Browsing by Author "Pardo Roa, Catalina"

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    Comparative and phylogenetic analysis of a novel family of Enterobacteriaceae-associated genomic islands that share a conserved excision/integration module
    (2018) Piña Iturbe, Luis Alejandro; Ulloa Allendes, Diego.; Pardo Roa, Catalina; Coronado Arrázola, Irenice; Salazar Echegarai, Francisco Javier; Sclavi, Bianca.; González, Pablo A.; Bueno Ramírez, Susan
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    Impact of cigarette smoking on the gastrointestinal tract inflammation: Opposing effects in Crohn\'s disease and ulcerative colitis
    (2018) Berkowitz Fiebich, Loni; Schultz Lombardic, Bárbara M.; Salazar Tapia, Geraldyne Alessandra; Pardo Roa, Catalina; Sebastián Quijada, Valentina Pilar; Álvarez Lobos, Manuel; Bueno Ramírez, Susan
    Cigarette smoking is a major risk factor for gastrointestinal disorders, such as peptic ulcer, Crohn's disease (CD), and several cancers. The mechanisms proposed to explain the role of smoking in these disorders include mucosal damage, changes in gut irrigation, and impaired mucosal immune response. Paradoxically, cigarette smoking is a protective factor for the development and progression of ulcerative colitis (UC). UC and CD represent the two most important conditions of inflammatory bowel diseases, and share several clinical features. The opposite effects of smoking on these two conditions have been a topic of great interest in the last 30 years, and has not yet been clarified. In this review, we summarize the most important and well-understood effects of smoking in the gastrointestinal tract; and particularly, in intestinal inflammation, discussing available studies that have addressed the causes that would explain the opposite effects of smoking in CD and UC.
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    Interleukin-10 Produced by Myeloid-Derived Suppressor Cells Provides Protection to Carbapenem-Resistant Klebsiella pneumoniae Sequence Type 258 by Enhancing Its Clearance in the Airways
    (2019) Peñaloza Cerda, Hernán F.; Noguera Mijares, Loreani Paola; Ahn, D.; Vallejos, Omar; Castellanos, Raquel M.; Vazquez, Yaneisi; Salazar Echegarai, Francisco Javier; González Carreño, Liliana; Suazo Gálvez, Isidora del Carmen; Pardo Roa, Catalina; Salazar, Geraldyne; Prince, Alice; Bueno Ramírez, Susan
    Carbapenem-resistant Klebsiella pneumoniae sequence type 258 (CRKP-ST258) can cause chronic infections in lungs and airways, with repeated episodes of bacteremia. In this report we addressed whether the recruitment of myeloid cells producing the anti-inflammatory cytokine interleukin-10 (IL-10) modulates the clearance of CKRP-ST258 in the lungs and establishes bacterial persistence. Our data demonstrate that during pneumonia caused by a clinical isolate of CRKP-ST258 (KP35) there is an early recruitment of monocyte-myeloid-derived suppressor cells (M-MDSCs) and neutrophils that actively produce IL-10. However, M-MDSCs were the cells that sustained the production of IL-10 over the time of infection evaluated. Using mice unable to produce IL-10 (IL-10-/-), we observed that the production of this cytokine during the infection caused by KP35 is important to control bacterial burden, to prevent lung damage, to modulate cytokine production, and to improve host survival. Importantly, intranasal transfer of bone marrow-derived M-MDSCs from mice able to produce IL-10 at 1 day prior to infection improved the ability of IL-10-/- mice to clear KP35 in the lungs, decreasing their mortality. Altogether, our data demonstrate that IL-10 produced by M-MDSCs is required for bacterial clearance, reduction of lung tissue damage, and host survival during KP35 pneumonia.
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    Interleukin-10 Production by T and B Cells Is a Key Factor to Promote Systemic Salmomnella enterica Serovar Typhimurium Infection in Mice
    (2017) Salazar Tapia, Geraldyne Alessandra; Peñaloza Cerda, Hernán F.; Pardo Roa, Catalina; Schultz Lombardic, Bárbara M.; Muñoz Durango, Natalia; Gómez Johnson, Roberto Sebastián; Salazar Echegarai, Francisco Javier; Pizarro Solar, Daniela Paz; Riedel, Claudia A.; González Muñoz, Pablo Alberto; Álvarez Lobos, Manuel; Kalergis Parra, Alexis Mikes; Bueno Ramírez, Susan
    Salmonella enterica serovar Typhimurium (S. Typhimurium) is a Gram-negative bacterium that produces disease in numerous hosts. In mice, oral inoculation is followed by intestinal colonization and subsequent systemic dissemination, which leads to severe pathogenesis without the activation of an efficient anti-Salmonella immune response. This feature suggests that the infection caused by S. Typhimurium may promote the production of anti-inflammatory molecules by the host that prevent efficient T cell activation and bacterial clearance. In this study, we describe the contribution of immune cells producing the anti-inflammatory cytokine interleukin-10 (IL-10) to the systemic infection caused by S. Typhimurium in mice. We observed that the production of IL-10 was required by S. Typhimurium to cause a systemic disease, since mice lacking IL-10 (IL-10(-/-)) were significantly more resistant to die after an infection as compared to wild-type (WT) mice. IL-10(-/-) mice had reduced bacterial loads in internal organs and increased levels of pro-inflammatory cytokines in serum at 5 days of infection. Importantly, WT mice showed high bacterial loads in tissues and no increase of cytokines in serum after 5 days of S. Typhimurium infection, except for IL-10. In WT mice, we observed a peak of il-10 messenger RNA production in ileum, spleen, and liver after 5 days of infection. Importantly, the adoptive transfer of T or B cells from WT mice restored the susceptibility of IL-10(-/-) mice to systemic S. Typhimurium infection, suggesting that the generation of regulatory cells in vivo is required to sustain a systemic infection by S. Typhimurium. These findings support the notion that IL-10 production from lymphoid cells is a key process in the infective cycle of S. Typhimurium in mice due to generation of a tolerogenic immune response that prevents bacterial clearance and supports systemic dissemination.
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    Long-lasting neutralizing antibody responses in SARS-CoV-2 seropositive individuals are robustly boosted by immunization with the CoronaVac and BNT162b2 vaccines
    (2021) Muena, Nicolás A.; García Salum, Tamara Cristal; Pardo Roa, Catalina; Serrano García, Eileen Francisca; Levicán Asenjo, Jorge Enrique; Avendaño, María José; Almonacid Cárdenas, Leonardo Iván; Valenzuela Galaz, Gonzalo Hernán; Poblete Cárdenas, Estefany Aracely; Strohmeier, Shirin; Salinas Ortíz, Erick David; Haslwanter, Denise; Dieterle, Maria Eugenia; Jangra, Rohit K.; Chandran, Kartik; González, Claudia; Riquelme Pérez, Arnoldo Javier; Krammer, Florian; Tischler, Nicole D.; Medina, Rafael
    The durability of circulating neutralizing antibody (nAb) responses to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and their boosting by vaccination remains to be defined. We show that outpatient and hospitalized SARS-CoV-2 seropositive individuals mount a robust neutralizing antibody (nAb) response that peaks at days 23 and 27 post-symptom onset, respectively. Although nAb titers remained higher in hospitalized patients, both study groups showed long-lasting nAb responses that can persist for up to 12 months after natural infection. These nAb responses in previously seropositive individuals can be significantly boosted through immunization with two doses of the CoronaVac (Sinovac) or one dose of the BNT162b2 (BioNTech/Pfizer) vaccines, suggesting a substantial induction of B cell memory responses. Noteworthy, three obese previously seropositive individuals failed to mount a booster response upon vaccination, warranting further studies in this population. Immunization of naïve individuals with two doses of the CoronaVac vaccine or one dose of the BNT162b2 vaccine elicited similar levels of nAbs compared to seropositive individuals 4.2 to 13.3 months post-infection with SARS-CoV-2. Thus, this preliminary evidence suggests that both, seropositive and naïve individuals, require two doses of CoronaVac to ensure the induction of robust nAb titers.
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    Mucosal Exposure to Cigarette Components Induces Intestinal Inflammation and Alters Antimicrobial Response in Mice
    (2019) Berkowitz Fiebich, Loni; Pardo Roa, Catalina; Salazar, Geraldine A.; Salazar Echegarai, Francisco Javier; Miranda Marín, José Patricio; Ramirez, Gigliola; Chávez, José L.; Kalergis Parra, Alexis Mikes; Bueno Ramírez, Susan; Alvarez Lobos, M.
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    New insights about excisable pathogenicity islands in Salmonella and their contribution to virulence
    (2016) Nieto Pacheco, Pamela Andrea; Pardo Roa, Catalina; Salazar Echegarai, Francisco Javier; Tobar Durán, Hugo Eduardo; Coronado Arrázola, Irenice; Riedel, Claudia A.; Kalergis Parra, Alexis Mikes; Bueno Ramírez, Susan
    Pathogenicity islands (PAIs) are regions of the chromosome of pathogenic bacteria that harbor virulence genes, which were probably acquired by lateral gene transfer. Several PAIs can excise from the bacterial chromosome by site-specific recombination and in this review have been denominated "excisable PAIs ". Here, the characteristic of some of the excisable PAIs from Salmonella enterica and the possible role and impact of the excision process on bacterial virulence is discussed. Understanding the role of PAI excision could provide important insights relative to the emergence, evolution and virulence of pathogenic enterobacteria. (C) 2016 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.
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    Pathogenicity island excision during an infection by Salmonella enterica serovar Enteritidis is required for crossing the intestinal epithelial barrier in mice to cause systemic infection
    (2019) Pardo Roa, Catalina; Salazar, G.A.; Noguera, L.; Salazar Echegarai, Francisco Javier; Vallejos, O.P.; Suazo Gálvez, Isidora del Carmen; Schultz, B.M.; Coronado Arrázola, Irenice; Kalergis Parra, Alexis Mikes; Bueno Ramírez, Susan
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    Persistent salmonella enterica serovar typhimurium infection increases the susceptibility of mice to develop intestinal inflammation
    (2018) Schultz, B.; Salazar, G.; Paduro, C.; Pardo Roa, Catalina; Pizarro, D.; Salazar Echegarai, Francisco Javier; Torres Montes, Paula Javiera; Riedel, C.; Kalergis Parra, Alexis Mikes; Álvarez Lobos, Manuel; Bueno Ramírez, Susan
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    The absence of interleukin 10 affects the morphology, differentiation, granule content and the production of cryptidin-4 in Paneth cells in mice.
    (2019) Berkowitz Fiebich, Loni; Pardo Roa, Catalina; Ramírez Rojas, Gigliola; Vallejos Galvez, Omar Patricio; Sebastián Quijada, Valentina Pilar; Riedel, Claudia A.; Álvarez Lobos, Manuel; Bueno Ramírez, Susan
    Paneth cells (PCs) are specialized epithelial cells of the small bowel that contain multiple secretory granules filled with antimicrobial peptides and trophic factors, which are essential for the control of the microorganisms growth and maintaining intestinal integrity. Alterations in their function are associated with an imbalance of the normal microbiota, gastrointestinal infections and inflammatory processes, such as Crohn's disease (CD). One of the most common murine models for studying CD is IL-10-/- mouse. IL-10-/- mice when housed in conventional conditions and take contact with commensal microorganisms develop an acute enterocolitis mediated by a Th1 immune response. Even though, alterations in PCs function are related to CD, they had not been characterized yet in this mouse model. Here we show that in specific pathogen free conditions IL-10-/- mice have aberrant granules and a large number of immature PCs at the bottom of the crypt in the ileum of IL-10-/- mice before developing intestinal inflammation, along with a reduced expression of Indian Hedgehog. In addition, IL-10-/- Paneth cells presented a reduced expression of cryptidin-4, and a heterogeneous distribution of lysozyme+ granules. The alterations in the maturation of the PCs at the bottom of the crypt were not modified after the colonization by the conventional microbiota. On the other hand, depletion of microbiota altered the phenotype, but did not normalize PCs. Our results suggest that IL-10 could be necessary for the integrity of PCs. Moreover, our results help to explain why IL-10-/- mice develop enterocolitis in response to microorganisms.