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 Katayama, H.
Right arrow Articles by Hirai, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Katayama, H.
Right arrow Articles by Hirai, K.

Am. J. Respir. Cell Mol. Biol., Volume 26, Number 4, April, 2002 398-403

Production of Eosinophilic Chemokines by Normal Pleural Mesothelial Cells

Hitoshi Katayama, Akihito Yokoyama, Nobuoki Kohno, Kimiko Sakai, Kunio Hiwada, Hirokazu Yamada, and Koichi Hirai

Second Department of Internal Medicine, Ehime University School of Medicine, Onsen-gun, Ehime; and Departments of Allergy and Rheumatology and Bioregulatory Function, University of Tokyo Graduate School of Medicine, Tokyo, Japan

Eosinophilic pleural effusion occurs in many diseases. The mechanisms of eosinophil accumulation are not well understood. We showed previously that eotaxin was readily detectable in most pleural effusions, and its concentration significantly correlated with eosinophil number. To test the hypothesis that pleural eotaxin is produced by resident mesothelial cells, we examined its production by normal pleural mesothelial cells (NPMC). Eotaxin was induced by tumor necrosis factor (TNF)-alpha or interleukin (IL)-4 and was drastically increased by their combination. In contrast, interferon (IFN)-gamma inhibited eotaxin production. Regulated on activation, normal T cells expressed and secreted (RANTES) was also induced by TNF-alpha and was drastically increased by the addition of IFN-gamma . These effects were observed at both protein and mRNA levels. Stabilization of RANTES mRNA was observed with IFN-gamma but not IL-4; neither cytokine stabilized eotaxin mRNA. Eosinophil chemoattractant activity in culture supernatants of NPMC stimulated with TNF-alpha plus IL-4 was diminished by an anti-eotaxin antibody; that induced by TNF-alpha plus IFN-gamma was attenuated by an anti-RANTES antibody. Thus, NPMC can produce eotaxin, and different cytokines act on NPMC to induce different chemokines by different mechanisms. IFN-gamma , a Th1 cytokine, acts at least at the posttranscriptional level to induce RANTES production, but it inhibits eotaxin production. In contrast, IL-4, a Th2 cytokine, acts at the transcriptional level to induce eotaxin.

Abbreviations: C-C chemokine receptor, CCR; ethylenediaminetetraacetic acid, EDTA; granulocyte macrophage-colony stimulating factor, GM-CSF; interferon, IFN; interleukin, IL; normal pleural mesothelial cells, NPMC; platelet activating factor, PAF; regulated on activation, normal T cells expressed and secreted, RANTES; saline sodium citrate, SSC; tumor necrosis factor, TNF




This article has been cited by other articles:


Home page
 Int ImmunolHome page
C. Penido, M. F. S. Costa, M. C. Souza, K. A. Costa, A. L. P. Candea, C. F. Benjamim, and M. d. G. M. O. Henriques
Involvement of CC chemokines in {gamma}{delta} T lymphocyte trafficking during allergic inflammation: the role of CCL2/CCR2 pathway
Int. Immunol., January 1, 2008; 20(1): 129 - 139.
[Abstract] [Full Text] [PDF]

Home page
 J. Pharmacol. Exp. Ther.Home page
C. Bandeira-Melo, A. G. C. Bonavita, B. L. Diaz, P. M. R. e Silva, V. F. Carvalho, P. J. Jose, R. J. Flower, M. Perretti, and M. A. Martins
A Novel Effect for Annexin 1-Derived Peptide Ac2-26: Reduction of Allergic Inflammation in the Rat
J. Pharmacol. Exp. Ther., June 1, 2005; 313(3): 1416 - 1422.
[Abstract] [Full Text] [PDF]

Home page
 Eur Respir JHome page
K. Irifune, A. Yokoyama, K. Sakai, A. Watanabe, H. Katayama, H. Ohnishi, H. Hamada, M. Nakajima, N. Kohno, and J. Higaki
Adoptive transfer of T-helper cell type 1 clones attenuates an asthmatic phenotype in mice
Eur. Respir. J., April 1, 2005; 25(4): 653 - 659.
[Abstract] [Full Text] [PDF]

Home page
 ChestHome page
I. Kalomenidis, Y. Guo, K. B. Lane, M. Hawthorne, and R. W. Light
Transforming Growth Factor-{beta}3 Induces Pleurodesis in Rabbits and Collagen Production of Human Mesothelial Cells
Chest, April 1, 2005; 127(4): 1335 - 1340.
[Abstract] [Full Text] [PDF]

Home page
 Arterioscler. Thromb. Vasc. Bio.Home page
R. B. Kodali, W. J.H. Kim, I. I. Galaria, C. Miller, A. D. Schecter, S. A. Lira, and M. B. Taubman
CCL11 (Eotaxin) Induces CCR3-Dependent Smooth Muscle Cell Migration
Arterioscler. Thromb. Vasc. Biol., July 1, 2004; 24(7): 1211 - 1216.
[Abstract] [Full Text] [PDF]

Home page
 Infect. Immun.Home page
S. Babayan, M.-N. Ungeheuer, C. Martin, T. Attout, E. Belnoue, G. Snounou, L. Renia, M. Korenaga, and O. Bain
Resistance and Susceptibility to Filarial Infection with Litomosoides sigmodontis Are Associated with Early Differences in Parasite Development and in Localized Immune Reactions
Infect. Immun., December 1, 2003; 71(12): 6820 - 6829.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Cell Mol. Bio.Home page
S. N. Georas, L. A. Beck, and C. Stellato
What Is Eotaxin Doing in the Pleura? . Insights into Innate Immunity from Pleural Mesothelial Cells
Am. J. Respir. Cell Mol. Biol., April 1, 2002; 26(4): 384 - 387.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Proc. Am. Thorac. Soc. Am. J. Respir. Crit. Care Med.
Copyright © 2002 American Thoracic Society.