Actinobacillus actinomycetemcomitans suppresses rat natural killer cell activity in vivo

Objective - To examine the immune suppressive effect of Actinobacillus actinomycetemcomitans (Aa) on rat natural killer (NK) cell activity in vivo. Material and Methods - Sprague-Dawley rats were given Aa in 2 different manners: (i) by mixing Aa with food at a dose of 10⁸ cells/rat/day for 3 months; or (ii) by a single i.m. injection of live Aa at doses of 10⁶ and 10⁷ cells/rat/day. NK cell activity was measured by means of a ⁵¹Cr-release assay using YAC-1 tumor cells as targets. Results - Rats that had been infected by Aa mixed with food experienced significant suppression of their NK cell activity; this reached ≈ 50% of control values at 2 and 3 months post-Aa infection. The suppression in NK cell activity was related to decreases in the extent of conjugate formation between effectors and YAC-1 target tumor cells (51.7%) and the extent of lysis of target cells (75.7%). The results also showed that addition of an admixture of Aa-treated NK cells to the control NK cells caused 75% and 53% decreases in activity at effector:target ratios of 25:1 and 50:1, respectively. In addition, a significant increase in the extent of T-suppressor cells (154.8% of control) was detected at 3 months post-Aa infection. In contrast, the single injection of live bacteria resulted in a remarkable, dose-dependent inhibition of NK cell activity (55% and 71% at doses of 10⁶ and 10⁷ cells/rat/day, respectively) as early as 2 days post-treatment. This also reflected significant suppression in the effector:target conjugate formation ratio (52% of control). The data also revealed a 150-188% increase in the number of splenic lymphocytes post-Aa injection. These effects were transient and normal levels were re-established by the fifth day. Conclusion - Aa treatment causes suppression of NK cell activity and the mode of action may be due to induction of T-suppressor cells or dilution of NK cells with other lymphoid cell populations. The degree of suppression is affected by the way in which Aa is introduced to the host. These results may contribute to the understanding of how Aa evades host defense.