HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Cook, A. D. Articles by Hamilton, J. A. Search for Related Content PubMed PubMed Citation Articles by Cook, A. D. Articles by Hamilton, J. A.

Stimulus-Dependent Requirement for Granulocyte-Macrophage Colony-Stimulating Factor in Inflammation¹

Arthritis and Inflammation Research Centre, Department of Medicine, Royal Melbourne Hospital, and Cooperative Research Centre for Chronic Inflammatory Diseases, University of Melbourne, Victoria, Australia

Data from several inflammation/autoimmunity models indicate that GM-CSF can be a key inflammatory mediator. Convenient models in readily accessible tissues are needed to enable the GM-CSF-dependent cellular responses to be elaborated. In this study, we show that, in contrast to the response to the commonly used i.p. irritant, thioglycolate medium, an Ag-specific methylated BSA-induced peritonitis in GM-CSF^–/– mice was severely compromised. The reduced response in the latter peritonitis model was characterized by fewer neutrophils and macrophages, as well as by deficiencies in the properties of the remaining macrophages, namely size and granularity, phagocytosis, allogeneic T cell triggering, and proinflammatory cytokine production. B1 lymphocytes were more evident in the GM-CSF^–/– Ag-specific exudates, indicating perhaps that GM-CSF can act on a common macrophage-B1 lymphocyte precursor in the inflamed peritoneum. We propose that these findings contribute to our understanding of how GM-CSF acts as a proinflammatory cytokine in many chronic inflammatory/autoimmune diseases. Of general significance, the findings also indicate that the nature of the stimulus is quite critical in determining whether a particular inflammatory mediator, such as GM-CSF, plays a role in an ensuing inflammatory reaction.

This article has been cited by other articles:

				Y.-C. Su, M. S. Rolph, N. G. Hansbro, C. R. Mackay, and W. A. Sewell Granulocyte-Macrophage Colony-Stimulating Factor Is Required for Bronchial Eosinophilia in a Murine Model of Allergic Airway Inflammation J. Immunol., February 15, 2008; 180(4): 2600 - 2607. [Abstract] [Full Text] [PDF]

				Y. Xu, Y. Zhan, A. M. Lew, S. H. Naik, and M. H. Kershaw Differential Development of Murine Dendritic Cells by GM-CSF versus Flt3 Ligand Has Implications for Inflammation and Trafficking J. Immunol., December 1, 2007; 179(11): 7577 - 7584. [Abstract] [Full Text] [PDF]

				W. Xu, A. Roos, N. Schlagwein, A. M. Woltman, M. R. Daha, and C. van Kooten IL-10-producing macrophages preferentially clear early apoptotic cells Blood, June 15, 2006; 107(12): 4930 - 4937. [Abstract] [Full Text] [PDF]

				J. R. Timoshanko, A. R. Kitching, T. J. Semple, S. R. Holdsworth, and P. G. Tipping Granulocyte Macrophage Colony-Stimulating Factor Expression by Both Renal Parenchymal and Immune Cells Mediates Murine Crescentic Glomerulonephritis J. Am. Soc. Nephrol., September 1, 2005; 16(9): 2646 - 2656. [Abstract] [Full Text] [PDF]