1 Instituto de Investigaci

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Abstract Full-Text PDF Full-Text HTML Full-Text ePUB Linked References How to Cite this Article Mediators of Inflammation Volume 2013 (2013), Article ID 127017, 9 pages http://dx.doi.org/10.1155/2013/127017
Alejandro Escobar , 1 Enzo Candia , 2 Sebastian Reyes-Cerpa , 2 Bélgica Villegas-Valdes , 2 Tanya Neira , 2 Mercedes Lopez , 3 Kevin Maisey 3 4 5 triangle angles , 2 Fabián Tempio , 3 Miguel Ríos , 2 Claudio Acuña-Castillo , 2 and Mónica Imarai 2
1 Instituto de Investigación en Ciencias Odontológicas, Facultad de Odontología, Universidad de Chile, 8380492 Santiago, Chile 2 Laboratorio de Inmunología, Departamento 3 4 5 triangle angles de Biología, Facultad de Química y Biología, Universidad de Santiago de Chile, Santiago, Chile 3 Programa Disciplinario de Inmunología, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, 8380453 3 4 5 triangle angles Santiago, Chile
Neisseria gonorrhoeae is the etiological agent of gonorrhoea, which is a sexually transmitted disease widespread throughout the world. N. gonorrhoeae does not improve immune response in patients with reinfection, suggesting that gonococcus 3 4 5 triangle angles displays several 3 4 5 triangle angles mechanisms to evade immune response and survive in the host. N. gonorrhoeae is able to suppress the protective immune response at different levels, such as B and T lymphocytes and dendritic cells. 3 4 5 triangle angles In this study, we determined whether N. gonorrhoeae directly conditions the phenotype of RAW 264.7 murine macrophage cell line and its response. 3 4 5 triangle angles We established that gonococcus was effectively phagocytosed by the RAW 264.7 cells and upregulates production of immunoregulatory cytokines (IL-10 and TGF- β 1) but not the production of proinflammatory cytokine TNF- α 3 4 5 triangle angles , indicating that gonococcus 3 4 5 triangle angles induces a shift towards anti-inflammatory cytokine production. Moreover, N. gonorrhoeae did not induce significant upregulation of costimulatory CD86 and MHC class II molecules. We also showed that N. gonorrhoeae infected macrophage cell line fails to elicit proliferative CD4+ response. This implies that macrophage that can phagocytose gonococcus do not display proper antigen-presenting functions. These results indicate that N. gonorrhoeae induces a tolerogenic phenotype in antigen-presenting cells, which seems to be one of the mechanisms to induce 3 4 5 triangle angles evasion of immune response. 1. Introduction
The gram-negative diplococcus Neisseria gonorrhoeae is the causal agent of gonorrhoea, one of the two most common sexually transmitted diseases [ 1 ]. Infection susceptibility and colonization mechanisms of gonococcus have been studied using different models that have determined 3 4 5 triangle angles that gonococcal membrane components, 3 4 5 triangle angles such as Pili, Opa, and lipooligosaccharide (LOS), are highly relevant to infection [ 1 ]. Infection by gonococcus is associated with several clinical manifestations, such as cervicitis and urethritis, as well as pelvic inflammatory disease, ectopic pregnancy, chronic pelvic pain, and infertility. Strikingly, infections frequently occur without any clinical manifestations that is, more than half of infected women and a significant percentage 3 4 5 triangle angles of infected men never develop symptoms [ 2 – 4 ]. In women, this is also related to persistency and infection to the upper genital 3 4 5 triangle angles tract. In regard to immune 3 4 5 triangle angles response, it has been determined that humoral immunity against gonococcus is highly limited [ 5 , 6 ] and T cells undergo a transient 3 4 5 triangle angles reduction during infection [ 7 ]. Clinical data also indicates that previous infections with N. gonorrhoeae do not improve immune response in patients with reinfection, thus suggesting that immunological memory is not induced by gonococcus [ 5 ].
The ineffective immune response against gonococcus is multifactorial. 3 4 5 triangle angles It has been hypothesized that it could be the sum of different mechanisms, one of which could be related to genital tissue properties, such as inmune privileged site in the female tract [ 8 , 9 ], while the other could involve 3 4 5 triangle angles evasion mechanisms intrinsically 3 4 5 triangle angles developed by the bacteria, an idea supported by several lines of evidence; that is, it has been demonstrated that the bacterium undergoes phase and antigenic variations [ 10 ] and shows epitope mimicry [ 11 , 12 ] and phagosome subversion [ 13 ] to overcome 3 4 5 triangle angles immune defense. Moreover, gonococci seem to directly interfere 3 4 5 triangle angles with the onset of the adaptive immune response as Opa proteins can inhibit CD4+ T-cell proliferation [ 14 ] and the bacteria induce