| First Author | Nishikawa S | Year | 1998 |
| Journal | Cell Immunol | Volume | 187 |
| Issue | 2 | Pages | 88-94 |
| PubMed ID | 9732696 | Mgi Jnum | J:49637 |
| Mgi Id | MGI:1277778 | Doi | 10.1006/cimm.1998.1329 |
| Citation | Nishikawa S, et al. (1998) Host resistance against Listeria monocytogenes is reciprocal during the course of infection in alymphoplastic aly mutant mice. Cell Immunol 187(2):88-94 |
| abstractText | The aly is a unique spontaneous autosomal recessive mutation in mice that causes a systemic defect of lymph nodes and Peyer's patches. We investigated host resistance against Listeria monocytogenes infection in the mutant. The 50% lethal dose oft. Monocytogenes in aly/aly mice was 10-fold higher than their heterozygotes, termed aly/+ mice, or their wild-type C57BL/6 mice. The bacterial growth in the spleens and livers of aly/aly mice was more efficient early in infection, and their listericidal activity of peritoneal macrophages was higher than those of aly/+ mice. In contrast, the complete elimination of bacteria from the spleens and livers of infected mice in the late stage of infection, in which a T-cell-dependent mechanism is required, was delayed in the aly/aly mice. Moreover, an acquired resistance against secondary infection with L. Monocytogenes was markedly diminished in the aly/aly mice. The production of endogenous interferon- gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF- alpha), which are critical in antilisterial resistance, was reduced in the aly/aly mice during the infection. The production of IFN-gamma, TNF-alpha, and interleukin-4 was also diminished in the spleen cell cultures of aly/aly mice when stimulated with heat-killed L. Monocytogenes or the T-cell receptors were directly stimulated with anti- CD3-epsilon monoclonal antibody. These results suggest that acquired immunity against L. Monocytogenes infection is attenuated in aly/aly mice, and that the insufficient production of IFN-gamma and TNF-alpha might be involved in the immunodeficiency. (C) 1998 Academic Press. |
