| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
- and IFN-
-Dependent Control of Infection with Chlamydia pneumoniae by Nonhemopoietic Cells1
* Microbiology and Tumorbiology Center, Karolinska Institute, Stockholm, Sweden; and
Laboratory of Virology, Instituto Superiore di Sanità, Rome, Italy
STAT1 mediates signaling in response to IFN-
, -
, and -
, cytokines required for protective immunity against several viral, bacterial, and eukaryotic pathogens. The protective role of STAT1 in the control of intranasal infection with the obligate intracellular bacterium Chlamydia pneumoniae was analyzed. IFN-–/– or IFN- receptor (R)–/– mice were highly susceptible to infection with C. pneumoniae. We found that STAT1–/– mice were even more susceptible to C. pneumoniae than IFN-–/– or IFN-R–/– mice. Phosphorylation of STAT1 was detected in the lungs of C. pneumoniae-infected wild-type, IFN-R–/–, and IFN-R–/– mice, but not in mice lacking both IFN-R and IFN-R. In line with this, IFN-R–/–/IFN-R–/– mice showed increased susceptibility to infection compared with IFN-R–/– mice. However, C. pneumoniae-infected IFN-R–/– or IFN regulatory factor 3–/– mice showed no increased susceptibility and similar IFN- expression compared with wild-type mice. CD4+ or CD8+ cells released IFN- in vivo and conferred protection against C. pneumoniae in a STAT1-independent manner. In contrast, STAT1 mediated a nonredundant protective role of nonhemopoietic cells but not of hemopoietic cells. Nonhemopoietic cells accounted for the expression of STAT1-mediated indoleamine 2, 3-dioxygenase and the p47 GTPase LRG-47, but not inducible NO synthase mRNA. In summary, we demonstrate that STAT1 mediates a cooperative effect of IFN- and IFN- on nonhemopoietic cells, resulting in protection against C. pneumoniae.
This article has been cited by other articles:
|
|
 |
|
  J. Baumert, K.-H. Schmidt, A. Eitner, E. Straube, and J. Rodel Host Cell Cytokines Induced by Chlamydia pneumoniae Decrease the Expression of Interstitial Collagens and Fibronectin in Fibroblasts Infect. Immun., February 1, 2009; 77(2): 867 - 876. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
U. M. Nagarajan, D. Prantner, J. D. Sikes, C. W. Andrews Jr., A. M. Goodwin, S. Nagarajan, and T. Darville Type I Interferon Signaling Exacerbates Chlamydia muridarum Genital Infection in a Murine Model Infect. Immun., October 1, 2008; 76(10): 4642 - 4648. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Qiu, Y. Fan, A. G. Joyee, S. Wang, X. Han, H. Bai, L. Jiao, N. Van Rooijen, and X. Yang Type I IFNs Enhance Susceptibility to Chlamydia muridarum Lung Infection by Enhancing Apoptosis of Local Macrophages J. Immunol., August 1, 2008; 181(3): 2092 - 2102. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Yang, P. Stark, K. Janik, H. Wigzell, and M. E. Rottenberg SOCS-1 Protects against Chlamydia pneumoniae-Induced Lethal Inflammation but Hampers Effective Bacterial Clearance J. Immunol., March 15, 2008; 180(6): 4040 - 4049. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. P. Shornick, A. G. Wells, Y. Zhang, A. C. Patel, G. Huang, K. Takami, M. Sosa, N. A. Shukla, E. Agapov, and M. J. Holtzman Airway Epithelial versus Immune Cell Stat1 Function for Innate Defense against Respiratory Viral Infection J. Immunol., March 1, 2008; 180(5): 3319 - 3328. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Trumstedt, E. Eriksson, A. M. Lundberg, T.-b. Yang, Z.-q. Yan, H. Wigzell, and M. E. Rottenberg Role of IRAK4 and IRF3 in the control of intracellular infection with Chlamydia pneumoniae J. Leukoc. Biol., June 1, 2007; 81(6): 1591 - 1598. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
