Subject Eosinophil

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. 

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. 

Djukanovic, R., Wilson, J.W., Britten, K.M. et al. 1990. Quantitation of mast cells and eosinophils in the bronchial mucosa of symptomatic atopic asthmatics and healthy control subjects using immunohistochemistry. Annu Res Respir Dis 142 863-871. 

In this chapter, we describe the radioactive and enzymic methods used to measure the accumulation of eosinophils in guinea pig skin. The mIn-labeled cell method provides results on the same day as the in vivo assay. This is especially useful when monitoring activity in HPLC fractions during purification of eosinophil chemoattractants because the speed of the assay facilitates progression to the next stage of purification. Although the EPO method takes at least one extra day to obtain results, it has the advantage that the eosinophils measured have not been subjected to isolation procedures which can modify their response to chemoattractant mediators. We first describe the isolation and purification of the eosinophils required for both methods as a source of cells to radiolabel and to provide a standard curve for the EPO assay. We then describe the mIn-labeled cell and EPO methods. 

L-(-f-)-Tartrate (0.05 M) inhibited isoenzymes Nos. 1-4 but had no appreciable effect on the reticular cell isoenzyme. No. 5 (M8, Yl). In cytochemical studies of blood smears from three patients with leukemic reticuloendotheliosis, the acid phosphatase activity in the monocytes, eosinophiles, neutrophiles, and other cells that could definitely be identified as lymphocytes did not differ appreciably from those of normal subjects. In all three patients the neoplastic reticulum cell showed various degrees of acid phosphatase activity most of them were strongly positive. The enzyme activity in these cells was resistant to to l-( + )-tartrate, whereas it was completely inhibited in other types of cells. 

Sehmi, R, Wardlaw, A.J., Cromwell, O., Kurthara, K., Waltmann, P. and Kay. A.B. (1992). IL-5 selectively enhances the chemotactic response of eosinophils obtained from normal but not eosinophilic subjects. Blood 79, 2952-2959. 

Bradley, B.L., Azzawi, M., Jacobson, M., Assoufi, B., Collins, J.V., Irani, A.A., Schwartz, L.B., Durham, S.R, Jeffery, P.K. and Kay, A.B. (1991). Eosinophils, T-lymphocytes, mast cells, neutrophils and macrophages in bronchial biopsy specimens from atopic subjects with asthma - comparison with biopsy specimens from atopic subjects without asthma and normal control subjects and relationship to bronchial hyperresponsiveness. J. Allergy Chn. Immunol. 88,661-674. 

Wardlaw, A.J., Dunnette, S., Gleich, G.J., Collins, J.V. and Kay, A.B. (1988). Eosinophils and mast cells in bronchoalveolar lavage in subjects with mild asthma. Relationship to bronchial hyperreactivity. Am. Rev. Respir. Dis. 137, 62-69. 

Elevated peripheral eosinophil counts in asthmatics have correlated with decreases in specific airway conductance, forced expiratory volume (FEVi), maximum mid-expiratory flow rate (Horn et al., 1975), bronchial hyperreactivity (BHR) to histamine (H Taylor and Luksza, 1987) and clinical severity scores (Aas Bousquet et al., 1990). When circulating eosinophils were isolated fi om asymptomatic asthmatics, a large proportion of cells (35%) was recovered with centrifugal density less than 1.082 gml compared to normal subjects (10% Frick et al., 1989). Alteration of centrifugal density of eosinophils is one of the phenotypic responses to cellular activation (Hansel et al., 1990 Fukuda and Makino, 1992). Not only is the number of cells increased in asthma, circulating eosinophils may be activated intravascularly as well. 

In an allergen inhalation model of asthma, subjects who develop the EAR have an initial drop in circulating eosinophil count followed by a rise at 48 h post-challenge (Cookson et al. 1989). The initial drop may reflect the recruitment of circulating eosinophils to the lung where they participate in the development of a late phase... 

Kroegel, C., Liu, M.C., Hubbard, W.C., Lichtenstein, L.M. and Bochner, B.S. (1994). Blood and bronchoalveolar eosinophils in allergic subjects after segmental antigen challenge surftice phenotype, density heterogeneity, and prostanoid production. J. Allergy Clin. Immunol. 93, 725-734. 

Moqbel, R, Lacy, P., Levi-Schafler, F., Manna, M., North, J., Gomperts, B. and Kay, A.B. (1995). Interleukin-6 as a granule-associated pre-formed mediator in peripheral blood eosinophils from asthmatic subjects. Am. J. Resp. Crit. Care Med., in press. 

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