IAI FigSearch
Home Help [Feedback] [For Subscribers] [Archive] [Search] [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 arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Jimenez, M. d. P.
Right arrow Articles by Fierer, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Jimenez, M. d. P.
Right arrow Articles by Fierer, J.

 Previous Article  |  Next Article 

Infection and Immunity, June 2006, p. 3387-3395, Vol. 74, No. 6
0019-9567/06/$08.00+0     doi:10.1128/IAI.01985-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

High Levels of Interleukin-10 Impair Resistance to Pulmonary Coccidioidomycosis in Mice in Part through Control of Nitric Oxide Synthase 2 Expression

Maria del Pilar Jimenez,1,{dagger} Lorraine Walls,1 and Joshua Fierer1,2*

VA Healthcare System,1 Departments of Medicine and Pathology, University of California San Diego School of Medicine, San Diego, California2

Received 7 December 2005/ Returned for modification 26 January 2006/ Accepted 2 March 2006

We have shown previously that there is a direct correlation between IL-10 levels and susceptibility to Coccidioides immitis peritonitis in C57BL/6 (B6), DBA/2, and BXD recombinant inbred mice. We now show that B6 mice are also more susceptible to C. immitis pneumonia and that interleukin-10 (IL-10)-deficient (IL-10–/–) B6 mice are more resistant to C. immitis pneumonia. In addition, we established that high levels of IL-10 are sufficient to make genetically resistant mice susceptible to both C. immitis peritonitis and pneumonia by infecting h.IL-10 transgenic mice. Infected h.IL-10 transgenic mice express lower levels of gamma interferon, IL-12 p40, and inducible nitric oxide synthetase 2 (NOS2) mRNA in their lungs, implicating inducible NOS as a defense mechanism in this disease. We treated DBA/2 mice with aminoguanidine, and they became more susceptible to C. immitis peritonitis and pneumonia. We conclude that high levels of IL-10 are both necessary and sufficient to make mice susceptible to C. immitis, regardless of the genetic background of the mice, and that IL-10 impairs resistance to C. immitis in part by suppressing NO synthesis.

* Corresponding author. Mailing address: Infectious Diseases Section (111F), VA San Diego Healthcare System, 3350 La Jolla Village Drive, San Diego, CA 92161. Phone: (858) 552-7446. Fax: (858) 552-4398. E-mail: jfierer{at}ucsd.edu.

Editor: A. Casadevall

{dagger} Present address: Grupo de Micología Médica y Experimental, Corporación para Investigaciones Biológicas, Medellín, Columbia.

Infection and Immunity, June 2006, p. 3387-3395, Vol. 74, No. 6
0019-9567/06/$08.00+0     doi:10.1128/IAI.01985-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 2006 by the American Society for Microbiology. All rights reserved.