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 Roach, D. R.
Right arrow Articles by Britton, W. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Roach, D. R.
Right arrow Articles by Britton, W. J.
Right arrowPubmed/NCBI databases
*Gene*GEO Profiles
*HomoloGene*UniGene
*Compound via MeSH
*Substance via MeSH
Medline Plus Health Information
*Listeria Infections

 Previous Article  |  Next Article 

Infection and Immunity, August 2005, p. 4787-4792, Vol. 73, No. 8
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.8.4787-4792.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Independent Protective Effects for Tumor Necrosis Factor and Lymphotoxin Alpha in the Host Response to Listeria monocytogenes Infection

D. R. Roach,1 H. Briscoe,2 B. M. Saunders,1,2 and W. J. Britton1,2*

Centenary Institute of Cancer Medicine and Cell Biology, Locked Bag No. 6, Newtown, NSW, 2042 Australia,1 Central Clinical School, University of Sydney, New South Wales, 2006 Australia2

Received 15 October 2004/ Returned for modification 23 November 2004/ Accepted 25 February 2005

Although the essential role of tumor necrosis factor (TNF) in resistance to Listeria monocytogenes infection is well established, the roles of the related cytokines lymphotoxin alpha (LT{alpha}) and lymphotoxin beta (LTß) are unknown. Using C57BL/6 mice in which the genes for these cytokines were disrupted, we examined the contributions of TNF, LT{alpha}, and LTß in the host response to Listeria. To overcome the lack of peripheral lymph nodes in LT{alpha}–/– and LTß–/– mice, bone marrow chimeras were constructed. TNF–/– and LT{alpha}–/– chimeras that lacked both secreted LT{alpha}3 and membrane-bound LT{alpha}1ß2 and LT{alpha}2ß1 were highly susceptible and succumbed 4.5 and 6 days, respectively, after a low-dose infection (200 CFU). LTß–/– chimeras, which lacked only membrane-bound LT, controlled the infection in a manner comparable to wild-type (WT) chimeras. The Listeria-specific proliferative and gamma interferon T-cell responses were equivalent in all five groups of infected mice (LT{alpha}–/– and LTß–/– chimeras, WT chimeras, and TNF–/– and WT mice). TNF–/– mice and LT{alpha}–/– chimeras, however, failed to generate the discrete foci of lymphocytes and macrophages that are essential for bacterial elimination. Rather, aberrant necrotic lesions comprised predominantly of neutrophils with relatively few lymphocytes and macrophages were observed in the livers and spleens of TNF–/– and LT{alpha}–/– chimeras. Therefore, in addition to TNF, soluble LT{alpha}3 plays a separate essential role in control of listerial infection through control of leukocyte accumulation and organization in infected organs.

* Corresponding author. Mailing address: Centenary Institute of Cancer Medicine and Cell Biology, Locked Bag No. 6, Newtown, NSW, 2042, Australia. Phone: 61-2-95155210. Fax: 61-2-93513968. E-mail: wbritton{at}medicine.usyd.edu.au.

Editor: J. L. Flynn

Infection and Immunity, August 2005, p. 4787-4792, Vol. 73, No. 8
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.8.4787-4792.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Hagge, D. A., Saunders, B. M., Ebenezer, G. J., Ray, N. A., Marks, V. T., Britton, W. J., Krahenbuhl, J. L., Adams, L. B. (2009). Lymphotoxin-{alpha} and TNF Have Essential but Independent Roles in the Evolution of the Granulomatous Response in Experimental Leprosy. Am. J. Pathol. 174: 1379-1389 [Abstract] [Full Text]  
  • Rutschmann, S., Hoebe, K., Zalevsky, J., Du, X., Mann, N., Dahiyat, B. I., Steed, P., Beutler, B. (2006). PanR1, a Dominant Negative Missense Allele of the Gene Encoding TNF-{alpha} (Tnf), Does Not Impair Lymphoid Development.. J. Immunol. 176: 7525-7532 [Abstract] [Full Text]  
  • Musicki, K., Briscoe, H., Tran, S., Britton, W. J., Saunders, B. M. (2006). Differential Requirements for Soluble and Transmembrane Tumor Necrosis Factor in the Immunological Control of Primary and Secondary Listeria monocytogenes Infection.. Infect. Immun. 74: 3180-3189 [Abstract] [Full Text]  
  • Liepinsh, D. J., Grivennikov, S. I., Klarmann, K. D., Lagarkova, M. A., Drutskaya, M. S., Lockett, S. J., Tessarollo, L., McAuliffe, M., Keller, J. R., Kuprash, D. V., Nedospasov, S. A. (2006). Novel Lymphotoxin Alpha (LT{alpha}) Knockout Mice with Unperturbed Tumor Necrosis Factor Expression: Reassessing LT{alpha} Biological Functions.. Mol. Cell. Biol. 26: 4214-4225 [Abstract] [Full Text]  
  • Bongartz, T., Sutton, A. J., Sweeting, M. J., Buchan, I., Matteson, E. L., Montori, V. (2006). Anti-TNF antibody therapy in rheumatoid arthritis and the risk of serious infections and malignancies: systematic review and meta-analysis of rare harmful effects in randomized controlled trials.. JAMA 295: 2275-2285 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»