Herpes simplex virus-induced suppression of macrophage-mediated tumoricidal activity in murine macrophages.

Herpes simplex virus (HSV) infections can enhance the progression of neoplastic diseases. Since macrophages can be activated to become tumorilytic and may figure prominently in host defense against cancer, the ability of HSV to modify macrophage-mediated tumoricidal functions was evaluated. Murine peritoneal macrophages treated with HSV could not be activated to a tumoricidal state by mouse recombinant gamma-interferon (IFN-gamma).

Regulatory effects on macrophages of human recombinant interferons-alpha.

The regulatory effects of human recombinant and hybrid interferons-alpha (IFN-alpha) on macrophage-mediated tumoricidal activity were examined. Recombinant hybrid IFN-alpha-A/D suppressed the capacity of murine interferon-gamma (IFN-gamma) to activate mouse peritoneal macrophages to a tumorilytic state, and blocked the killing of syngeneic syngeneic melanoma target cells by macrophages previously committed to the cytotoxic phenotype with a 4-h pretreatment with IFN-gamma. This suppressive activity was limited to IFN-alpha-A/D, as IFN-alpha-A and IFN-alpha-D were not effective.

Catecholamine-induced suppression of interleukin-1 production.

Recent evidence indicates that stress can suppress immune responses and thus increase the severity of viral and neoplastic diseases. Although, the mechanisms for stress-induced modulation of immunologic competence are unclear, neuroendocrine hormones are thought to be involved. A direct suppressive effect could result from the action of neuroendocrine hormones on lymphokine and monokine release.

Neuroendocrine hormones suppress macrophage-mediated lysis of herpes simplex virus-infected cells.

Herpes simplex viruses (HSV) remain latent in sensory and peripheral ganglia and can be reactivated to cause recurrent HSV infections. Recent evidence has suggested that stress can induce an immunosuppressive state and increase the frequency and severity of recurrent herpes infections. Because macrophages play a central role in the host defense against HSV, the effects of stress-related neuroendocrine hormones on macrophage-HSV interactions were examined.

Modulation of macrophage-mediated tumoricidal activity by neuropeptides and neurohormones.

Recent evidence has suggested that stress may suppress the immune system and increase the frequency and severity of viral and neoplastic disease. The mechanisms for stress-induced modulation of immune function are unclear, but several neuropeptides are thought to be involved. Because macrophages play an important role in the host defense against infection and neoplasia, several stress-related neuropeptides were screened in efforts to determine whether these substances affect macrophage-mediated tumoricidal activity.