HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Hayder, H. Articles by Müllbacher, A. Search for Related Content PubMed PubMed Citation Articles by Hayder, H. Articles by Müllbacher, A. Pubmed/NCBI databases Compound via MeSH Substance via MeSH

Adenovirus-Induced Liver Pathology Is Mediated Through TNF Receptors I and II but Is Independent of TNF or Lymphotoxin

Hikmat Hayder^*, Robert V. Blanden^*, Heinrich Körner^1,, D. Sean Riminton, Jonathon D. Sedgwick^2, and Arno Müllbacher^3,*

^* Division of Immunology and Cell Biology, John Curtin School of Medical Research, Australian National University, Canberra, Australia; and Centenary Institute of Cancer Medicine and Cell Biology, Royal Prince Alfred Hospital, Sydney, Australia

Mice infected with an adenovirus mutant in which the E3 region is deleted, including TNF-resistance genes, develop fatal liver pathology within 3–4 days after infection. At least 10-fold more wild-type virus was needed to cause comparable pathology. These results indicate that the E3 region is critically involved in modulating the pathogenesis of adenovirus infection and that TNF may play a role in liver damage. To explore the latter possibility, the course of disease was examined in infected mice lacking TNFR-I and/or TNFRII, TNF only, or both TNF and lymphotoxin-. Only mice lacking both TNFRI and TNFRII were protected from the lethal affects of the mutant adenovirus. Mice deficient in TNF or TNF and lymphotoxin- displayed the fatal pathology. This outcome is consistent with the existence of another related ligand that binds TNFRI/II to mediate liver damage during infection with this mutant.

This article has been cited by other articles:

				P. J. Shaw, P. E. Ganey, and R. A. Roth Tumor Necrosis Factor{alpha} Is a Proximal Mediator of Synergistic Hepatotoxicity from Trovafloxacin/Lipopolysaccharide Coexposure J. Pharmacol. Exp. Ther., January 1, 2009; 328(1): 62 - 68. [Abstract] [Full Text] [PDF]

				S. Akai, H. Hosomi, K. Minami, K. Tsuneyama, M. Katoh, M. Nakajima, and T. Yokoi Knock Down of {gamma}-Glutamylcysteine Synthetase in Rat Causes Acetaminophen-induced Hepatotoxicity J. Biol. Chem., August 17, 2007; 282(33): 23996 - 24003. [Abstract] [Full Text] [PDF]

				D. Cai, M. Xaymardan, J. M. Holm, J. Zheng, J. R. Kizer, and J. M. Edelberg Age-associated impairment in TNF-{alpha} cardioprotection from myocardial infarction Am J Physiol Heart Circ Physiol, July 11, 2003; 285(2): H463 - H469. [Abstract] [Full Text] [PDF]

				J. Schumann, K. Muhlen, A. K. Kiemer, A. M. Vollmar, and G. Tiegs Parenchymal, But Not Leukocyte, TNF Receptor 2 Mediates T Cell-Dependent Hepatitis in Mice J. Immunol., February 15, 2003; 170(4): 2129 - 2137. [Abstract] [Full Text] [PDF]

				S. Balkow, A. Kersten, T. T. T. Tran, T. Stehle, P. Grosse, C. Museteanu, O. Utermohlen, H. Pircher, F. von Weizsacker, R. Wallich, et al. Concerted Action of the FasL/Fas and Perforin/Granzyme A and B Pathways Is Mandatory for the Development of Early Viral Hepatitis but Not for Recovery from Viral Infection J. Virol., September 15, 2001; 75(18): 8781 - 8791. [Abstract] [Full Text] [PDF]

				P. Wilhelm, U. Ritter, S. Labbow, N. Donhauser, M. Rollinghoff, C. Bogdan, and H. Korner Rapidly Fatal Leishmaniasis in Resistant C57BL/6 Mice Lacking TNF J. Immunol., March 15, 2001; 166(6): 4012 - 4019. [Abstract] [Full Text] [PDF]