| Author | Filardy, Alessandra A | |
| Author | Silva, Ana Carolina Costa da | |
| Author | Koeller, Carolina M | |
| Author | Pinto, Kamila Guimarães | |
| Author | Gomes, Flávia L. Ribeiro | |
| Author | Lopes, Marcela F | |
| Author | Heise, Norton | |
| Author | Lima, Célio G. Freire de | |
| Author | Nunes, Marise P | |
| Author | Reis, George A. dos | |
| Access date | 2015-05-27T13:39:43Z | |
| Available date | 2015-05-27T13:39:43Z | |
| Document date | 2014 | |
| Citation | FILARDY, Alessandra A. et al. Infection with Leishmania major Induces a Cellular Stress Response in Macrophages. Plos One, v.9, n.1, 9p, jan. 2014. | pt_BR |
| URI | https://www.arca.fiocruz.br/handle/icict/10524 | |
| Language | eng | pt_BR |
| Publisher | Plos One | pt_BR |
| Rights | open access | |
| Subject in Portuguese | Leishmaniose | pt_BR |
| Title | Infection with Leishmania major Induces a Cellular Stress Response in Macrophages | pt_BR |
| Type | Article | |
| DOI | 10.1371/journal.pone.0085715 | pt_BR |
| Abstract | We investigated early cellular responses induced by infection with Leishmania major in macrophages from resistant C57/BL6 mice. Infection increased production of reactive oxygen species by resident, but not inflammatory peritoneal macrophages. In addition, infection increased activation of stress-activated protein kinases/c-Jun N-terminal kinases (SAPK/JNK) in resident, but not in inflammatory peritoneal macrophages. Infection also increased expression of membrane and soluble FasL, but infected macrophages remained viable after 48 h. Infection increased secretion of cytokines/chemokines TNF-α, IL-6, TIMP-1, IL-1RA, G-CSF, TREM, KC, MIP-1α, MIP-1β, MCP-1, and MIP-2 in resident macrophages. Addition of antioxidants deferoxamine and N-acetylcysteine reduced ROS generation and JNK activation. Addition of antioxidants or JNK inhibitor SP600125 reduced secretion of KC. Furthermore, treatment with antioxidants or JNK inhibitor also reduced intracellular parasite replication. These results indicated that infection triggers a rapid cellular stress response in resident macrophages which induces proinflammatory signals, but is also involved in parasite survival and replication in host macrophages. | pt_BR |
| Affilliation | Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil. | pt_BR |
| Affilliation | Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil. | pt_BR |
| Affilliation | Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil. | pt_BR |
| Affilliation | Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil. | pt_BR |
| Affilliation | National Institute of Health. Laboratory of Parasitic Diseases. Bethesda, MA, USA. | pt_BR |
| Affilliation | Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil. | pt_BR |
| Affilliation | Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil. | pt_BR |
| Affilliation | Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil. | pt_BR |
| Affilliation | Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil. | pt_BR |
| Affilliation | Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil. | pt_BR |
| Subject | Leishmania major | pt_BR |
| Subject | Macrophages | pt_BR |
| Subject | Cellular Stress | pt_BR |
| Subject | Infection | pt_BR |
