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J Int AIDS Soc. 2016 May 16;19(1):20759. doi: 10.7448/IAS.19.1.20759. eCollection 2016.

The impact of HIV infection on blood leukocyte responsiveness to bacterial stimulation in asymptomatic patients and patients with bloodstream infection.

Author information

1
Center of Experimental and Molecular Medicine, Division of Infectious Diseases, Academic Medical Center, University of Amsterdam, Amsterdam, Netherlands.
2
Center of Tropical Medicine and Travel Medicine, Division of Infectious Diseases, Academic Medical Center, University of Amsterdam, Amsterdam, Netherlands.
3
Centre des Recherches Médicales de Lambaréné, Lambaréné, Gabon; m.a.huson@amc.uva.nl.
4
Centre des Recherches Médicales de Lambaréné, Lambaréné, Gabon.
5
Institute of Tropical Medicine, University of Tübingen, Tübingen, Germany.

Abstract

INTRODUCTION:

HIV-induced changes in cytokine responses to bacteria may influence susceptibility to bacterial infections and the consequent inflammatory response.

METHODS:

We examined the impact of HIV on whole blood responsiveness to bacterial stimulation in asymptomatic subjects and patients with bacterial bloodstream infection (BSI). Whole blood was stimulated ex vivo with two bacterial Toll-like receptor agonists (lipopolysaccharide and lipoteichoic acid) and two pathogens (Streptococcus pneumoniae and non-typhoidal Salmonella), which are relevant in HIV-positive patients. Production of interferon-γ, tumour necrosis factor-α, interleukin-1β and interleukin-6 was used as a read-out.

RESULTS:

In asymptomatic subjects, HIV infection was associated with reduced interferon-γ, release after stimulation and priming of the pro-inflammatory cytokine response to non-typhoidal Salmonella. In patients with BSI, we found no such priming effect, nor was there evidence for more profound sepsis-induced immunosuppression in BSI patients with HIV co-infection.

CONCLUSIONS:

These results suggest a complex effect of HIV on leukocyte responses to bacteria. However, in patients with sepsis, leukocyte responses were equally blunted in patients with and without HIV infection.

KEYWORDS:

HIV; bacterial infections; cytokines; innate immunity; leukocyte reprogramming; sepsis

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