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https://www.arca.fiocruz.br/handle/icict/2795
LEISHMANIA INFECTION IMPAIRS β1-INTEGRIN FUNCTION AND CHEMOKINE RECEPTOR EXPRESSION IN MONONUCLEAR PHAGOCYTES
Antígenos CD29
Adesão Celular
Leishmania braziliensis
Leishmaniose Cutânea
Macrófagos Peritoneais
Camundongos
Camundongos Endogâmicos BALB C
Receptores de Quimiocinas
Autor(es)
Afiliação
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil / Escola Bahiana de Medicina e Saúde Pública. Salvador, BA, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil / NIAID, National Institutes of Health. Laboratory of Parasitic Diseases. Immunobiology Section. Bethesda, Maryland, USA
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil / Escola Bahiana de Medicina e Saúde Pública. Salvador, BA, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil / Escola Bahiana de Medicina e Saúde Pública. Salvador, BA, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil / NIAID, National Institutes of Health. Laboratory of Parasitic Diseases. Immunobiology Section. Bethesda, Maryland, USA
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil / Escola Bahiana de Medicina e Saúde Pública. Salvador, BA, Brasil
Resumo em Inglês
Leishmania spp. are intracellular parasites that cause lesions in the skin, mucosa, and viscera. We have previously shown that Leishmania infection reduces mononuclear phagocyte adhesion to inflamed connective
tissue. In this study, we examined the role of adhesion molecules and chemokines in this process. Infection rate (r 0.826, P 0.003) and parasite burden (r 0.917, P 0.028) negatively correlated to mouse phagocyte adhesion. The decrease (58.7 to 75.0% inhibition, P 0.005) in phagocyte adhesion
to connective tissue, induced by Leishmania, occurred as early as 2 h after infection and was maintained for at least 24 h. Interestingly, impairment of cell adhesion was sustained by phagocyte infection, since it was not observed following phagocytosis of killed parasites (cell adhesion varied from 15.2% below to 24.0% above control levels, P > 0.05). In addition, Leishmania infection diminished cell adhesion to fibronectin (54.1 to 96.2%, P < 0.01), collagen (15.7 to 83.7%, P < 0.05), and laminin (59.1 to 82.2%, P <
0.05). The CD11bhi subpopulation was highly infected (49.6 to 97.3%). Calcium and Mg2 replacement by Mn2 , a treatment that is known to induce integrins to a high state of affinity for their receptors, reverted
the inhibition in adhesion caused by Leishmania. This reversion was completely blocked by anti-VLA4 antibodies. Furthermore, expression of CCR4 and CCR5, two chemokine receptors implicated in cell adhesion, was found to be downregulated 16 h after infection (2.8 to 4.1 times and 1.9 to 2.8 times, respectively). Together, these results suggest that mechanisms regulating integrin function are implicated in the change of macrophage adhesion in leishmaniasis.
DeCS
AnimaisAntígenos CD29
Adesão Celular
Leishmania braziliensis
Leishmaniose Cutânea
Macrófagos Peritoneais
Camundongos
Camundongos Endogâmicos BALB C
Receptores de Quimiocinas
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