help button home button
AJRCMB
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Cheng, G.
Right arrow Articles by Fukuda, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cheng, G.
Right arrow Articles by Fukuda, T.

Am. J. Respir. Cell Mol. Biol., Volume 25, Number 2, August, 2001 212-218

A549 Cells Can Express Interleukin-16 and Stimulate Eosinophil Chemotaxis

Gang Cheng, Takashi Ueda, Fukiko Eda, Masafumi Arima, Nozomi Yoshida, and Takeshi Fukuda

Department of Pulmonary Medicine and Clinical Immunology, Dokkyo University School of Medicine, Tochigi, Japan

Alveolar epithelial cells produce many types of chemokines such as regulated on activation, normal T cells expressed and secreted (RANTES), eotaxin induced by interleukin (IL)-1beta , or tumor necrosis factor (TNF)-alpha and may contribute to allergic disease by recruiting eosinophils. However, identification of the eosinophil chemotacic activity (ECA) release from A549 cells, an alveolar type II cell line, has not yet been completed. Recently, IL-16 was also reported to be a potent chemotactic stimulus for CD4+ T lymphocytes and eosinophils in asthma and other pulmonary diseases. To test the possibility that alveolar epithelial cells produce IL-16, we analyzed RNA and culture supernatant from A549 cells by reverse transcription/ polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). The release of ECA from A549 cells was assessed using a blind-well chemotactic chamber. IL-16 release was increased in a concentration-dependent manner by stimulation with IL-1beta or TNF-alpha . A549 cells also expressed IL-16 messenger RNA. The combination of IL-4 and IL-1beta or TNF-alpha had an additive effect on IL-16 production. The release of ECA was induced by IL-1beta or TNF-alpha in a dose-dependent manner. The combination of these cytokines had a greater effect than one alone. The blockade of eotaxin and IL-16 caused 70% inhibition of ECA, but anti-RANTES antibodies only caused 30% inhibition and anti-IL-8 antibodies failed to affect inhibition. These findings suggest a role for chemokines released by alveolar epithelial cells in the recruitment of eosinophils into the lung in pulmonary disorders such as asthma and interstitial lung diseases, and suggested that eotaxin and IL-16 are potent and effective eosinophil chemoattractants.

Abbreviations: bronchoalveolar lavage fluid, BALF; complementary DNA, cDNA; deoxynucleotide triphosphate, dNTP; eosinophil chemotactic activity, ECA; immunoglobulin, Ig; interleukin, IL; monoclonal antibody, mAb; messenger RNA, mRNA; regulated on activation, normal T cells expressed and secreted, RANTES; reverse transcription/polymerase chain reaction, RT-PCR; tumor necrosis factor, TNF.




This article has been cited by other articles:


Home page
 J. Immunol.Home page
F. Cagnoni, S. Oddera, J. Giron-Michel, A. M. Riccio, S. Olsson, P. Dellacasa, G. Melioli, G. W. Canonica, and B. Azzarone
CD40 on Adult Human Airway Epithelial Cells: Expression and Proinflammatory Effects
J. Immunol., March 1, 2004; 172(5): 3205 - 3214.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Proc. Am. Thorac. Soc. Am. J. Respir. Crit. Care Med.
Copyright © 2001 American Thoracic Society. 		  New Orleans Int'l Conf