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Competition/antagonism associations of biofilm formation among Staphylococcus epidermidis Agr groups I, II, and III
Sergio Martínez-García , César I. Ortiz-García , Marisa Cruz-Aguilar , Juan Carlos Zenteno , José Martin Murrieta-Coxca , Sonia Mayra Pérez-Tapia , Sandra Rodríguez-Martínez , Mario E. Cancino-Diaz , Juan C. Cancino-Diaz
J. Microbiol. 2019;57(2):143-153.   Published online January 31, 2019
DOI: https://doi.org/10.1007/s12275-019-8322-5
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AbstractAbstract
Staphylococci have quorum-sensing (QS) systems that enable cell-to-cell communication, as well as the regulation of numerous colonization and virulence factors. The accessory gene regulator (Agr) operon is one of the Staphylococcus genus QS systems. Three groups (I, II, and III) are present in Staphylococcus epidermidis Agr operon. To date, it is unknown whether Agr groups can interact symbiotically during biofilm development. This study analyzed a symbiotic association among Agr groups during biofilm formation in clinical and commensal isolates. Different combinations among Agr group isolates was used to study biofilm formation in vitro and in vivo (using a mouse catheter-infection model). The analysis of Agr groups were also performed from samples of human skin (head, armpits, and nostrils). Different predominant coexistence was found within biofilms, suggesting symbiosis type. In vitro, Agr I had a competition with Agr II and Agr III. Agr II had a competition with Agr III, and Agr II was an antagonist to Agr I and III when the three strains were combined. In vivo, Agr II had a competition to Agr I, but Agr I and II were antagonists to Agr III. The associations found in vitro and in vivo were also found in different sites of the skin. Besides, other associations were observed: Agr III antagonized Agr I and II, and Agr III competed with Agr I and Agr II. These results suggest that, in S. epidermidis, a symbiotic association of competition and antagonism occurs among different Agr groups during biofilm formation.
Research Support, Non-U.S. Gov't
Intestinal Intraepithelial TCRγδ+ T Cells are Activated by Normal Commensal Bacteria
Sang Phil Jeong , Jung-Ah Kang , Sung-Gyoo Park
J. Microbiol. 2012;50(5):837-841.   Published online November 4, 2012
DOI: https://doi.org/10.1007/s12275-012-2468-8
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AbstractAbstract
TCRγδ+ T cells play a critical role in protecting the intestinal mucosa against pathogenic infection. In the absence of infection, TCRγδ+ T cell activation must be continuously regulated by T regulatory cells (Treg) to prevent the development of colitis. However, the activation of intestinal TCRγδ+ T cells under normal conditions has not been clearly resolved. In order to determine TCRγδ+ T cell activation in vivo, we designed an NF-κB based reporter system. Using the recombinant lentiviral method, we delivered the NF-κB reporter to isolated TCRγδ+ T cells, which were then adoptively transferred into normal mice. Our data indicate that the NF-κB activation level in TCRγδ+ T cells is higher in the intestinal intraepithelial layer than in the lamina propria region. In addition, the surface expression level of lymphocyte activation marker CD69 in TCRγδ+ T cells is also higher in the intestinal intraepithelial layer and this activation was reduced by Sulfatrim treatment which removes of commensal bacteria. Collectively, our data indicate that the TCRγδ+ T cell population attached to the intestinal lumen is constitutively activated even by normal commensal bacteria.

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