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    Vagus nerve mediated liver-brain-axis is a major regulator of the metabolic landscape in the liver
    (Universidade Federal de Minas Gerais, 2025) Camila de Fátima Carvalho Brito; Roberta Cristelli Fonseca; Lucas Rodrigues-Ribeiro; João S. F. Guimarães; Bruna F. Vaz; Gabriel S. S. Tofani; Ana C. S. Batista; Ariane Barros Diniz; Paola Fernandes; Núbia A. M. Nunes; Rafaela Miranda Pessoa; Amanda C. C. Oliveira; Ivana Silva Lula; Valbert Nascimento Cardoso; Simone Odília Antunes Fernandes; Maristela Oliveira Poletini; Jacqueline Isaura Alvarez-Leite; Gustavo Batista de Menezes; Adaliene Versiani Matos Ferreira; Mariana Torquato Quezado de Magalhães; Vladimir Gorshkov; Frank Kjeldsen; Thiago Verano-Braga; Alan Moreira de Araujo
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    Serodiagnosis and therapeutic monitoring of New-World tegumentary leishmaniasis using synthetic type-2 glycoinositolphospholipid-based neoglycoproteins
    (Universidade Federal de Minas Gerais, 2022) Sayonara Melo Viana; Alba Lucia Montoya; Augusto Marcelino Carvalho; Brunele Silva Dias de Mendonça; Susana Portillo; Janet Olivas; Nasim Karimi; Igor Estevao; Uriel Ortega Rodriguez; Edgar Marcelino de Carvalho; Walderez Ornelas Dutra; Rosa Maldonaldo; Katja Michael; Camila Indiani de Oliveira; Igor Correia de Almeida
    American tegumentary leishmaniasis (TL) caused by Leishmania braziliensis is characterized by a spectrum of clinical presentations, ranging from localized cutaneous ulcers (CL), mucosal (ML), or disseminated (DL) disease, to a subclinical (SC) asymptomatic form. Current diagnosis based on parasite culture and/or microscopy lacks sensitivity and specificity. Previous studies showed that patients with CL and ML have very high levels of Leishmania-specific anti-α-Gal antibodies. However, the native parasite α-Gal glycotope(s) is(are) still elusive, thus they have not yet been explored for a more accurate TL diagnosis. Using a chemiluminescent immunoassay, we evaluated the seroreactivity of TL patients across its clinical spectrum, and of endemic (EC) and nonendemic healthy controls (NEC) against three synthetic neoglycoproteins (NGP29b, NGP30b, and NGP28b), respectively comprising the L. major-derived type-2 glycoinositolphospholipid (GIPL)-1 (Galfβ1,3Manα), GIPL-2 (Galα1,3Galfβ1,3Manα), and GIPL-3 (Galα1,6Galα1,3Galfβ) glycotopes. Contrary to NGP29b and NGP30b, NGP28b exhibited high sensitivity and specificity to a CL serum pool. More importantly, NGP28b reacted strongly and specifically with individual sera from distinct clinical forms of TL, especially with SC sera, with 94% sensitivity and 97% specificity, by post-two-graph receiver-operating characteristic curve analysis. Contrary to NGP29b, NGP28b showed low cross-reactivity with Chagas disease and control (NEC/EC) sera. Additionally, seroreactivity of CL patients against NGP28b was significantly decreased after successful chemotherapy, indicating that L. braziliensis-specific anti-α-Gal antibodies may serve as an early biomarker of cure in CL. Our data also points towards the applicability of L. major type-2 GIPL-3-derived Galα1,6Galα1,3Galfβ glycotope for the serological diagnosis of American TL, particularly of the subclinical form.
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    Editorial: clinical and molecular features of infectious cardiomyopathies: implications for prevention, treatment and management
    (Universidade Federal de Minas Gerais, 2022) Maria do Carmo Pereira Nunes; Lívia Silva Araújo Passos; Walderez Ornelas Dutra
    This editorial aimed to synthesize advances regarding the clinical and molecular characteristics of infectious cardiomyopathies—with an emphasis on Chagasic cardiomyopathy—by highlighting factors related to the parasite, the host, and the environment. The methodology involved analyzing and integrating studies published within the research topic, encompassing clinical investigations, systematic reviews, and experimental studies on biomarkers, immune responses, *Trypanosoma cruzi* genetic variability, environmental factors, and therapeutic strategies. The conclusion is that these studies expand knowledge regarding the epidemiology, pathogenesis, diagnosis, and treatment of infectious cardiomyopathies; identify potential biomarkers and therapeutic targets; and provide insights to improve the prevention, prognosis, and clinical management of these diseases.
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    Cytotoxic CD4+ T cells driven by T-cell intrinsic IL-18R/MyD88 signaling predominantly infiltrate Trypanosoma cruzi-infected hearts
    (Universidade Federal de Minas Gerais, 2022) Carlos Henrique Dantas Barbosa; Fábio Canto; Ariel Gomes; Layza Mendes Brandão; Jéssica Ribeiro de Lima; Guilherme Afonso Melo; Alessandra Granato; Eula Graciele Amorim Neves; Walderez Ornelas Dutra; Ana Carolina Oliveira; Alberto Nóbrega; Maria Bellio
    Increasing attention has been directed to cytotoxic CD4+ T cells (CD4CTLs) in different pathologies, both in humans and mice. The impact of CD4CTLs in immunity and the mechanisms controlling their generation, however, remain poorly understood. Here, we show that CD4CTLs abundantly differentiate during mouse infection with the intracellular parasite Trypanosoma cruzi. CD4CTLs display parallel kinetics to Th1 cells in the spleen, mediate specific cytotoxicity against cells presenting pathogen-derived antigens and express immunoregulatory and/or exhaustion markers. We demonstrate that CD4CTL absolute numbers and activity are severely reduced in both Myd88-/- and Il18ra-/- mice. Of note, the infection of mixed-bone marrow chimeras revealed that wild-type (WT) but not Myd88-/- cells transcribe the CD4CTL gene signature and that Il18ra-/- and Myd88-/- CD4+ T cells phenocopy each other. Moreover, adoptive transfer of WT CD4+GzB+ T cells to infected Il18ra-/- mice extended their survival. Importantly, cells expressing the CD4CTL phenotype predominate among CD4+ T cells infiltrating the infected mouse cardiac tissue and are increased in the blood of Chagas patients, in which the frequency of CD4CTLs correlates with the severity of cardiomyopathy. Our findings describe CD4CTLs as a major player in immunity to a relevant human pathogen and disclose T-cell intrinsic IL-18R/MyD88 signaling as a key pathway controlling the magnitude of the CD4CTL response.

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