The eosinophil and the pathophysiology of asthma

The international consensus report on diagnosis and treatment of asthma was published in 1992 (Clin ExpAllergy 22: 1-72). According to the report, asthma is a chronic inflammatory disorder of the airways in which many cells play a role, including mast cells and eosinophils.Airway inflammation causes various symptoms of asthma which are usually associated with widespread but variable airflow obstruction and causes an associated increase in airway responsiveness to a variety of stimuli. The definition of asthma, provided in this report, is an epoch-making revision of the conventional recognition of asthma based on respiratory physiology and does not contradict the empirical knowledge that asthma responds well to steroid therapy. One reason, which led airway inflammation to be understood as a major factor in the pathophysiology of asthma is the technological advance and the widespread use of bronchoscopes. The use of bronchoscopyas a research tool has markedly improved the understanding of the pathology of asthma. It became also possible to link biopsy findings to autopsy findings in patients who died of asthma. However, it is relatively difficult to repeat a biopsy of the airway mucosal membranes in individual asthmatic patients. Here, animal models of asthma play a significant role. Findings from animal models can provide a clue for the development of new anti-asthmatic drugs. This paper will deal with the paradigm of allergic asthma and focus on recent topics of interleukin (IL)-4 and IL-5, which seem to play a central role in allergic asthma. The causative relationship between airway inflammation and hyperresponsiveness will be discussed. (Internal Medicine 42: 636-643, 2003)

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“…This view is based on the findings that eosinophils contain eosinophil peroxidase (27), major basic protein (28-30), LTC4 (28) and PAF (31).…”

Section: Inflammation and Airway Hyperresponsivenessmentioning

confidence: 99%

Allergic Bronchial Asthma: Airway Inflammation and Hyperresponsiveness

et al. 2003

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“…The 1970s and 1980s witnessed an upsurge in interest in the capacity of the eosinophil to adhere to and kill metazoan helminth parasites, in vitro (3,4). Circa the same era, elegant clinical observations of Gleich and others established a close correlation between secreted eosinophil crystalloid granule-stored cationic proteins and tissue damage in asthma (5,6). Subsequently, attention became focused on understanding eosinophil effector function.…”

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confidence: 99%

The rise of the phoenix: the expanding role of the eosinophil in health and disease

Adamko

Odemuyiwa

Vethanayagam

et al. 2004

Allergy

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We have entered a new phase in the evolution of our understanding of the role of the eosinophil with a greater appreciation of novel potential functions that may be ascribed to this enigmatic cell type. This review not only provides an update to our current understanding of the various immunobiological roles for the eosinophil, but also attracts attention to some novel observations predicting functions beyond its putative effector role. These observations include the intriguing possibility that the eosinophil may posses the capacity to regulate the immune and inflammatory responses in diseases such as asthma.

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“…It has been shown that levels of eosinophil granule proteins in the bronchoalveolar lavage fluids are elevated in the pulmonary late-phase reaction induced by challenge with ragweed extract (1). Tissue eosinophilia and the deposition of eosinophil granule proteins in the affected tissues are observed in bronchial asthma (2). Moreover, in bronchial asthma, major basic protein (MBP) is present in increased concentrations in the sputum ( 3 ) .…”

Section: Effects Of Interleukin (Il)mentioning

confidence: 99%

Effects of interleukin (IL)‐3 and IL‐5 on human eosinophil degranulation induced by complement components C3a and C5a*

Takafuji

Tadokoro

Itō

1996

Allergy

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It is suggested that eosinophils (Eos) play an important role in the pathogenesis of bronchial asthma by releasing cytotoxic cationic eosinophil granule proteins and damaging bronchial epithelial cells. However, the exact nature of the actual inducer of eosinophil degranulation in vivo is unclear. We examined eosinophil cationic protein (ECP) release from human Eos in response to soluble agonists such as C5a, C3a, platelet‐activating factor, and FMLP with or without interleukin (IL)‐3 or IL‐5 priming. Eosinophil degranulation induced by these soluble agonists required the pretreatment of Eos by cytochalasin B even in IL‐3 priming. Among four agonists, C5a was the most effective stimulus of ECP release either with or without IL‐5 priming. IL‐3 and IL‐5 remarkably enhanced ECP release in Eos triggered by C3a and C5a. The enhancement of ECP release by IL‐3 and IL‐5 occurred at 0.1–0.3 ng/ml and became maximal at 10–30 ng/ml, concentration‐dependently. The enhancement of ECP release by cytokines became optimal at an interval of 10 min. Our data support the importance of complement components and cytokines in eosinophil degranulation in vivo.

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The eosinophil and the pathophysiology of asthma

Cited by 567 publications

References 66 publications

Allergic Bronchial Asthma: Airway Inflammation and Hyperresponsiveness

Allergic Bronchial Asthma: Airway Inflammation and Hyperresponsiveness

The rise of the phoenix: the expanding role of the eosinophil in health and disease

Effects of interleukin (IL)‐3 and IL‐5 on human eosinophil degranulation induced by complement components C3a and C5a*

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