Asthma eosinophils

Eosinophils are important effector granulocytes in asthma. Eosinophils possess a unique array of biological functions. As effector granulocytes, they contribute to... 

Lung diseases with possible and/or mild pulmonary eosinophilia Asthma, eosinophilic bronchitis Organizing pneumonia Idiopathic interstitial pneumonias Langerhans cell granulomatosis Sarcoidosis Lymphoma... 

Microfilariae in the tissues of the lung (ie, eosinophilic lung or tropical eoskiophiha) produce symptoms of chest pain, cough, and asthma, which are often reheved by the administration of diethylcarbama2iae. 

Bronchial Asthma. Figure 2 Mechanisms of bronchial hyperresponsiveness. Toxic products from eosinophils [cationic peptides, reactive oxygen species (ROS)] cause epithelial injury. Nerve endings become easily accessible to mediators from mast cells, eosinophils [eosinophil-derived neurotoxin (EDN)], and neutrophils, and to airborne toxicants such as S02. Activation of nerve endings stimulates effector cells like mucosal glands and airway smooth muscle either directly or by cholinergic reflexes. 

Siroux V. Curt F. Oryszczyn MP, Maccario J, Kauff-mann F Role of gender and hormone-related events on IgE. atopy, and eosinophils in the Epidemiological Study on the Genetics and Environment of Asthma, dO bronchial hyperresponsiveness and atopy. J Allergy Clin Immunol 2004 114 491-498. 

The term refers to a distinct clinical syndrome characterized by aggressive and continuous inflammatory disease of the airways with chronic eosinophilic rhinosinus-itis, asthma and often nasal polyposis [6-8]. Aspirin and other NSAIDs that inhibit COX-1 exacerbate the condition, precipitating violent asthmatics attacks. This is a hallmark of the syndrome. The prevalence of aspirin hypersensitivity in the general population ranges from 0.6 to 2.5%, but is much more frequent in adult asthmatic subjects where it reaches 10-15%, although it is often underdiagnosed. 

Th2 lymphocytes are one of the primary factors initiating and perpetuating the inflammatory response.7 In addition, proinflammatory mediators such as the leukotrienes generated during mast cell degranulation can increase vascular permeability, leading to airway edema and increased mucus production.8 Eosinophilic infiltration of the airways is a hallmark of asthma, and activated eosinophils can cause bronchoconstriction and AHR.9... 

Increased serum concentrations of IgE or eosinophils may help confirm the diagnosis of asthma but are not diagnostic for asthma. 

Inflammation is present in the lungs of all smokers. It is unclear why only 15% to 20% of smokers develop COPD, but susceptible individuals appear to have an exaggerated inflammatory response.5 O The inflammation of COPD differs from that seen in asthma, so the use of anti-inflammatory medications and the response to those medications are different. The inflammation of asthma is mainly mediated through eosinophils and mast cells. In COPD the primary inflammatory cells include neutrophils, macrophages, and CD8+ T lymphocytes. 

Key Words Allergy asthma lung pulmonary T cell mast cell eosinophil inflammation dendritic cell IgE B cell. 

Robinson DS, North J, Zeibecoglou K, et al. Eosinophil development and bone marrow and tissue eosinophils in atopic asthma. Int Arch Allergy Immunol 1999 118(2-4) 98-100. 

Zeibecoglou K, Ying S, Yamada T, et al. Increased mature and immature CCR3 messenger RNA+ eosinophils in bone marrow from patients with atopic asthma compared with atopic and nonatopic control subjects. J Allergy Clin Immunol 1999 103(1 Pt 1) 99-106. 

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