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. 2000 Apr;120(1):107-12.
doi: 10.1046/j.1365-2249.2000.01201.x.

Impact of highly active anti-retroviral therapy (HAART) on cytokine production and monocyte subsets in HIV-infected patients

N Amirayan-Chevillard  1 , H Tissot-Dupont, C Capo, C Brunet, F Dignat-George, Y Obadia, H Gallais, J L Mege
Affiliations

Impact of highly active anti-retroviral therapy (HAART) on cytokine production and monocyte subsets in HIV-infected patients

N Amirayan-Chevillard et al. Clin Exp Immunol. 2000 Apr.

Abstract

HIV infection is associated with cytokine production by monocytes and expansion of a monocyte subset that expresses high levels of CD16. Our study was designed to investigate the effects of anti-retroviral therapies on these immune parameters. Four groups of HIV+ patients were included in the study. The first group comprised drug-naive patients (n = 20); the second included patients who received two inhibitors of HIV reverse transcriptase (n = 45); the third group received a therapy combining these two inhibitors and one inhibitor of HIV protease (HAART) (n = 35); the fourth consisted of patients who had stopped their treatment (n = 20). The release of inflammatory cytokines (tumour necrosis factor, IL-1beta, IL-6) and immunoregulatory cytokines such as IL-10 by monocytes was determined by ELISA. The monocyte subsets expressing low or high levels of CD16 were studied by flow cytometry. Monocytes from patients naive of treatment released higher amounts of inflammatory cytokines and IL-10 than HIV- individuals. Each anti-retroviral therapy restored a normal pattern of cytokine secretion. Nevertheless, the release of cytokines increased again after the arrest of the treatment. The expansion of the monocyte subset that expresses high levels of CD16 was significantly decreased by HAART but not by the treatment including two inhibitors of reverse transcriptase. These results suggest that only HAART controls monocyte activation in the treatment of HIV infection.

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Figures

Fig. 1
Fig. 1
Spontaneous release of monocyte cytokines and anti-retroviral therapy. Adherent monocytes were isolated from controls (n = 20), HIV-infected patients naive of treatment (n = 20), patients treated with two reverse transcriptase (RT) inhibitors (double therapy, n = 45), patients undergoing HAART (n = 35), or patients who had discontinued treatment (n = 20). Monocytes were cultured for 16 h at 37°C and cell supernatants were assayed by ELISA for cytokines. Results are expressed as means ± s.e.m. *P = 0·0001; **P = 0·0002; ***P = 0·002, compared with HIV-infected patients naive of treatment.
Fig. 2
Fig. 2
Lipopolysaccharide (LPS)-stimulated production of cytokines and anti-retroviral therapy. The status of patients is described in Fig. 1. Monocytes were cultured in the presence of LPS (1 μg/ml) for 16 h at 37°C and cell supernatants were assayed by ELISA for cytokines. Results are expressed as means ± s.e.m. *P = 0·003; **P = 0·02; ***P = 0·01, compared with HIV-infected patients naive of treatment.
Fig. 3
Fig. 3
Monocyte subsets and anti-retroviral therapy. Blood cells were double-stained with FITC-conjugated anti-CD14 MoAbs and PE-conjugated anti-CD16 MoAbs. The cell analysis was performed with a flow cytometer. (a) The left panel represents monocytes from a control individual while the right panel corresponds to a representative HIV-infected patient naive of treatment. (b) Monocytes from controls, HIV-infected patients naive of treatment, patients treated with two reverse transcriptase (RT) inhibitors (double therapy), patients undergoing HAART, or patients who had stopped their treatment were analysed. The number of CD16high monocytes was calculated as percentage ± s.e.m. of CD14-expressing cells. *P = 0·05 compared with HIV-infected patients naive of treatment.
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