ROLES FOR TUMOR-NECROSIS-FACTOR AND GAMMA-INTERFERON IN RESISTANCE TOENTERIC LISTERIOSIS

Listeria monocytogenes normally infects the host by translocating from the intestinal lumen. Experiments mere carried out to determine if, w hen, and where tumor necrosis factor (TNF) and gamma interferon (IFN-g amma) function in antibacterial resistance during enteric listeriosis. Groups of normal mice and severe combined immunodeficient (SCID) mice were injected with neutralizing monoclonal antibodies (MAb) specific for each cytokine and then inoculated intragastrically with L. monocyt ogenes. The course of infection was monitored by enumerating listeriae in gut-associated lymphoid tissues, livers, and spleens. By the third day of infection, bacterial numbers in infected tissues and organs we re greatly exacerbated in all mice treated with anti-TNF MAb, whereas bacterial numbers in the organs of mice treated with anti-IFN-gamma MA b did not differ fi-om those present in the respective organs of contr ol mice. However, by the fifth day of infection, bacterial numbers in the organs of anti-IFN-gamma MAb-treated normal mice and SCID mice wer e much greater than in the corresponding organs of control mice. Exper iments with Listeria-immune mice revealed that TNF and IFN-gamma are i nvolved in the expression of anti-listeria memory immunity; however, i t was also found that the anti-IFN-gamma MAb was relatively ineffectiv e in inhibiting the expression of anti-Listeria immunity, whereas a po lyclonal anti-IFN-gamma was quite effective.