These data suggest that oestrogen contributes to the persistence

These data suggest that oestrogen contributes to the persistence of autoreactive T cells through the defective control of apoptosis, and may also provide a clue as to how oestrogen triggers SLE

activity. However, it remains unclear as to whether oestrogen affects the survival of peripheral T cells reactive to self-antigens in vivo. In addition, we did not examine the tripartite relationship among oestrogen, T cell apoptosis and disease activity in SLE patients. Further longitudinal study is required to clarify these issues. This research was supported by Basic Science Research Program through JNK inhibitor the National Research Foundation funded by the Ministry of Education, Science and Technology (No. 314-2008-1-E00113) and by a grant from the Korea Association of Internal Medicine. None. “
“Increased susceptibility to tuberculosis following

HIV-1 seroconversion contributes significantly to the tuberculosis epidemic in sub-Saharan Africa. Lung-specific mechanisms underlying the interaction between HIV-1 and Mycobacterium tuberculosis infection are incompletely understood. Here we address these questions by examining the effect of HIV-1 and latent M. tuberculosis co-infection on the expression of viral-entry receptors and ligands in bronchoalveolar lavage (BAL) of HIV-1-infected and -uninfected patients with and without latent M. tuberculosis infection. Irrespective of HIV-1 status, T cells from BAL expressed higher levels of the beta-chemokine receptor (CCR)5 than peripheral blood T cells, in particular the CD8+ T cells of HIV-1-infected persons showed elevated CCR5 expression. The concentrations of Fludarabine solubility dmso the CCR5 ligands RANTES and MIP-1β were elevated Staurosporine order in the BAL of HIV-1-infected persons compared with that in HIV-1-uninfected controls.

CCR5 expression and RANTES concentration correlated strongly with HIV-1 viral load in the BAL. In contrast, these alterations were not associated with M. tuberculosis sensitisation in vivo, nor did M. tuberculosis infection of BAL cells ex vivo change RANTES expression. These data suggest ongoing HIV-1 replication predominantly drives local pulmonary CCR5+ T-cell activation in HIV/latent M. tuberculosis co-infection. “
“Biofilm infections may not simply be the result of colonization by one bacterium, but rather the consequence of pathogenic contributions from several bacteria. Interspecies interactions of different organisms in mixed-species biofilms remain largely unexplained, but knowledge of these is very important for understanding of biofilm physiology and the treatment of biofilm-related infectious diseases. Here, we have investigated interactions of two of the major bacterial species of cystic fibrosis lung microbial communities –Pseudomonas aeruginosa and Staphylococcus aureus– when grown in co-culture biofilms. By growing co-culture biofilms of S. aureus with P.

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