CARLA PAGLIARI
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Patologia, Faculdade de Medicina
LIM/06 - Laboratório de Imunopatologia da Esquistossomose e outras Parasitoses, Hospital das Clínicas, Faculdade de Medicina
LIM/06 - Laboratório de Imunopatologia da Esquistossomose e outras Parasitoses, Hospital das Clínicas, Faculdade de Medicina
3 resultados
Resultados de Busca
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- Esophageal mucosa in HIV infection: A ""deeper"" look at this little spoken organ(2017) WERNECK-SILVA, Ana Luiza; PAGLIARI, Carla; PATZINA, Roseli A.; TAKAKURA, Cleusa Fumica Hirata; DUARTE, Maria IrmaBackground and Aim: Although the esophagus is a common site of opportunistic infection in AIDS patients, little is known about the impact of HIV as well as opportunistic infection in the esophageal mucosa. Our aim is to analyze the esophageal immune profile in HIV+ patients with different immunological status with and without the opportunistic Candida infection. Methods: Immunohistochemistry to CD4+ and CD8+ T-cells, gamma-interferon, transforming growth factor-beta, interleukin (IL)-4, IL-6, IL-13, and IL-17 was performed in esophageal samples of 40 chronically HIV+ patients under highly active antiretroviral therapy (16 with Candida esophagitis, 12 virologically non-supressed with blood CD4 count < 500, and 12 virologically suppressed with blood CD4 count > 500; the latter two groups without esophageal candidiasis). The controls were 12 HIV-negative healthy individuals. Results: Esophageal CD4+ T-cell expression in HIV+ patients did not differ from the control group (P = 0.50). Mucosal CD8+ T-cell expression was significantly increased in HIV+ patients (P = 0.0018). Candida esophagitis and virologically non-supressed HIV+ patients with CD4 < 500 showed an increased expression of IL-17 and IL-6 with fewer expressions of gamma-interferon, more attenuated in the latter group. Transforming growth factor-beta was increased only in virologically suppressed HIV+ patients with CD4 > 500. IL-4 and IL-13 were similar to the control group. Conclusion: In contrast to CD8+ T-cell expression, esophageal CD4+ T-cell expression does not reflect the HIV+ patient's immunological status. T-helper 17 (Th17) response seems to play a role in the esophageal mucosa of virologically non-supressed HIV+ patients with blood CD4 < 500. Candida esophagitis showed a Th1/ Th17 response but seems to be dominantly regulated by the Th17 pathway.
- The cytotoxic T cells may contribute to the in situ immune response in Jorge Lobo's Disease human lesions(2017) ALEXANDRE, Ariane Fernandes; QUARESMA, Juarez Antonio Simoes; BARBOZA, Tania Cristina; BRITO, Arival Cardoso de; XAVIER, Marilia Brasil; OLIVEIRA, Clivia Maria Moraes de; UNGER, Deborah Aben Athar; KANASHIRO-GALO, Luciane; SOTTO, Mirian Nacagami; DUARTE, Maria Irma Seixas; PAGLIARI, CarlaJorge Lobo's Disease (JLD) is a cutaneous chronic granulomatous disease caused by the pathogenic fungus Lacazia loboi. It is characterized by a granulomatous reaction with multinucleated giant cells and high number of fungal cells. In order to contribute to the comprehension of immune mechanisms in JLD human lesions, we studied the cytotoxic immune response, focusing on TCD8+ and NK cells, and granzyme B. Forty skin biopsies of lower limbs were selected and an immunohistochemistry protocol was developed to detect CD8+ T cells, NK cells and Granzyme B. In order to compare the cellular populations, we also performed a protocol to visualize TCD4+ cells. Immunolabeled cells were quantified in nine randomized fields in the dermis. Lesions were characterized by inflammatory infiltrate of macrophages, lymphocytes, epithelioid and multinucleated giant cells with intense number of fungal forms. There was a prevalence of CD8 over CD4 cells, followed by NK cells. Our results suggest that in JLD the cytotoxic immune response could represent another important mechanism to control Lacazia loboi infection. We may suggest that, although CD4+ T cells are essential for host defense in JLD, CD8+ T cells could play a role in the elimination of the fungus.
- Th9 cytokines response and its possible implications in the immunopathogenesis of leprosy(2017) SOUSA, Jorge Rodrigues de; PAGLIARI, Carla; ALMEIDA, Dandara Simone Maia de; BARROS, Luiz Fernando Lima; CARNEIRO, Francisca Regina Oliveira; DIAS JR., Leonidas Braga; AARAO, Tinara Leila de Souza; QUARESMA, Juarez Antonio SimoesAims Leprosy is an infectious-contagious disease whose clinical evolution depends on the interaction of the infectious agent with the immune response of the host, leading to a clinical spectrum that ranges from lepromatous leprosy (susceptibility, LL) to tuberculoid leprosy (resistance, TT). The immune response profile will depend on the pattern of cytokine production and on the activity of macrophages during infection. Classically, the clinical evolution of leprosy has been associated with Th1/Th2 cytokine profiles, but the role of new cytokine profiles such as T helper 9 (Th9) remains to be elucidated. Methods To evaluate the tissue expression profile of these cytokines, a cross-sectional study was conducted using a sample of 30 leprosy skin lesion biopsies obtained from patients with leprosy, 16 TT and 14 lepromatous LL. Results Immunohistochemical analysis revealed a significant difference in interleukin (IL)-9, IL-4 transforming growth factor (TGF)-beta and IL-10 levels between the two groups. IL-9 was more expressed in TT lesions compared with LL lesions. Higher expression of IL-4, IL-10 and TGF-beta was observed in LL compared with TT. IL-4, IL-10 and TGF-beta tended to be negatively correlated with the expression of IL-9, indicating a possible antagonistic activity in tissue. Conclusions The results suggest that Th9 lymphocytes may be involved in the response to Mycobacterium leprae, positively or negatively regulating microbicidal activity of the local immune system in the disease.