First Author | Jacobs M | Year | 2000 |
Journal | Clin Immunol | Volume | 94 |
Issue | 3 | Pages | 192-9 |
PubMed ID | 10692238 | Mgi Jnum | J:60961 |
Mgi Id | MGI:1354129 | Doi | 10.1006/clim.2000.4835 |
Citation | Jacobs M, et al. (2000) Fatal Mycobacterium bovis BCG infection in TNF-LT-alpha-deficient mice. Clin Immunol 94(3):192-9 |
abstractText | Neutralization of TNF or disruption of TNF-R1 leads to fatal Mycobacterium bovis BCG infection. Here we used TNF-LT-alpha-deficient mice to test whether a complete disruption of TNF and LT-alpha reduces further host resistance to BCG infection. The bacterial burden especially in the lungs of TNF-LT-alpha-deficient mice was significantly increased and the mice succumbed to infection between 8 and 10 weeks. In the absence of TNF-LT-alpha the granulomatous response was severely impaired and delayed. The cells in the granulomas of TNF-LT-alpha-deficient mice expressed low levels of MHC class II and ICAM-1. They contained a few T cells and F4/80-positive macrophages expressing little iNOS and acid phosphatase activity. By contrast, the lethal action of endotoxin was dramatically reduced in BCG-infected TNF-LT-alpha-deficient mice. In summary, in the absence of TNF-LT-alpha the recruitment and activation of mononuclear cells in response to BCG infection were significantly delayed and reduced resulting in immature granulomas allowing uncontrolled fatal infection. Copyright 2000 Academic Press. |