHR), one of the hallmarks of bronchial asthma, is a risk factor for the development of asthma and chronic obstructive pulmonary diseases (1, 2), and has been used as a clinical endpoint for therapeutic intervention in asthma addition, BHR has been shown to be associated with an accelerated decline in lung function (3, 4) and with respiratory. Reserve your copy now. This two volume book is an outstanding reference source on all aspects of allergy and allergic diseases. Covering virtually every allergic condition, from the immunological and molecular basis of the allergic response to future trends in allergic disease prevention, this new international editorial team (, Jean Bousquet, Pat Holt and Allen Kaplan) have completely.