To evaluate the effects of cannabis and/or cocaine use on inflammatory, oxidative stress status and circulating monocyte subsets in HIV-infected individuals under antiretroviral therapy.
Soluble CD14 (sCD14), intestinal fatty acid-binding protein (IFABP), tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, IL-8, IL-10, C-reactive protein (CRP) and oxidative stress markers were examined. The monocyte subsets and their activation and cytokine production by peripheral blood mononuclear cells (PBMCs) of HIV-1 infected individuals upon lipopolysaccharide (LPS)-stimulation were also investigated.
sCD14, IFABP, TNF-α, IL-6, IL-8 and IL-10 levels were evaluated using ELISA, CRP by turbidimetry; lipid peroxidation (TBARS) spectrofluometrically and total thiol levels by using 5–5′-dithio-bis (2-nitrobenzoic acid) reagent. Monocyte subsets and activation were assessed by flow cytometry.
All HIV-infected drug user groups showed higher sCD14 levels compared to HIV+ non-drug users. IFABP was increased in HIV+ drug-users in relation to healthy individuals. Cannabis use lowered the percentages of inflammatory, non-classical, activated-classic, and activated-inflammatory monocytes. Cocaine users showed increased plasmatic TNF-α and TBARS levels, decreased thiols content and lower activated-classic and inflammatory-monocyte percentages. Cannabis-plus-cocaine use increased CRP, IL-8 and IL-6/IL-10 ratio, but decreased thiols content, and inflammatory and activated-classic monocyte percentages. PBMCs of cannabis and cannabis-plus-cocaine users showed low potential cytokine production either spontaneously or under LPS-stimulation.
In HIV infection the use of cannabis induces predominantly an anti-inflammatory profile. The use of cocaine and cannabis-plus-cocaine showed a mixed pro- and anti-inflammatory profile, with predominance of inflammatory status. Further studies are required to better understand the action of these drugs in HIV infection.
aInstituto de Patologia Tropical e Saúde Pública, Universidade Federal de Goiás, Goiânia, Goiás, Brasil
bLaboratório de Imunologia Celular e Molecular, Programa de Pós-Graduação em Ciências da Saúde, Programa de Pós-Graduação em Ciências da Reabilitação, Universidade Federal de Ciências da Saúde de Porto Alegre, Porto Alegre, RS, Brasil
cPontifícia Universidade Católica de Goiás, PUC Goiás, Goiânia, Goiás, Brasil
dHospital de Doenças Tropicais de Goiás, HDT, Goiânia, Goiás, Brasil
eHospital das Clínicas Dr Serafim de Carvalho, Jataí, Goiás, Brasil
fDepartamento de Farmacociências, Universidade Federal de Ciências da Saúde de Porto Alegre, Porto Alegre, RS, Brasil
giii-INCT-Instituto de Investigação em Imunologia – Instituto Nacional de Ciência e Tecnologia, Brasil.
Correspondence to Simone Gonçalves da Fonseca, Instituto de Patologia Tropical e Saúde Pública – Universidade Federal de Goiás, Rua 235 S/N – Setor Universitário, 74605-050, Goiânia, Goiás, Brazil. Tel: 55 62 32096111; fax: 55 62 32096363; e-mail: email@example.com; Irmtraut Araci Hoffmann Pfrimer, Pontifícia Universidade Católica de Goiás (PUC Goiás), Rua 232 n° 128, Área V, 3° andar - Setor Leste Universitário, CEP: 74605-140 - Goiânia, GO, Brasil. Tel: 55 62 39461346; e-mail: firstname.lastname@example.org
Received 27 March, 2018
Revised 14 April, 2019
Accepted 21 May, 2019
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