help button home button Am J Pathol Epitomics
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
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 Sato, J.
Right arrow Articles by Castellino, F. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sato, J.
Right arrow Articles by Castellino, F. J.
(American Journal of Pathology. 2003;163:517-531.)
© 2003 American Society for Investigative Pathology

The Fibrinolytic System in Dissemination and Matrix Protein Deposition During a Mycobacterium Infection

Jun Sato*{dagger}, Jeffrey Schorey{ddagger}, Victoria A. Ploplis*{dagger}, Erijka Haalboom*, Liana Krahule* and Francis J. Castellino*{dagger}

From the W. M. Keck Center for Transgene Research* and the Departments of Chemistry and Biochemistry{dagger} and Biological Sciences,{ddagger} University of Notre Dame, Notre Dame, Indiana

The fibrinolytic system is known to play an important role in the inflammatory response to bacterial infections. In the present study, relationships between protein components of the fibrinolytic system and infectivity by Mycobacterium avium were analyzed. Infections were initiated through noninvasive intratracheal administration of M. avium 724 in mice individually deficient for plasminogen, tissue-type plasminogen activator, urokinase-type plasminogen activator, and urokinase-type plasminogen activator receptor, along with wild-type control mice. There were no differences in lung colony counts among all mouse genotypes throughout a 10-week infection. However, in tissue-type plasminogen activator and plasminogen-deficient mice an earlier dissemination of M. avium to other organs was observed. Nevertheless, the M. avium growth rates in the liver, spleen, and lung did not differ between the various mouse populations throughout a 10-week infection. Histochemical and immunohistochemical analyses at 5 and 10 weeks after infection demonstrated that plasminogen-deficient mice, compared to wild-type mice, had enhanced fibrin and fibronectin deposition, as well as increased neutrophil infiltration within liver granulomas. These results suggest that plasmin(ogen) plays a role in the turnover of extracellular matrix proteins within granulomas and has a limited effect in the early dissemination of M. avium from lungs. Thus, plasmin(ogen) functions in limiting progressive fibrosis in the granuloma during a chronic mycobacterial infection.





This article has been cited by other articles:


Home page
Nephrol Dial TransplantHome page
J. J. T. H. Roelofs, K. M. A. Rouschop, G. J. D. Teske, G. T. M. Wagenaar, N. Claessen, J. J. Weening, T. van der Poll, and S. Florquin
Endogenous tissue-type plasminogen activator is protective during ascending urinary tract infection
Nephrol. Dial. Transplant., March 1, 2009; 24(3): 801 - 808.
[Abstract] [Full Text] [PDF]


Home page
BloodHome page
S. Weijer, C. W. Wieland, S. Florquin, and T. van der Poll
A thrombomodulin mutation that impairs activated protein C generation results in uncontrolled lung inflammation during murine tuberculosis
Blood, October 15, 2005; 106(8): 2761 - 2768.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2003 by the American Society for Investigative Pathology.