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Eosinophil degranulation in the presence of bronchial epithelial cells. Effect of cytokines and role of adhesion.
J Immunol. 1996 May 15; 156(10):3980-5.JI

Abstract

It has been suggested that eosinophils (Eos) are responsible for damage to bronchial epithelial cells by releasing toxic eosinophil granule proteins in bronchial asthma. We examined eosinophil cationic protein (ECP) release from human Eos cultured in the presence of human bronchial epithelial cell line BEAS-2B (Ep). ECP release was potentiated only when both Eos and Ep were activated by IL-5 and TNF, respectively, while it was not potentiated when either Eos or Ep were activated. ECP release from Eos activated by IL-5 was also enhanced when Ep was stimulated by IFN-gamma. Paraformaldehyde fixation of Ep had no effect on ECP enhancement, excluding the possibility that soluble factors from Ep contribute to ECP potentiation. Coculture of Eos and Ep with cytokine treatment resulted in the enhancement of eosinophil adhesion and ECP release, and eosinophil adhesion preceded ECP release in the kinetic study. The enhancement of ECP release was partially inhibited by anti-CD18 mAb, which caused partial and comparable inhibition on the potentiation of eosinophil adhesion. These results suggest that the activation of Ep may profoundly affect the ability of cocultured Eos to release ECP and that CD18-dependent adhesion of Eos to Ep may be considered as one of the mechanisms of ECP enhancement.

Authors+Show Affiliations

Department of Medicine and Physical Therapy, Faculty of Medicine, University of Tokyo, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

8621939

Citation

Takafuji, S, et al. "Eosinophil Degranulation in the Presence of Bronchial Epithelial Cells. Effect of Cytokines and Role of Adhesion." Journal of Immunology (Baltimore, Md. : 1950), vol. 156, no. 10, 1996, pp. 3980-5.
Takafuji S, Ohtoshi T, Takizawa H, et al. Eosinophil degranulation in the presence of bronchial epithelial cells. Effect of cytokines and role of adhesion. J Immunol. 1996;156(10):3980-5.
Takafuji, S., Ohtoshi, T., Takizawa, H., Tadokoro, K., & Ito, K. (1996). Eosinophil degranulation in the presence of bronchial epithelial cells. Effect of cytokines and role of adhesion. Journal of Immunology (Baltimore, Md. : 1950), 156(10), 3980-5.
Takafuji S, et al. Eosinophil Degranulation in the Presence of Bronchial Epithelial Cells. Effect of Cytokines and Role of Adhesion. J Immunol. 1996 May 15;156(10):3980-5. PubMed PMID: 8621939.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Eosinophil degranulation in the presence of bronchial epithelial cells. Effect of cytokines and role of adhesion. AU - Takafuji,S, AU - Ohtoshi,T, AU - Takizawa,H, AU - Tadokoro,K, AU - Ito,K, PY - 1996/5/15/pubmed PY - 1996/5/15/medline PY - 1996/5/15/entrez SP - 3980 EP - 5 JF - Journal of immunology (Baltimore, Md. : 1950) JO - J Immunol VL - 156 IS - 10 N2 - It has been suggested that eosinophils (Eos) are responsible for damage to bronchial epithelial cells by releasing toxic eosinophil granule proteins in bronchial asthma. We examined eosinophil cationic protein (ECP) release from human Eos cultured in the presence of human bronchial epithelial cell line BEAS-2B (Ep). ECP release was potentiated only when both Eos and Ep were activated by IL-5 and TNF, respectively, while it was not potentiated when either Eos or Ep were activated. ECP release from Eos activated by IL-5 was also enhanced when Ep was stimulated by IFN-gamma. Paraformaldehyde fixation of Ep had no effect on ECP enhancement, excluding the possibility that soluble factors from Ep contribute to ECP potentiation. Coculture of Eos and Ep with cytokine treatment resulted in the enhancement of eosinophil adhesion and ECP release, and eosinophil adhesion preceded ECP release in the kinetic study. The enhancement of ECP release was partially inhibited by anti-CD18 mAb, which caused partial and comparable inhibition on the potentiation of eosinophil adhesion. These results suggest that the activation of Ep may profoundly affect the ability of cocultured Eos to release ECP and that CD18-dependent adhesion of Eos to Ep may be considered as one of the mechanisms of ECP enhancement. SN - 0022-1767 UR - https://www.unboundmedicine.com/medline/citation/8621939/Eosinophil_degranulation_in_the_presence_of_bronchial_epithelial_cells__Effect_of_cytokines_and_role_of_adhesion_ L2 - https://www.jimmunol.org/lookup/pmidlookup?view=long&pmid=8621939 DB - PRIME DP - Unbound Medicine ER -