Immune Response Against Salmonella Enteritidis Is Unsettled by HIV Infection

Abstract

The human immunodeficiency virus (HIV) is responsible for more than 2 million new infections per year and opportunistic infections such as Salmonella spp. Gastroenteritis is an important cause of mortality and morbidity in developing countries. Monocytes and macrophages play a critical role in the innate immune response against bacterial infections. However during HIV infection the virus can infect these cells and although they are more resistant to the cytopathic effects, they represent an important viral reservoir in these patients. Our aim was to evaluate the monocyte functions from HIV-1 infected patients after in vitro exposition to Salmonella Enteritidis. Our results suggest impairment of monocytes phagocytic and microbicidal activity in HIV-1 non-treated patients, which was more evident in women, if compared with men. Moreover, monocytes from HIV-1 infected and non-treated patients after stimulation with the bacteria, produced more pro-inflammatory cytokines than monocytes from HIV-treated patients, suggesting that HIV-1 infected patients have their functions unbalanced, once in the presence of an opportunistic infection in vitro.

HIV and Mediterranean Zoonoses: A Review of the Literature

“…The severity of iNTS in PLWH may be due to an impaired immune response to the infection, as suggested in a study by MacLennan et al [ 84 ]; specifically, it was reported that an excess of antibodies against Salmonella lipopolysaccharide (LPS) is associated with a reduction in Salmonella killing. Other reasons behind the severity of iNTS in PLWH may be found in the dysregulation of proinflammatory cytokine release, such as TNF alpha, IL-10 and IL-12 [ 85 ], the attenuation of transcription factor nuclear κB (NFκB)-mediated inflammation [ 86 ], the defective activity of monocytes phagocytosis [ 87 ] and the apparent enhanced capacity of a specific sequence type 313 (ST313) of S. typhimurium of surviving in HIV-infected macrophages and their defective phagocytic ability [ 88 , 89 ].…”