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and tumour necrosis factor- synergistically activates mouse macrophages after infection with herpes simplex virus type 2Institute of Medical Microbiology, University of Aarhus, DK-8000 Aarhus C, Denmark
Resistance of mice to infection with herpes simplex virus type 2 (HSV-2) is strongly dependent on the function of macrophages (M
). Infection of mouse M with HSV-2 results in an early (4 to 10 h) activation of the cells with an enhanced respiratory burst generated after membrane triggering with a phorbol ester. The role of monokines produced during this infection was analysed. Both interferon-
/
(IFN-/) and tumour necrosis factor- (TNF-) were produced within the very first hours after infection of M with HSV-2. Exogenously added IFN-/ conferred to M a respiratory burst capacity comparable to that seen after virus infection, whereas TNF- by itself was unable to prime M for a respiratory burst. In fact concentrations of TNF- comparable to those found in HSV-2-infected M cultures generally suppressed the response. However, when TNF- was added together with IFN-/ a dose-dependent synergistic enhancement of the IFN-induced M activation was seen. The kinetics of the synergistic activation by the two monokines was similar to that seen with IFN-/ alone. Neutralizing antibodies to IFN-/ and TNF- were able to diminish the HSV-induced priming of M for a respiratory burst. When the two antibodies were used together in subneutralizing concentrations an additional diminution of the responsiveness was seen, indicating that both monokines are involved in the virus-induced priming of M. However, high concentrations of antibodies to IFN-/ alone were able to abolish the activation completely, whereas this was not the case with anti-TNF-. Collectively these data demonstrate that autocrine secretion of IFN-/ by M infected with HSV-2 is a sine qua non for the activation of M during the infection, and that this effect of IFN is synergistically enhanced, also in an autocrine manner, by TNF-. It is suggested that this reciprocal M-monokine interaction may be of importance in resistance to virus infections.
Received 9 February 1993;
accepted 28 May 1993.
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