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Priming of eosinophil migration across lung epithelial cell monolayers and upregulation of CD11b/CD18 are elicited by extracellular Ca2+.
Am J Respir Cell Mol Biol. 2003 Jun; 28(6):713-21.AJ

Abstract

In patients with asthma, eosinophils are primed and massively infiltrate lung tissues and migrate across epithelia into airways. Using blocking monoclonal antibodies, we found that eosinophil transmigration across a lung epithelial cell monolayer depended on the functions of alphaMbeta2 integrin CD11b/CD18. To study the role of Ca2+ in eosinophil priming and transepithelial migration, we treated eosinophils with eotaxin or thapsigargin (TG), reagents that increase cytoplasmic free Ca2+ concentrations by receptor- or nonreceptor-mediated mechanisms, respectively. Pretreatment of eosinophils with TG enhanced CD11b/CD18-dependent transmigration across lung epithelium. Within minutes, TG time- and dose-dependently upregulated the expression of CD11b/CD18 but did not upregulate the expression of alphaL (CD11a) or beta1 (CD29) integrin. The upregulation of CD11b/CD18 expression by eotaxin or TG was prevented when Ca2+ entry was blocked. The priming of eosinophil transmigration by TG was also abrogated by the blockade of Ca2+ entry. Our results indicate that induction of Ca2+ entry by the depletion of Ca2+ from intracellular stores upregulates CD11b/CD18 expression on eosinophils and primes eosinophil transmigration across lung epithelium. Both responses are therefore elicited by extracellular Ca2+. We suggest that, as an important priming signal for human eosinophil functional responses, store-operated Ca2+ entry may be one of the underlying mechanisms of eosinophilic inflammation in asthma.

Authors+Show Affiliations

Department of Medical Sciences, Clinical Chemistry, Uppsala University, Uppsala, Sweden. lixliu@ucalgary.caNo 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

12760968

Citation

Liu, Lixin, et al. "Priming of Eosinophil Migration Across Lung Epithelial Cell Monolayers and Upregulation of CD11b/CD18 Are Elicited By Extracellular Ca2+." American Journal of Respiratory Cell and Molecular Biology, vol. 28, no. 6, 2003, pp. 713-21.
Liu L, Hakansson L, Ridefelt P, et al. Priming of eosinophil migration across lung epithelial cell monolayers and upregulation of CD11b/CD18 are elicited by extracellular Ca2+. Am J Respir Cell Mol Biol. 2003;28(6):713-21.
Liu, L., Hakansson, L., Ridefelt, P., Garcia, R. C., & Venge, P. (2003). Priming of eosinophil migration across lung epithelial cell monolayers and upregulation of CD11b/CD18 are elicited by extracellular Ca2+. American Journal of Respiratory Cell and Molecular Biology, 28(6), 713-21.
Liu L, et al. Priming of Eosinophil Migration Across Lung Epithelial Cell Monolayers and Upregulation of CD11b/CD18 Are Elicited By Extracellular Ca2+. Am J Respir Cell Mol Biol. 2003;28(6):713-21. PubMed PMID: 12760968.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Priming of eosinophil migration across lung epithelial cell monolayers and upregulation of CD11b/CD18 are elicited by extracellular Ca2+. AU - Liu,Lixin, AU - Hakansson,Lena, AU - Ridefelt,Peter, AU - Garcia,Rodolfo C, AU - Venge,Per, PY - 2003/5/23/pubmed PY - 2003/7/11/medline PY - 2003/5/23/entrez SP - 713 EP - 21 JF - American journal of respiratory cell and molecular biology JO - Am J Respir Cell Mol Biol VL - 28 IS - 6 N2 - In patients with asthma, eosinophils are primed and massively infiltrate lung tissues and migrate across epithelia into airways. Using blocking monoclonal antibodies, we found that eosinophil transmigration across a lung epithelial cell monolayer depended on the functions of alphaMbeta2 integrin CD11b/CD18. To study the role of Ca2+ in eosinophil priming and transepithelial migration, we treated eosinophils with eotaxin or thapsigargin (TG), reagents that increase cytoplasmic free Ca2+ concentrations by receptor- or nonreceptor-mediated mechanisms, respectively. Pretreatment of eosinophils with TG enhanced CD11b/CD18-dependent transmigration across lung epithelium. Within minutes, TG time- and dose-dependently upregulated the expression of CD11b/CD18 but did not upregulate the expression of alphaL (CD11a) or beta1 (CD29) integrin. The upregulation of CD11b/CD18 expression by eotaxin or TG was prevented when Ca2+ entry was blocked. The priming of eosinophil transmigration by TG was also abrogated by the blockade of Ca2+ entry. Our results indicate that induction of Ca2+ entry by the depletion of Ca2+ from intracellular stores upregulates CD11b/CD18 expression on eosinophils and primes eosinophil transmigration across lung epithelium. Both responses are therefore elicited by extracellular Ca2+. We suggest that, as an important priming signal for human eosinophil functional responses, store-operated Ca2+ entry may be one of the underlying mechanisms of eosinophilic inflammation in asthma. SN - 1044-1549 UR - https://www.unboundmedicine.com/medline/citation/12760968/Priming_of_eosinophil_migration_across_lung_epithelial_cell_monolayers_and_upregulation_of_CD11b/CD18_are_elicited_by_extracellular_Ca2+_ L2 - https://www.atsjournals.org/doi/10.1165/rcmb.4771?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -