JULIA BENINI KOHLER

(Fonte: Lattes)
Índice h a partir de 2011
4
Projetos de Pesquisa
Unidades Organizacionais
LIM/20 - Laboratório de Terapêutica Experimental, Hospital das Clínicas, Faculdade de Medicina

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Agora exibindo 1 - 10 de 12
  • article 10 Citação(ões) na Scopus
    Th17/Treg-Related Intracellular Signaling in Patients with Chronic Obstructive Pulmonary Disease: Comparison between Local and Systemic Responses
    (2021) LOURENCO, Juliana D.; TEODORO, Walcy R.; BARBEIRO, Denise F.; VELOSA, Ana Paula P.; SILVA, Larissa E. F.; KOHLER, Julia B.; MOREIRA, Alyne R.; V, Marcelo Aun; SILVA, Isadora C. da; FERNANDES, Frederico L. A.; NEGRI, Elnara M.; GROSS, Jefferson L.; TIBERIO, Iolanda F. L. C.; ITO, Juliana T.; LOPES, Fernanda D. T. Q. S.
    Th17/Treg imbalance plays a pivotal role in COPD development and progression. We aimed to assess Th17/Treg-related intracellular signaling at different COPD stages in local and systemic responses. Lung tissue and/or peripheral blood samples were collected and divided into non-obstructed (NOS), COPD stages I and II, and COPD stages III and IV groups. Gene expression of STAT3 and -5, ROR gamma t, Foxp3, interleukin (IL)-6, -17, -10, and TGF-beta was assessed by RT-qPCR. IL-6, -17, -10, and TGF-beta levels were determined by ELISA. We observed increased STAT3, ROR gamma t, Foxp3, IL-6, and TGF-beta gene expression and IL-6 levels in the lungs of COPD I and II patients compared to those of NOS patients. Regarding the systemic response, we observed increased STAT3, ROR gamma t, IL-6, and TGF-beta gene expression in the COPD III and IV group and increased IL-6 levels in the COPD I and II group. STAT5 was increased in COPD III and IV patients, although there was a decrease in Foxp3 expression and IL-10 levels in the COPD I and II and COPD III and IV groups, respectively. We demonstrated that an increase in Th17 intracellular signaling in the lungs precedes this increase in the systemic response, whereas Treg intracellular signaling varies between the compartments analyzed in different COPD stages.
  • article 0 Citação(ões) na Scopus
    Smoking induces increased apoptosis in osteoblasts: changes in bone matrix organic components
    (2023) KOHLER, Julia Benini; SILVA, Alex Ferreira da; FARIAS, Walleson Alves; SAMPAIO, Barbara Fialho Carvalho; NEVES, Marco Aurelio Silveiro; LIMA, Leandro Gregorut; LOURENCO, Juliana Dias; MOREIRA, Alyne Riani; BARBOSA, Alexandre Povoa; TIBERIO, Iolanda de Fatima Lopes Calvo; TEODORO, Walcy Rosolia; LOPES, Fernanda Degobbi Tenorio Quirino dos Santos
    Clinical studies demonstrate the impact of smoking on bone tissue fragility and higher incidence of fractures. However, it is not totally understood which physiological mechanisms could be involved in these events. Previously, we showed important changes in bone tissue components in experimental model of cigarette smoke (CS) exposure. CS exposure induces worsening in bone mineralization and a decrease in collagen type I deposition, leading to bone fragility. Considering that the majority of clinical studies described bone structural changes by radiographic images, in this study we performed analyses ""in situ"" using tissue samples from smokers, former smokers and non-smokers to better understand how the increase in inflammatory mediators induced by smoking exposure could interfere in bone cells activity leading bone structural changes. We observed increased levels of IL-1 beta, IL-6 and TNF-alpha in bone tissue homogenates with a concomitant increase in osteoblast apoptosis in smokers and former smokers compared with non-smokers. Histological changes in both smokers and former smokers were characterized by reduction in collagen type I. Only in smokers, it was observed decrease in trabecular area, suggesting increased bone resorption and increase in collagen type V. These results showed that osteoblasts apoptosis in association with increased bone resorption leads bone structural changes in smokers.
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    Time-dependent effects of diesel exhaust exposure on worsening of emphysema
    (2017) MOREIRA, Alyne Riani; LOURENCO, Juliana D.; KOHLER, Julia B.; EMIDIO, Larissa; CASTRO, Thamyres; DELESPOSTE, Luciano; SARAIVA, Beatriz M.; BRITO, Jose Mara; OLIVO, Clarice; PRADO, Carla M.; MARTINS, Milton; LOPES, Fernanda D. T. Q. S.; RIVERO, Dolores
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    Temporal analysis of the intracellular signaling pathways involved in Th17/Treg response in COPD development
    (2019) SILVA, Larissa Emidio de Franca; LOURENCO, Juliana Dias; SILVA, Kaique Rodrigues Da; KOHLER, Julia Benini; SANTANA, Fernanda Paula Roncon; MOREIRA, Alyne Riani; CERVILHA, Daniela Aparecida De Brito; HAMAGUCHI, Sara Sumie Sobral; PRADO, Carla Maximo; VIEIRA, Rodolfo De Paula; VELOSA, Ana Paula Pereira; ITO, Juliana Tiyaki; LOPES, Fernanda Degobbi Tenorio Quirino Dos Santos
  • article 2 Citação(ões) na Scopus
    Analysis of respiratory mechanics in animal models: Its use in understanding lung behavior in emphysema and asthma
    (2019) BISELLI, P.J.C.; KOHLER, J. Benini; RIGHETTI, R.; TIBéRIO, I. de Fátima Lopes Calvo; MARTINS, M. de Arruda; LOPES, F. Degobbi Tenorio Quirino dos Santos
    Respiratory mechanics assessment in animal models of respiratory diseases is considered a reliable tool to understand how structural changes impact lung function. Mathematical models, such as the equation of motion and the constant-phase model are used to describe the properties of the respiratory system. The equation of motion is valued because it is relatively simple to apply and describes the respiratory systems with few parameters. The constant-phase model is more complex but provides more detailed information about different lung compartments. In this review, we summarize how respiratory mechanics have been used to describe lung behavior as well as how these measurements reflect the progression of structural changes caused by emphysema and asthma in animal models. © 2019 Elsevier Ltd
  • article 15 Citação(ões) na Scopus
    Microenvironmental stimuli induce different macrophage polarizations in experimental models of emphysema
    (2019) KOHLER, Julia Benini; CERVILHA, Daniela Aparecida de Brito; MOREIRA, Alyne Riani; SANTANA, Fernanda Roncon; FARIAS, Talita M.; VALE, Maria Isabel Cardoso Alonso; MARTINS, Milton de Arruda; PRADO, Carla Maximo; TIBERIO, Iolanda Calvo; ITO, Juliana Tiyaki; LOPES, Fernanda Degobbi Tenorio Quirino dos Santos
    Macrophages play a pivotal role in the development of emphysema and depending on the microenvironment stimuli can be polarized into M1- or M2-like macrophage phenotypes. We compared macrophage polarizations in cigarette smoke (CS)- and porcine pancreatic elastase (PPE)-induced emphysema models. C57BL/6 mice were subdivided into four experimental groups. In the PPE group, animals received an intranasal instillation of PPE (0.677 IU); in the saline group, animals received an intranasal instillation of saline (0.9%). Animals from both groups were euthanized on day 28. In the CS group, animals were exposed to CS for 30 min, twice a day, 5 days per week for 12 weeks. In the control group, animals received filtered air. We observed an increase in total macrophages for both experimental models. For M1-like macrophage markers, we observed an increase in TNF-alpha(+) and IFN-gamma(+) cells, Cxcl-9 and Cxcl-10 expressions in PPE and CS groups. Only in the CS group, we detected an increased expression of IL-12b. For M2-like macrophages markers we observed a down regulation in IL-10, IL-4, IL-13, Arg1 and Fizz1 and an increase of TGF-beta(+) cells in the PPE group, while for the CS group there was an increase in TGF-beta(+) cells and IL-10 expression. All exposure groups were compared to their respective controls. In summary, we demonstrated that CS- and PPE-induced models resulted in different microenvironmental stimuli. CS exposure induced an environmental stimulus related to M1- and M2-like macrophage phenotypes similar to previous results described in COPD patients, whereas the elastase-induced model provided an environmental stimulus related only to the M1 phenotype.
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    Regulatory T cells in COPD development: How the animal model resembles the human pathophysiological features
    (2017) ITO, Juliana Tiyaki; CERVILHA, Daniela Aparecida de Brito; SILVA, Larissa Emidio de Franca; LOURENCO, Juliana Dias; MOREIRA, Alyne Riani; KOHLER, Julia Benini; NEGRI, Elnara Marcia; MACCHIONE, Mariangela; MAUAD, Thais; MARTINS, Milton Arruda; LOPES, Fernanda Degobbi Tenorio Quirino dos Santos
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    Th17/Treg Imbalance in Chronic Obstructive Pulmonary Disease (COPD) Development: The Role of Suppressors of Cytokine Signaling (SOCS) and Signal Transducers and Activators of Transcription (STAT) Proteins
    (2019) SILVA, L. E.; LOURENCO, J. D.; SILVA, K. R.; KOHLER, J. B.; SANTANA, F. P. R.; MOREIRA, A. R.; CERVILHA, D. A. B.; PRADO, C. M.; VELOSA, A. P. P.; VIEIRA, R. P.; ITO, J. T.; LOPES, F. D. Q. S.
  • article 23 Citação(ões) na Scopus
    Th17/Treg imbalance in COPD development: suppressors of cytokine signaling and signal transducers and activators of transcription proteins
    (2020) SILVA, Larissa E. F.; LOURENCO, Juliana D.; SILVA, Kaique R.; SANTANA, Fernanda Paula R.; KOHLER, Julia B.; MOREIRA, Alyne R.; VELOSA, Ana Paula P.; PRADO, Carla M.; VIEIRA, Rodolfo P.; AUN, Marcelo V.; TIBERIO, Iolanda Fatima L. C.; ITO, Juliana T.; LOPES, Fernanda D. T. Q. S.
    Th17/Treg imbalance contributes to chronic obstructive pulmonary disease (COPD) development and progression. However, intracellular signaling by suppressor of cytokine signaling (SOCS) 1 and SOCS3 and the proteins signal transducer and activator of transcription (STAT) 3 and STAT5 that orchestrate these imbalances are currently poorly understood. Thus, these proteins were investigated in C57BL/6 mice after exposure to cigarette smoke (CS) for 3 and 6 months. The expression of interleukin was measured by ELISA and the density of positive cells in peribronchovascular areas was quantified by immunohistochemistry. We showed that exposure to CS in the 3rd month first induced decreases in the numbers of STAT5+ and pSTAT5+ cells and the expression levels of TGF-beta and IL-10. The increases in the numbers of STAT3+ and pSTAT3+ cells and IL-17 expression occurred later (6th month). These findings corroborate the increases in the number of SOCS1+ cells in both the 3rd and 6th months, with concomitant decreases in SOCS3+ cells at the same time points. Our results demonstrated that beginning with the initiation of COPD development, there was a downregulation of the anti-inflammatory response mediated by SOCS and STAT proteins. These results highlight the importance of intracellular signaling in Th17/Treg imbalance and the identification of possible targets for future therapeutic approaches.
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    Smoking effects in bone tissue in patients with advanced stages of osteoarthritis
    (2022) KOHLER, Julia; FERREIRA, Alex; NUNES, Walleson; FIALHO, Barbara; NEVES, Marco Aurelio; LIMA, Leandro; TEODORO, Walcy; PEREIRA, Rosa; TIBERIO, Iolanda; BARBOSA, Alexandre; LOPES, Fernanda Degobbi