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Infection and Immunity, January 2003, p. 365-373, Vol. 71, No. 1
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.1.365-373.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Selective Early Production of CCL20, or Macrophage Inflammatory Protein 3{alpha}, by Human Mast Cells in Response to Pseudomonas aeruginosa

Tong-Jun Lin,1,2 Lauren H. Maher,1 Kaede Gomi,1 Jeffrey D. McCurdy,1 Rafael Garduno,1 and Jean S. Marshall1,3*

Departments of Microbiology & Immunology,1 Pediatrics,2 Pathology, Dalhousie University, Halifax, Nova Scotia, B3H 4H7 Canada3

Received 17 May 2002/ Returned for modification 5 August 2002/ Accepted 16 October 2002

Mast cells are important as sentinel cells in host defense against bacterial infection. Much of their effectiveness depends upon recruiting other immune cells; however, little is known about the mechanisms of this response. CCL20, also known as macrophage inflammatory protein-3{alpha} (MIP-3{alpha}), Exodus, and LARC, is a chemokine known to be a potent chemoattractant for immature dendritic cells and T cells. In this study, we examined the human mast cell production of both CCL20 and granulocyte-macrophage colony-stimulating factor (GM-CSF), a critical cytokine for innate immune responses in the lung, in response to Pseudomonas aeruginosa. Reverse transcription-PCR and Western blot analysis demonstrated that the human mast cells (HMC-1) express CCL20 mRNA and are able to produce a significant amount (32.4 ng/ml) of CCL20 protein following stimulation by calcium ionophore and phorbol myristate acetate. Importantly, P. aeruginosa potently stimulated CCL20 production in human cord blood-derived mast cells (CBMC), with production peaking at 6 h after stimulation. This time course of expression was distinct from that of GM-CSF, which peaked after 24 to 48 h. Significant CCL20 production did not occur following immunoglobulin E-mediated activation of CBMC under conditions which induced a substantial GM-CSF response. Interestingly, the CCL20 response of mast cells to P. aeruginosa was relatively resistant to inhibition by the corticosteroid dexamethasone, interleukin-10, or cyclosporine, while GM-CSF production was potently inhibited. However, P. aeruginosa-induced CCL20 production was blocked by the protein kinase C (PKC) inhibitor Ro 31-8220 and a PKC pseudosubstrate. These results support a role for human mast cells in the initiation of immune responses to P. aeruginosa infection.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Dalhousie University, Sir Charles Tupper Medical Building, 5859 University Ave., Halifax, Nova Scotia, B3H 3H7 Canada. Phone: (902) 494-5118. Fax: (902) 494-5125. E-mail: Jean.Marshall{at}Dal.ca.

Editor: B. B. Finlay

Infection and Immunity, January 2003, p. 365-373, Vol. 71, No. 1
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.1.365-373.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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