Abstract:
:Disseminated infection with virulent Mycobacterium avium in C57Bl/6 (B6) mice leads to severe lymphocyte depletion in secondary lymphoid organs. In this study, we found an up-regulation of caspase-8 activity in spleen cell extracts from M. avium 25291-infected B6 mice compared to non-infected mice. The activation of this extrinsic apoptotic pathway correlated with an increase in inter-nucleosomal DNA fragmentation in CD4(+) spleen cells, as analysed by the terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) assay. These data suggest the involvement of death receptors in the induction of lymphocyte loss in the spleen, but previous work has excluded a role for tumour necrosis factor (TNF) receptors and Fas/CD95 in M. avium-induced lymphopenia. TNF-related apoptosis-inducing ligand (TRAIL) is expressed by different cell types of the immune system and induces apoptosis and killing of tumour cells while sparing normal cells. Here we used TRAIL(-/-) mice to determine if the absence of TRAIL prevented M. avium-induced immune pathology. We found that TRAIL-deficient mice still developed splenic lymphopenia during disseminated infection or granuloma necrosis during low-dose infections while exhibiting slightly increased susceptibility to M. avium 25291 when compared to B6 mice. However, in vivo proliferation of less virulent strains of M. avium was not influenced by TRAIL deficiency despite a decrease in interferon-γ production in infected B6.TRAIL(-/-) mice compared to B6 mice. Our results show that TRAIL does not play a significant role in either M. avium-induced pathology or protective immunity.
journal_name
Clin Exp Immunoljournal_title
Clinical and experimental immunologyauthors
Borges M,Rosa GT,Appelberg Rdoi
10.1111/j.1365-2249.2011.04385.xsubject
Has Abstractpub_date
2011-06-01 00:00:00pages
407-16issue
3eissn
0009-9104issn
1365-2249journal_volume
164pub_type
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