Inhibition of Human Monocyte Function by Prophylactic Doses of Chloroquine

Lm, Osorio; Fonte, Luis; Cm, Finlay

doi:10.4269/ajtmh.1992.46.165

Cited by 12 publications

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“…Six of the patients treated with prednisolone also received treatment with chloroquine. Chloroquine inhibits phagocytosis [42] and superoxide production [43] by monocytes. No reports are available on the effect of chloroquine on monocyte adhesion receptors.…”

Section: Discussionmentioning

confidence: 99%

Monocyte activation in rheumatoid arthritis (RA): increased integrin, Fcγ and complement receptor expression and the effect of glucocorticoids

Torsteinsdottir¹,

Arvidson

Hällgren

et al. 1999

Clinical and Experimental Immunology

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SUMMARYThe aim of this work was to study the expression of b 1 -and b 2 -integrins, CR1, CD44 and Fcg receptors on peripheral blood monocytes in RA. The expression of these receptors was measured by flow cytometry, before and after treatment with low-dose prednisolone. Expression of the same receptors was also measured before and after treatment with metyrapone, a substance that inhibits the synthesis of cortisol in the adrenals. The expression of the b 2 -integrins CD11a, CD11b and CD18, of CD35 (CR1), and of FcgRII and FcgRI (CD32 and CD64) on monocytes was elevated in the RA patients compared with healthy controls, while the expression of the b 1 -integrins (CD29, CD49d, CD49f) was unaffected. A significant correlation between monocyte expression of CD64 and C-reactive protein (CRP), and blood platelet count, respectively, was found in the group of patients with RA. After 4-6 weeks of treatment with low-dose prednisolone, the expression on the monocytes of CD11a, CD11b, CD18, CD35, CD32 and CD64 was normalized. A significant correlation (r ¼ 0·64, P ¼ 0·02) was found between the decrease in expression of CD11b and clinical improvement after prednisolone treatment. Two days of metyrapone treatment, which significantly lowered the serum cortisol levels, elevated the expression of CD35 and CD49f. Priming of peripheral monocytes seems to be one of the mechanisms behind the recruitment of monocytes to the rheumatoid synovium. One reason for the good clinical effects of prednisolone in RA could be a down-regulation of adhesion and phagocytosis receptors on monocytes.

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Section: Discussionmentioning

confidence: 99%

Monocyte activation in rheumatoid arthritis (RA): increased integrin, Fcγ and complement receptor expression and the effect of glucocorticoids

Torsteinsdottir¹,

Arvidson

Hällgren

et al. 1999

Clinical and Experimental Immunology

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“…However, the finding that chloroquine enhances the production of IL‐10 in the absence of antigen and mitogen stimulation and that TT does not further increase the number of IL‐10‐producing cells, suggests that it is the APCs that produce the IL‐10. Also resembling alternatively activated APCs, monocytes from individuals on chloroquine prophylaxis show inhibited phagocytosis in vitro [44–46]. Thus, it might be that chloroquine affects the maturation and/or stimulation of monocytes in an alternative way, resulting in anti‐inflammatory signals or tolerance in the immune system.…”

Section: Discussionmentioning

confidence: 99%

Chloroquine Enhances the Number of IL‐10 Producing Cells and the Expression of B7‐2 and ICAM‐1 in In Vitro‐Cultured PBMC

Hugosson

Björkman

2002

Scand J Immunol

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Chloroquine is prescribed as both an anti-malarial and an anti-inflammatory drug. However, its immunomodulating effects remain largely unclear. Previous studies have shown that chloroquine inhibits antigeninduced proliferation, implying immuno-suppressive effects. In this study, we examined whether the inhibition of the proliferation reflects changes in the surface molecules that are important for T-cell activation and whether chloroquine affects the balance between pro-and anti-inflammatory cytokines. Chloroquine elevated the expression of the costimulatory and adhesion molecules B7-2 (CD86) and ICAM-1 (CD54) in peripheral mononuclear cells (PBMC). An increased percentage of CD14 cells was also observed, and within this cell population, an increase in ICAM-1 expression was revealed by double-staining experiments. Assessment of the frequencies of interleukin (IL)-10 and interferon (IFN)-g-producing cells in in vitro-cultivated PBMCs showed that the ratio between pro-and antiinflammatory cytokines changed after exposure to chloroquine, favouring anti-inflammatory immune responses. This effect was mainly because of increased frequencies of IL-10-producing cells and was seen with or without the presence of stimulating antigens or mitogens. Our findings indicate that chloroquine affects the direction of the lymphocyte stimulation towards an anti-inflammatory response by affecting the antigen-presenting cells (APC) and the balance between pro-and anti-inflammatory cytokines, rather than generally inhibiting cytokine production.

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“…Essa última ação dependeu do tempo e da dose da droga agindo sobre os fagócitos (Prasad, 1987). A cloroquina diminuiu também a fagocitose de eritrócitos de carneiro sensibilizados com IgG e de S. cerevisiae por monócitos de indivíduos tratados com cloroquina (Osorio e cols, 1992). Entretanto, diferentemente, a cloroquina aumentou a atividade de fagócitos mononucleares humanos para C. neoformans, por mecanismo independente de ferro, mas dependente do aumento do pH no fagolissosomo do fagócito (Levitz e cols, 1997).…”

Section: Produção De óXido Nítricounclassified

Influência das drogas antiparasitárias cloroquina, primaquina e sulfato de quinina sobre a capacidade fagocitária, expressão de corpúsculo lipidico e produção de radicais de oxigênio e nitrogênio pelos monócitos humanos estimulados com eritrócitos parasitados pelo Plasmodium falciparum

Oliveira¹

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Agradeço a Deus pela minha vida e por me manter firme em meus propósitos de vida. À minha mãe, que é tudo na minha e maior exemplo de amor ao próximo. Aos meus irmãos e irmãs, pelo carinho e incentivo. Aos meus sobrinhos, por serem a alegria da minha vida. Ao meu marido Jean Claude Ribeiro, pelo companheirismo, paciência e amor. Às minhas cunhadas, pelo incentivo. À professora Maria Imaculada Muniz Barbosa Junqueira, minha orientadora e chefe, pela oportunidade que me foi confiada, pelo incentivo e apoio em momentos de fraqueza. Pelo conhecimento a mim transmitido, pela paciência e persistênica, generosidade, dedicação, reconhecimento e amorozidade. Muito obrigada por tudo! Ao meu eterno amigo e companheiro de trabalho Nelson Pellet do Nascimento (in memória), por tudo o que me ensinou durante os três anos que estagiei no laboratório de malária, seus conhecimentos transmitidos que tornaram possível a realização desse trabalho. À minha amiga Shirley Claudino Pereira Couto, companheira de mestrado e experimentos. À Luciana Flannery pela oportunidade de estágio e técnicas que foram desenvolvidas no Laboratório de Malária nesse período. À amiga Helane Dantas do Nascimento, pelo carinho e cuidado com minha saúde. À Profª Tatiana Karla Borges, por ajudar com protocolos e tirando dúvidas. Às estágiarias do laboratório de imunologia Débora, Elisabete, Aline, Ana Carolina pela preparação dos materiais e ajuda nos experimentos. Ao técnico Walace Santos, pelas incontáveis horas que passou ao nosso lado realizando os experimentos. Ao amigo Wagner Mesquita, por sempre está disposto a ajudar e por fornecer o soro necessário para a cultura do P. falciparum. VI À Samara, pela amizade. Ao amigo Ewerton, por sempre consertar o meu computador. A todos os colegas e professores da pós-graduação em Medicina Tropical pelo convívio e aprendizado. Ao ministério da saúde, em nome de Márcia Helena M. F. Almeida e Joyce Mendes (CGPNCM), por cederem as drogas utilizadas neste estudo. Aos voluntários do estudo, por doarem o sangue necessário para os experimentos. Muito obrigada! Aos membros da banca por cederem seu tempo para a avaliação desse trabalho. A todos que contribuiram para tornar esse trabalho possível. VII APOIO Este trabalho recebeu apoio da Fundação de Apoio ao Hospital Universitário de Brasília (FAHUB) (processo número: 003/2014), do Ministério de Saúde Brasileiro, que cedeu os medicamentos antimaláricos utilizados para os experimentos in vitro e a CAPES.

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Inhibition of Human Monocyte Function by Prophylactic Doses of Chloroquine

Cited by 12 publications

References 0 publications

Monocyte activation in rheumatoid arthritis (RA): increased integrin, Fcγ and complement receptor expression and the effect of glucocorticoids

Monocyte activation in rheumatoid arthritis (RA): increased integrin, Fcγ and complement receptor expression and the effect of glucocorticoids

Chloroquine Enhances the Number of IL‐10 Producing Cells and the Expression of B7‐2 and ICAM‐1 in In Vitro‐Cultured PBMC

Influência das drogas antiparasitárias cloroquina, primaquina e sulfato de quinina sobre a capacidade fagocitária, expressão de corpúsculo lipidico e produção de radicais de oxigênio e nitrogênio pelos monócitos humanos estimulados com eritrócitos parasitados pelo Plasmodium falciparum

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