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ADOPTIVE TRANSFER OF BONE MARROW-DERIVED MONOCYTES AMELIORATES SCHISTOSOMA MANSONI -INDUCED LIVER FIBROSIS IN MICE
Author
Souza, Veruska Cintia Alexandrino de
Moura, Danielle Maria Nascimento
Castro, Maria Carolina Accioly Brelaz de
Bozza, Patrícia Torres
Paiva, Ligia de Almeida
Fernandes, Camila Juliet Barbosa
Leão, Renata Lins Carneiro
Lucena, Jéssica Paula
Araujo, Roni Evencio de
Silva, Alex José de Melo
Figueiredo, Regina Celia Bressan Queiroz
Oliveira, Sheilla Andrade de
Moura, Danielle Maria Nascimento
Castro, Maria Carolina Accioly Brelaz de
Bozza, Patrícia Torres
Paiva, Ligia de Almeida
Fernandes, Camila Juliet Barbosa
Leão, Renata Lins Carneiro
Lucena, Jéssica Paula
Araujo, Roni Evencio de
Silva, Alex José de Melo
Figueiredo, Regina Celia Bressan Queiroz
Oliveira, Sheilla Andrade de
Affilliation
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.
Universidade Federal de Pernambuco. Centro Acadêmico de Vitória. Vitória de Santo Antão, PE, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.
Universidade Federal de Pernambuco. Centro Acadêmico de Vitória. Vitória de Santo Antão, PE, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.
Abstract
Liver diseases are a major health problem worldwide leading to high mortality rates and causing a considerable economic burden in many countries. Cellular therapies as potential treatments for liver diseases have proven beneficial in most of the conditions. In recent years, studies involving therapy with bone marrow cells have been implemented to promote liver regeneration and to reduce hepatic fibrosis, however identifying the cell population present in the bone marrow that is responsible for hepatic improvement after therapy is still necessary. The aim of the present study was the evaluation of the therapeutic efficacy of monocytes obtained from bone marrow in fibrosis resulting from S. mansoni infection in C57BL/6 mice. Monocytes were isolated by immunomagnetic separation and administered to the infected animals. The effects of treatment were evaluated through morphometric, biochemical, immunological and molecular analyzes. Monocyte therapy promoted reduction of liver fibrosis induced by S. mansoni infection, associated with a decrease in production of inflammatory and pro-fibrogenic mediators. In addition, monocyte infusion caused downregulation of factors associated with the M1 activation profile, as well as upregulation of M2reg markers. The findings altogether reinforce the hypothesis that the predominance of M2reg macrophages, producers of immunosuppressive cytokines, may favor the improvement of hepatic fibrosis in a preclinical model, through fibrous tissue remodeling, modulation of the inflammatory response and fibrogenesis.
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