Does Prolactin treatment trigger imunoendocrine alterations during experimental T. cruzi infection?

• Published in: Cytokine (Philadelphia, Pa.) Vol. 121; p. 154736
• Main Authors: Del Vecchio Filipin, Marina, Brazão, Vânia, Santello, Fabricia Helena, da Costa, Cássia Mariana Bronzon, Paula Alonso Toldo, Míriam, Rossetto de Morais, Fabiana, do Prado Júnior, José Clóvis
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.09.2019
• Subjects: Cytokines; Immune response; Prolactin, Trypanosoma cruzi; Cytokines; Prolactin, Trypanosoma cruzi; Immune response
• ISSN: 1043-4666; 1096-0023
• DOI: 10.1016/j.cyto.2019.154736

[Display omitted] •We have investigated the influence of prolactin on the magnitude of the immune response in male Wistar rats infected with the Y strain of T. cruzi. The highest and significant percentages of NK cells and B lymphocytes were observed in the infected PRL treated animals (14th dpi).•Early and late apoptosis as well as CD4+T and CD8+ T levels were reduced for the same groups.•Proliferation of polyclonal stimulated T cells were significantly higher in PRL treated and infected animals than in untreated rats (7th dpi).•On 60th day post-infection, CD4+ T lymphocytes IFN-γ producers were significantly reduced in prolactin-treated rats comparing to infected and untreated rats.•Our present results demonstrated that PRL can influence many aspects of the immune response during the experimental Chagas' disease, and this substance could be used as a supporting trial along with the conventional drug treatment. Prolactin (PRL) is a pleiotropic polypeptide hormone produced by the anterior pituitary gland and negatively controlled by dopamine. Some researchers have associated the immune regulatory functions of PRL with some infectious diseases like Toxoplasma gondii and T. cruzi. This work aimed to analyze the possible immuno-modulatory effects of this hormone through the subcutaneous administration of PRL during the experimental Chagas disease. On the 14th day post-infection (dpi), PRL triggered increased percentages of NK cells in treated infected animals as compared to the infected and untreated ones. For early and late apoptosis, our results showed that in chronically infected groups, PRL counteracted splenocyte apoptosis as revealed by the reduced percentages of both, early and late apoptosis. Reduced percentages of spleen CD4+ and CD8+ T cells were detected in infected PRL treated rats (60 days post-infection). Concerning to B cells, a significant increased percentage of these cells was found for all PRL treated infected animals (14th dpi), but no statistically significant alteration was observed on the 60th days post-infection. Furthermore, PRL treatment triggered a significant increase in the percentage of CD4+ T lymphocytes IFN-γ producers, while on the 60th dpi, a reduced percentage of IFN-γ in these cells was observed in prolactin-treated rats compared to infected and untreated ones. Enhanced serum IL-12 levels were detected in infected and PRL treated subjects (60th dpi). Only on 7th day post-infection, the flow cytometric analysis of CFSE-stained CD3+ T cells showed an enhanced proliferation of polyclonal stimulated T cells in PRL-treated and infected animals. In this study, we demonstrated that PRL can influence many aspects of the immune response during the experimental Chagas' disease, and this substance could be used as a supporting trial along with the conventional drug treatment.