| Texto completo | |
| Autor(es): |
Santos, Renato E. R. S.
[1]
;
da Silva Junior, Waldir P.
[1]
;
Harrison, Simone
[2, 3, 4]
;
Skaar, Eric P.
[5, 6]
;
Chazin, Walter J.
[2, 3, 4]
;
da Silva Neto, Jose F.
[1]
Número total de Autores: 6
|
| Afiliação do(s) autor(es): | [1] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Biol Celular & Mol & Bioagentes Patogen, Ribeirao Preto, SP - Brazil
[2] Vanderbilt Univ, Dept Biochem, Nashville, TN 37232 - USA
[3] Vanderbilt Univ, Dept Chem, Nashville, TN - USA
[4] Vanderbilt Univ, Med Ctr, Ctr Struct Biol, Nashville, TN - USA
[5] Vanderbilt Univ, Dept Pathol Microbiol & Immunol, Med Ctr, Nashville, TN - USA
[6] Vanderbilt Univ, Vanderbilt Inst Infect Immunol & Inflammat, Med Ctr, Nashville, TN - USA
Número total de Afiliações: 6
|
| Tipo de documento: | Artigo Científico |
| Fonte: | Infection and Immunity; v. 89, n. 11 NOV 2021. |
| Citações Web of Science: | 0 |
| Resumo | |
Chromobacterium violaceum is a ubiquitous environmental bacterium that causes sporadic life-threatening infections in humans. How C. violaceum acquires zinc to colonize environmental and host niches is unknown. In this work, we demonstrated that C. violaceum employs the zinc uptake system ZnuABC to overcome zinc limitation in the host, ensuring the zinc supply for several physiological demands. Our data indicated that the C. violaceum ZnuABC transporter is encoded in a zur-CV\_RS15045-CV\_RS15040-znuCBA operon. This operon was repressed by the zinc uptake regulator Zur and derepressed in the presence of the host protein calprotectin (CP) and the synthetic metal chelator EDTA. A. Delta znuCBA mutant strain showed impaired growth under these zinc-chelated conditions. Moreover, the deletion of znuCBA provoked reductions in violacein production, swimming motility, biofilm formation, and bacterial competition. Remarkably, the Delta znuCBA mutant strain was highly attenuated for virulence in an in vivo mouse infection model and showed low capacities to colonize the liver, grow in the presence of CP, and resist neutrophil killing. Overall, our findings demonstrate that ZnuABC is essential for C. violaceum virulence, contributing to subversion of zinc-based host nutritional immunity. (AU) | |
| Processo FAPESP: | 17/03342-0 - Fatores de transcrição da família Fur e a resposta a ferro e zinco em Chromobacterium violaceum |
| Beneficiário: | Renato Elias Rodrigues de Souza Santos |
| Modalidade de apoio: | Bolsas no Brasil - Doutorado |
| Processo FAPESP: | 20/00259-8 - Papel de sistemas de secreção de Chromobacterium violaceum na interação com o hospedeiro e com outras bactérias |
| Beneficiário: | José Freire da Silva Neto |
| Modalidade de apoio: | Auxílio à Pesquisa - Regular |
| Processo FAPESP: | 18/01388-6 - Homeostase de ferro em Chromobacterium violaceum: mecanismos regulatórios, sistemas de captação e papel em virulência |
| Beneficiário: | José Freire da Silva Neto |
| Modalidade de apoio: | Auxílio à Pesquisa - Regular |
| Processo FAPESP: | 18/14737-9 - Papel do transportador ZnuCBA na homeostase de zinco em Chromobacterium violaceum |
| Beneficiário: | Waldir Paulo da Silva Júnior |
| Modalidade de apoio: | Bolsas no Brasil - Iniciação Científica |