The effects of HIV viral load on the phagocytic activity of monocytes activated with lipopolysaccharide from oral microorganisms

A study was undertaken to determine whether viral load status in HIV+ patients has any potential effect on monocyte phagocytic function both before and after challenge of the monocytes with lipopolysaccharide (LPS) isolated from oral microorganisms. LPS of two putative periodontal pathogens Porphyromonas gingivalis (P. gingivalis) and Fusobacterium nucleatum (F. nucleatum) was prepared. Whole blood samples in EDTA were collected from 30 HIV+ patients presenting for dental care at the University of Maryland. Control samples were prepared from appropriate uninfected individuals. Viral load was determined using quantitative RT-PCR (Amplicor(R), Roche Diagnostics). Phagocytic function was determined using FITC labeled Saccharomyces species in resting isolated monocytes and in cells after 24 h stimulation with 1 mu g/ml of LPS of P. gingivalis or F. nucleatum. Immunohistochemical staining was performed for complement receptor CR-1 (CD-35) on phagocyte cells. In HIV+ patients with high viral load (>10,000 copies/ml), 13.5% of isolated resting monocytes demonstrated phagocytic activity, while 23% of the resting control monocytes from noninfected individuals showed phagocytic function. When the monocytes were stimulated with 1 mu g/ml of LPS of F. nucleatum, phagocytic activity was observed in 18.5% of monocytes in patients with high viral load, 33.5% with moderate viral load (400-10,00 copies/ml) and 51% with low viral load (<400 copies/ml), while 62% of the control monocytes demonstrated phagocytic activity. Stimulation of monocytes with LPS of P. gingivalis showed similar results. Complement receptor CD-35 showed a 50% decrease in expression in HIV+ patients with high viral load. A progressive decrease in monocyte/macrophage phagocytic function and CD-35 expression with and without: oral LPS activation occurs after HIV infection and this trend appears to be accentuated in patients with high viral load. This relationship may contribute to increased susceptibility to oral opportunistic infections in advanced HIV+ patients.