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+ patie nts has any potential effect on monocyte phagocytic function both before an d after challenge of the monocytes with lipopolysaccharide (LPS) isolated f rom oral microorganisms. LPS of two putative periodontal pathogens Porphyro monas gingivalis (P. gingivalis) and Fusobacterium nucleatum (F. nucleatum) was prepared. Whole blood samples in EDTA were collected from 30 HIV+ pati ents presenting for dental care at the University of Maryland. Control samp les were prepared from appropriate uninfected individuals. Viral load was d etermined using quantitative RT-PCR (Amplicor(R), Roche Diagnostics). Phago cytic function was determined using FITC labeled Saccharomyces species in r esting isolated monocytes and in cells after 24 h stimulation with 1 mu g/m l 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 resti ng monocytes demonstrated phagocytic activity, while 23% of the resting con trol monocytes from noninfected individuals showed phagocytic function. Whe n the monocytes were stimulated with 1 mu g/ml of LPS of F. nucleatum, phag ocytic activity was observed in 18.5% of monocytes in patients with high vi ral 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 demons trated phagocytic activity. Stimulation of monocytes with LPS of P. gingiva lis showed similar results. Complement receptor CD-35 showed a 50% decrease in expression in HIV+ patients with high viral load. A progressive decreas e in monocyte/macrophage phagocytic function and CD-35 expression with and without: oral LPS activation occurs after HIV infection and this trend appe ars to be accentuated in patients with high viral load. This relationship m ay contribute to increased susceptibility to oral opportunistic infections in advanced HIV+ patients.