Níveis séricos de CXCL12 nas diferentes formas e fases clínicas da Leishmaniose Visceral

• Ano de defesa: 2024
• Autor(a) principal: Santos, Rogério Silva
• Orientador(a): Santos, Priscila Lima dos
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Programa de Pós-Graduação: Pós-Graduação em Ciências Aplicadas à Saúde
• Palavras-chave em Português: Quimiocinas; Quimiocina CXCL12; Leishmaniose Visceral
• Palavras-chave em Inglês: Chemokines; Chemokine CXCL12; Leishmaniasis, Visceral
• Área do conhecimento CNPq: CIENCIAS DA SAUDE
• Link de acesso: https://ri.ufs.br/jspui/handle/riufs/23953

Introduction: Leishmaniasis is an endemic disease in tropical regions that can manifest in cutaneous, mucocutaneous, and visceral (VL) forms, known as kala-azar. The immune response to parasitic infection is complex, and its course depends on the cellular and molecular agents present at the time of infection. The chemokine CXCL12 plays a pleiotropic and crucial role in physiological processes such as embryogenesis, hematopoiesis, angiogenesis, and inflammation, as it activates and induces the migration of hematopoietic stem cells and endothelial cells in most leukocytes. Given this molecule's significant role in hematopoietic activation and differentiation, which is targeted by Leishmania sp., it is necessary to investigate its involvement in this comorbidity. Objective: To evaluate serum levels of the chemokine CXCL12 in different forms and clinical stages of VL. Methodology:This is a case-control study conducted at LIBM of HU-UFS, following ethical standards. Participants were divided into case groups (diagnosed with VL) and control groups (DTH+ and endemic controls). Serum was extracted and analyzed for cytokines and chemokines using multiplex. Clinical and laboratory data were collected from medical records, and statistical analysis employed Kruskal-Wallis tests and Spearman correlation, considering p-values <0.05 as significant. Results: Individuals with the symptomatic and active form of VL had elevated serum levels of CXCL12 compared to asymptomatic individuals. During treatment, CXCL12 concentration decreased to levels similar to the control group. The correlations between chemokines were predominantly positive, indicating a synergistic interaction among the molecules. The correlation between CXCL12 and hematocrit showed a Spearman coefficient (Rho) of -0.48, while the correlation between CXCL12 and hemoglobin had Rho=-0.53 with significant p-values. These negative values indicate that as CXCL12 expression increases, hematocrit and hemoglobin levels tend to decrease. This inverse relationship suggests that CXCL12 may play a regulatory role in decreasing hematocrit and hemoglobin levels, possibly interfering with the normal balance of these molecules in the blood. The lack of studies on CXCL12 in humans with VL is noted, although studies in murine models indicate that CXCL12 influences the attraction of hematopoietic progenitors. Conclusion: The study indicates that serum expression of CXCL12 decreases during VL treatment, aligning with the clinical recovery of patients. The research contributes to understanding the immunological dynamics in VL and suggests that CXCL12 may be an important biomarker for monitoring treatment. However, further studies are needed to explore the involvement of CXCL12 in the development of VL.