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The T cell-specific CXC chemokines IP-10, Mig, and I-TAC are expressed by activated human bronchial epithelial cells.
J Immunol. 1999 Mar 15; 162(6):3549-58.JI

Abstract

Recruitment of activated T cells to mucosal surfaces, such as the airway epithelium, is important in host defense and for the development of inflammatory diseases at these sites. We therefore asked whether the CXC chemokines IFN-induced protein of 10 kDa (IP-10), monokine induced by IFN-gamma (Mig), and IFN-inducible T-cell alpha-chemoattractant (I-TAC), which specifically chemoattract activated T cells by signaling through the chemokine receptor CXCR3, were inducible in respiratory epithelial cells. The effects of proinflammatory cytokines, including IFN-gamma (Th1-type cytokine), Th2-type cytokines (IL-4, IL-10, and IL-13), and dexamethasone were studied in normal human bronchial epithelial cells (NHBEC) and in two human respiratory epithelial cell lines, A549 and BEAS-2B. We found that IFN-gamma, but not TNF-alpha or IL-1 beta, strongly induced IP-10, Mig, and I-TAC mRNA accumulation mainly in NHBEC and that TNF-alpha and IL-1 beta synergized with IFN-gamma induction in all three cell types. High levels of IP-10 protein (> 800 ng/ml) were detected in supernatants of IFN-gamma/TNF-alpha-stimulated NHBEC. Neither dexamethasone nor Th2 cytokines modulated IP-10, Mig, or I-TAC expression. Since IFN-gamma is up-regulated in tuberculosis (TB), using in situ hybridization we studied the expression of IP-10 in the airways of TB patients and found that IP-10 mRNA was expressed in the bronchial epithelium. In addition, IP-10-positive cells obtained by bronchoalveolar lavage were significantly increased in TB patients compared with normal controls. These results show that activated bronchial epithelium is an important source of IP-10, Mig, and I-TAC, which may, in pulmonary diseases such as TB (in which IFN-gamma is highly expressed) play an important role in the recruitment of activated T cells.

Authors+Show Affiliations

Infectious Disease Unit, Massachusetts General Hospital, Charlestown 02129, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

10092813

Citation

Sauty, A, et al. "The T Cell-specific CXC Chemokines IP-10, Mig, and I-TAC Are Expressed By Activated Human Bronchial Epithelial Cells." Journal of Immunology (Baltimore, Md. : 1950), vol. 162, no. 6, 1999, pp. 3549-58.
Sauty A, Dziejman M, Taha RA, et al. The T cell-specific CXC chemokines IP-10, Mig, and I-TAC are expressed by activated human bronchial epithelial cells. J Immunol. 1999;162(6):3549-58.
Sauty, A., Dziejman, M., Taha, R. A., Iarossi, A. S., Neote, K., Garcia-Zepeda, E. A., Hamid, Q., & Luster, A. D. (1999). The T cell-specific CXC chemokines IP-10, Mig, and I-TAC are expressed by activated human bronchial epithelial cells. Journal of Immunology (Baltimore, Md. : 1950), 162(6), 3549-58.
Sauty A, et al. The T Cell-specific CXC Chemokines IP-10, Mig, and I-TAC Are Expressed By Activated Human Bronchial Epithelial Cells. J Immunol. 1999 Mar 15;162(6):3549-58. PubMed PMID: 10092813.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The T cell-specific CXC chemokines IP-10, Mig, and I-TAC are expressed by activated human bronchial epithelial cells. AU - Sauty,A, AU - Dziejman,M, AU - Taha,R A, AU - Iarossi,A S, AU - Neote,K, AU - Garcia-Zepeda,E A, AU - Hamid,Q, AU - Luster,A D, PY - 1999/3/27/pubmed PY - 1999/3/27/medline PY - 1999/3/27/entrez SP - 3549 EP - 58 JF - Journal of immunology (Baltimore, Md. : 1950) JO - J Immunol VL - 162 IS - 6 N2 - Recruitment of activated T cells to mucosal surfaces, such as the airway epithelium, is important in host defense and for the development of inflammatory diseases at these sites. We therefore asked whether the CXC chemokines IFN-induced protein of 10 kDa (IP-10), monokine induced by IFN-gamma (Mig), and IFN-inducible T-cell alpha-chemoattractant (I-TAC), which specifically chemoattract activated T cells by signaling through the chemokine receptor CXCR3, were inducible in respiratory epithelial cells. The effects of proinflammatory cytokines, including IFN-gamma (Th1-type cytokine), Th2-type cytokines (IL-4, IL-10, and IL-13), and dexamethasone were studied in normal human bronchial epithelial cells (NHBEC) and in two human respiratory epithelial cell lines, A549 and BEAS-2B. We found that IFN-gamma, but not TNF-alpha or IL-1 beta, strongly induced IP-10, Mig, and I-TAC mRNA accumulation mainly in NHBEC and that TNF-alpha and IL-1 beta synergized with IFN-gamma induction in all three cell types. High levels of IP-10 protein (> 800 ng/ml) were detected in supernatants of IFN-gamma/TNF-alpha-stimulated NHBEC. Neither dexamethasone nor Th2 cytokines modulated IP-10, Mig, or I-TAC expression. Since IFN-gamma is up-regulated in tuberculosis (TB), using in situ hybridization we studied the expression of IP-10 in the airways of TB patients and found that IP-10 mRNA was expressed in the bronchial epithelium. In addition, IP-10-positive cells obtained by bronchoalveolar lavage were significantly increased in TB patients compared with normal controls. These results show that activated bronchial epithelium is an important source of IP-10, Mig, and I-TAC, which may, in pulmonary diseases such as TB (in which IFN-gamma is highly expressed) play an important role in the recruitment of activated T cells. SN - 0022-1767 UR - https://www.unboundmedicine.com/medline/citation/10092813/The_T_cell_specific_CXC_chemokines_IP_10_Mig_and_I_TAC_are_expressed_by_activated_human_bronchial_epithelial_cells_ L2 - http://www.jimmunol.org/cgi/pmidlookup?view=long&pmid=10092813 DB - PRIME DP - Unbound Medicine ER -