دورية أكاديمية
Interaction between peripheral blood mononuclear cells and Trypanosoma cruzi -infected adipocytes: implications for treatment failure and induction of immunomodulatory mechanisms in adipose tissue.
| العنوان: | Interaction between peripheral blood mononuclear cells and Trypanosoma cruzi -infected adipocytes: implications for treatment failure and induction of immunomodulatory mechanisms in adipose tissue. |
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| المؤلفون: | Moreira LR; Department of Tropical Medicine, Federal University of Pernambuco, Recife, Brazil.; Department of Immunology, Aggeu Magalhães Institute, Recife, Brazil., Silva AC; Department of Immunology, Aggeu Magalhães Institute, Recife, Brazil., da Costa-Oliveira CN; Department of Immunology, Aggeu Magalhães Institute, Recife, Brazil., da Silva-Júnior CD; Department of Tropical Medicine, Federal University of Pernambuco, Recife, Brazil.; Department of Immunology, Aggeu Magalhães Institute, Recife, Brazil., Oliveira KKDS; Department of Immunology, Aggeu Magalhães Institute, Recife, Brazil., Torres DJL; Department of Tropical Medicine, Federal University of Pernambuco, Recife, Brazil.; Department of Immunology, Aggeu Magalhães Institute, Recife, Brazil., Barros MD; Department of Immunology, Aggeu Magalhães Institute, Recife, Brazil., Rabello MCDS; Department of Immunology, Aggeu Magalhães Institute, Recife, Brazil., de Lorena VMB; Department of Immunology, Aggeu Magalhães Institute, Recife, Brazil. |
| المصدر: | Frontiers in immunology [Front Immunol] 2024 Mar 12; Vol. 15, pp. 1280877. Date of Electronic Publication: 2024 Mar 12 (Print Publication: 2024). |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: Frontiers Research Foundation] Country of Publication: Switzerland NLM ID: 101560960 Publication Model: eCollection Cited Medium: Internet ISSN: 1664-3224 (Electronic) Linking ISSN: 16643224 NLM ISO Abbreviation: Front Immunol Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: [Lausanne : Frontiers Research Foundation] |
| مواضيع طبية MeSH: | Trypanosoma cruzi* , Chagas Disease* , Nitroimidazoles*, Humans ; Interleukin-8 ; Leukocytes, Mononuclear ; Complement Factor D ; Interleukin-2/therapeutic use ; Adipose Tissue ; Adipocytes ; Tumor Necrosis Factor-alpha/therapeutic use ; Immunity ; Treatment Failure |
| مستخلص: | Background/introduction: Adipose tissue (AT) has been highlighted as a promising reservoir of infection for viruses, bacteria and parasites. Among them is Trypanosoma cruzi , which causes Chagas disease. The recommended treatment for the disease in Brazil is Benznidazole (BZ). However, its efficacy may vary according to the stage of the disease, geographical origin, age, immune background of the host and sensitivity of the strains to the drug. In this context, AT may act as an ally for the parasite survival and persistence in the host and a barrier for BZ action. Therefore, we investigated the immunomodulation of T. cruzi-infected human AT in the presence of peripheral blood mononuclear cells (PBMC) where BZ treatment was added. Methods: We performed indirect cultivation between T. cruzi-infected adipocytes, PBMC and the addition of BZ. After 72h of treatment, the supernatant was collected for cytokine, chemokine and adipokine assay. Infected adipocytes were removed to quantify T. cruzi DNA, and PBMC were removed for immunophenotyping. Results: Our findings showed elevated secretion of interleukin (IL)-6, IL-2 and monocyte chemoattractant protein-1 (MCP-1/CCL2) in the AT+PBMC condition compared to the other controls. In contrast, there was a decrease in tumor necrosis factor (TNF) and IL-8/CXCL-8 in the groups with AT. We also found high adipsin secretion in PBMC+AT+T compared to the treated condition (PBMC+AT+T+BZ). Likewise, the expression of CD80+ and HLA-DR+ in CD14+ cells decreased in the presence of T. cruzi. Discussion: Thus, our findings indicate that AT promotes up-regulation of inflammatory products such as IL-6, IL-2, and MCP-1/CCL2. However, adipogenic inducers may have triggered the downregulation of TNF and IL-8/CXCL8 through the peroxisome proliferator agonist gamma (PPAR-g) or receptor expression. On the other hand, the administration of BZ only managed to reduce inflammation in the microenvironment by decreasing adipsin in the infected culture conditions. Therefore, given the findings, we can see that AT is an ally of the parasite in evading the host's immune response and the pharmacological action of BZ. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2024 Moreira, Silva, Costa-Oliveira, Silva-Júnior, Oliveira, Torres, Barros, Rabello and de Lorena.) |
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| فهرسة مساهمة: | Keywords: Trypanosoma cruzi; adipokine; adipose tissue; benznidazole; chemokine; cytokine; immunomodulation |
| المشرفين على المادة: | 0 (Interleukin-8) EC 3.4.21.46 (Complement Factor D) 0 (Interleukin-2) YC42NRJ1ZD (benzonidazole) 0 (Tumor Necrosis Factor-alpha) 0 (Nitroimidazoles) |
| تواريخ الأحداث: | Date Created: 20240327 Date Completed: 20240328 Latest Revision: 20240328 |
| رمز التحديث: | 20240329 |
| مُعرف محوري في PubMed: | PMC10963431 |
| DOI: | 10.3389/fimmu.2024.1280877 |
| PMID: | 38533504 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 1664-3224 |
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| DOI: | 10.3389/fimmu.2024.1280877 |