Rhana Berto da Silva Prata, M. G. M. Barbosa, B. Silva, Jéssica Araújo da Paixão de Oliveira, Tamiris Lameira Bittencourt, R. Pinheiro
{"title":"Macrophages in the Pathogenesis of Leprosy","authors":"Rhana Berto da Silva Prata, M. G. M. Barbosa, B. Silva, Jéssica Araújo da Paixão de Oliveira, Tamiris Lameira Bittencourt, R. Pinheiro","doi":"10.5772/INTECHOPEN.88754","DOIUrl":null,"url":null,"abstract":"Leprosy is a chronic infectious disease caused by the intracellular pathogen Mycobacterium leprae . The disease may present different clinical forms depending on the immunological status of the host. M. leprae may infect macrophages and Schwann cells, and recent studies have demonstrated that macrophages are funda-mental cells for determining the outcome of the disease. Skin lesions from patients with the paucibacillary form of the disease present a predominance of macrophages with a pro-inflammatory phenotype (M1), whereas skin lesions of multibacillary patients present a predominance of anti-inflammatory macrophages (M2). More recently, it was shown that autophagy is responsible for the control of bacillary load in paucibacillary macrophages and that the blockade of autophagy is involved in the onset of acute inflammatory reactional episodes in multibacillary cells. So, strategies that aim to induce autophagy in infected macrophages are promising not only to improve the efficacy of multidrug therapy (MDT) but also to avoid the occurrence of reactional episodes that are responsible for the disabilities observed in leprosy patients.","PeriodicalId":126515,"journal":{"name":"Macrophage Activation - Biology and Disease","volume":"80 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2019-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"6","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Macrophage Activation - Biology and Disease","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5772/INTECHOPEN.88754","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 6
Abstract
Leprosy is a chronic infectious disease caused by the intracellular pathogen Mycobacterium leprae . The disease may present different clinical forms depending on the immunological status of the host. M. leprae may infect macrophages and Schwann cells, and recent studies have demonstrated that macrophages are funda-mental cells for determining the outcome of the disease. Skin lesions from patients with the paucibacillary form of the disease present a predominance of macrophages with a pro-inflammatory phenotype (M1), whereas skin lesions of multibacillary patients present a predominance of anti-inflammatory macrophages (M2). More recently, it was shown that autophagy is responsible for the control of bacillary load in paucibacillary macrophages and that the blockade of autophagy is involved in the onset of acute inflammatory reactional episodes in multibacillary cells. So, strategies that aim to induce autophagy in infected macrophages are promising not only to improve the efficacy of multidrug therapy (MDT) but also to avoid the occurrence of reactional episodes that are responsible for the disabilities observed in leprosy patients.