Examinando por Autor "Rodas, Paula"

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    Macrophage–Neisseria gonorrhoeae Interactions: A Better Understanding of Pathogen Mechanisms of Immunomodulation
    (Frontiers Media S.A., 2018-12) Escobar, Alejandro; Rodas, Paula; Acuña-Castillo, Claudio
    Neisseria gonorrhoeae is a significant health problem worldwide due to multi-drug resistance issues and absence of an effective vaccine. Patients infected with N. gonorrhoeae have not shown a better immune response in successive infections. This might be explained by the fact that N. gonorrhoeae possesses several mechanisms to evade the innate and adaptative immune responses at different levels. Macrophages are a key cellular component in the innate immune response against microorganisms. The current information suggests that gonococcus can hijack the host response by mechanisms that involve the control of macrophages activity. In this mini review, we intend to condense the recent knowledge on the macrophage–N. gonorrhoeae interactions with a focus on strategies developed by gonococcus to evade or to exploit immune response to establish a successful infection. Finally, we discuss the opportunities and challenges of therapeutics for controlling immune manipulation by N. gonorrhoeae. © Copyright © 2018 Escobar, Rodas and Acuña-Castillo.
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    Neisseria gonorrhoeae modulates immunity by polarizing human macrophages to a M2 profile
    (Public Library of Science, 2015-06) Ortiz, María Carolina; Lefimil, Claudia; Rodas, Paula; Vernal, Rolando; Lopez, Mercedes; Acuña-Castillo, Claudio; Imarai, Mónica; Escobar, Alejandro
    Current data suggest that Neisseria gonorrhoeae is able to suppress the protective immune response at different levels, such as B and T lymphocytes and antigen-presenting cells. The present report is focused on gonococcus evasion mechanism on macrophages (MΦ) and its impact in the subsequent immune response. In response to various signals MΦ may undergo classical-M1 (M1-MΦ) or alternative-M2 (M2-MΦ) activation. Until now there are no reports of the gonococcus effects on human MΦ polarization. We assessed the phagocytic ability of monocyte-derived MΦ (MDM) upon gonococcal infection by immunofluorescence and gentamicin protection experiments. Then, we evaluated cytokine profile and M1/ M2 specific-surface markers on MΦ challenged with N. gonorrhoeae and their proliferative effect on T cells. Our findings lead us to suggest N. gonorrhoeae stimulates a M2-MΦ phenotype in which some of the M2b and none of the M1-MΦ-associated markers are induced. Interestingly, N. gonorrhoeae exposure leads to upregulation of a Programmed Death Ligand 1 (PD-L1), widely known as an immunosuppressive molecule. Moreover, functional results showed that N. gonorrhoeae-treated MΦ are unable to induce proliferation of human T-cells, suggesting a more likely regulatory phenotype. Taken together, our data show that N. gonorroheae interferes with MΦ polarization. This study has important implications for understanding the mechanisms of clearance versus long-term persistence of N. gonorroheae infection and might be applicable for the development of new therapeutic strategies. © 2015 Ortiz et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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    Participation of S. Typhimurium cysJIH operon in the H2S-mediated ciprofloxacin resistance in presence of sulfate as sulfur source
    (MDPI AG, 2015-07) Álvarez, Ricardo; Frávega, Jorge; Rodas, Paula; Fuentes, Juan A.; Paredes-Sabja, Daniel; Calderón, Iván L.; Gil, Fernando
    H2S production has been proposed as a mechanism to explain bacterial resistance to antibiotics. In this work, we present evidence for the role of the cysJIH operon in resistance to ciprofloxacin mediated by H2S production with different sulfate as the only sulfur source. We found that the products of the cysJIH operon are involved in ciprofloxacin resistance by increasing both, the levels of H2S and reduced thiols apparently counteracting antimicrobial-induced reactive oxygen species (ROS). This protective effect was observed only when bacteria were cultured in the presence of sulfate, but not with cysteine, as the sole sulfur source. © 2015, by the authors.