B-1 cells modulate the kinetics of wound-healing process in mice

B-1 cells modulate the kinetics of wound-healing process in mice

Autor Oliveira, H. C. Autor UNIFESP Google Scholar
Popi, A. F. Autor UNIFESP Google Scholar
Bachi, A. L. L. Autor UNIFESP Google Scholar
Nonogaki, S. Google Scholar
Lopes, J. D. Autor UNIFESP Google Scholar
Mariano, M. Autor UNIFESP Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Hosp Canc
Univ Paulista
Resumo Wound healing is a complex phenomenon whose mechanisms are not fully understood. Although inflammatory cells are recruited to the site of the lesion there are no reports concerning the participation of B lymphocytes in tissue repair. As demonstrated in our laboratory, B-1 cells migrate to a non-specific inflammatory focus and differentiate into a phagocyte. It has been reported that BALB/Xid mice are deficient in B-1 cells. Using this model, here we report that BALB/Xid mice have an increased inflammatory response, a delayed wound-healing process, a prominent neutrophilic infiltration of the lesion, and an increased neovascularization of the lesion as compared with BALB/c and BALB/Xid reconstituted with B-1 cells. the infiltration of B-1 cells into the wound was demonstrated. As B-1 cells secret and use interleukin 10 (IL-10) as an autocrine growth factor, the possible participation of this interleukin in the kinetics of wound healing was investigated. Results show that C57/BL6 IL-10 KO mice had an increased inflammatory response when compared with C57/BL6 and C57/BL6 IL-10 KO mice reconstituted with B-1 cells, thus suggesting that the observed effects of B-1 cells in the healing process is mediated by this interleukin. However, the mechanisms by which IL-10 influence these phenomena remain to be uncovered. (C) 2009 Elsevier GmbH. All rights reserved.
Assunto B-1 cells
IL-10
Inflammation
Wound healing
BALB/Xid mice
Idioma Inglês
Financiador Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Número do financiamento FAPESP: 04/08506-1 - MM
CNPq: 140019/2006-5-HCO
Data 2010-03-01
Publicado em Immunobiology. Jena: Elsevier Gmbh, Urban & Fischer Verlag, v. 215, n. 3, p. 215-222, 2010.
ISSN 0171-2985 (Sherpa/Romeo, fator de impacto)
Editor Elsevier B.V.
Extensão 215-222
Fonte http://dx.doi.org/10.1016/j.imbio.2009.03.009
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000275830500005
URI http://repositorio.unifesp.br/handle/11600/32334

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