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Upregulation of p75 Tumor Necrosis Factor Alpha Receptor in Mycobacterium avium-Infected Mice: Evidence for a Functional Role

By Angelo Corti, Lanfranco Fattorini, Ove Fredrik Thoresen, Maria Luisa Ricci, Anna Gallizia, Micaela Pelagi, Yongjun Li and Graziella Orefici


The bacterial growth and the production of tumor necrosis factor alpha (TNF-α) and TNF receptors (TNF-Rs) in the spleen and blood of BALB/c mice challenged with Mycobacterium avium complex (MAC) were monitored. Infection developed in two phases: the first, up to day 21, was associated with rapid MAC multiplication in the spleen and a drop in the mycobacteremia, and the second was associated with control of the infection in both compartments. In the spleen, TNF-α and TNF-RII mRNA levels peaked on day 21 and then slowly decreased; however, no increase in the level of TNF-RI mRNA was observed throughout these experiments. The level of circulating soluble TNF-RII (sTNF-RII) was transiently increased after day 21. In a model in which overproduction of bioactive TNF-α was triggered in response to a second infection with MAC, an increased production of sTNF-RII by cultured splenocytes was also observed. Administration of an antagonist anti-TNF-RII monoclonal antibody (MAb 6G1) to infected mice inhibited the bacterial growth in the spleen, suggesting that the TNF-RII and/or sTNF-RII was functionally involved in the mechanisms that control the infection. Overall, these observations suggest that upregulation of TNF-RII or sTNF-RII contributes to modulation of the TNF-α antibacterial activity in MAC infections

Topics: Host Response and Inflammation
Publisher: American Society for Microbiology
Year: 1999
OAI identifier: oai:pubmedcentral.nih.gov:96952
Provided by: PubMed Central
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