Suppressed phagocytosis but promoted bacterial growth upon the effect of virus free supernatants of infected lymphocytes.

ABSTRACT

The pathomechanism of suppressed phagocytosis and bacterial superinfections which follow viral diseases is not completely understood. Both polymorphonuclear leukocytes (PMNL) and mononuclear phagocytes (MNPh) as well as bacterial growth are controlled by several cytokines produced by other immune cells. The effect of disturbed production of cytokines on phagocytes and microbes have not been studied yet. Peripheral T lymphocytes were infected with human adenoviruses (Ad) and herpes simplex virus type 1 (HSV-1) or were activated by phytohaemagglutinin (PHA), then culture supernatants containing no infectious virus were mixed to phagocytes swallowing viable Staphylococcus aureus. Influence of supernatants on eukaryotic and bacterial cell growth was compared to cytokine assays. Supernatant mediators, different from interferon (IFN) and tumour necrosis factor (TNF), induced by oncogenic Ad-12 or HSV-1 diminished phagocytosis of both PMNL and MNPh in a dose dependent manner, promoted bacterial growth free and inside MNPh, while those of latent Ad-5 and nononcogenic Ad-8 exerted moderate effects. Plating efficiency of HEp-2 cells was decreased by all of them. Supernatants of PHA treated lymphocytes containing IFN-gamma enhanced both phagocytosis and bacterial replication free and inside MNPh, while it suppressed HEp-2 plating. Neither viruses nor PHA affected phagocytic process directly. Staphylococci inside PMNL were not affected. Presumably, production of a single mediator by infected T lymphocytes is responsible for the multiple effects. Relationship with another soluble factors is discussed.