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Publicações Científicas e Culturais 23073
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Editorial: the Role of Pentraxins: from inflammation, tissue repair and immunity to biomarkers
(Universidade Federal de Minas Gerais, 2019) Barbara Bottazzi; Cecília Garlanda; Mauro Martins Teixeira
Pentraxins are conserved proteins, such as CRP, SAP, and PTX3, involved in innate immunity, inflammation, and tissue repair. They act in complement activation, opsonization, and tissue remodeling. They also have clinical relevance as biomarkers and therapeutic targets in various diseases, including infections, cancer, and cardiovascular conditions.
Interleukin-33 Receptor (ST2) Deficiency Improves the Outcome of Staphylococcus aureus-Induced Septic Arthritis
(Universidade Federal de Minas Gerais, 2018) Larissa Staurengo Ferrari; Silvia Cellone Trevelin; Victor Fattori; Daniele Carvalho Nascimento; Kalil Alves de Lima; Jacinta Sanchez Pelayo; Florêncio Figueiredo; Rubia Casagrande; Sandra Yasuyo Fukada; Mauro Martins Teixeira; Thiago Mattar Cunha; Foo Yew Liew; Rene Oliveira; Paulo Louzada Junior; Fernando de Queiroz Cunha; José Carlos Alves Filho; Waldiceu Aparecido Verri
The ST2 receptor is a member of the Toll/IL-1R superfamily and interleukin-33 (IL-33) is its agonist. Recently, it has been demonstrated that IL-33/ST2 axis plays key roles in inflammation and immune mediated diseases. Here, we investigated the effect of ST2 deficiency in Staphylococcus aureus-induced septic arthritis physiopathology. Synovial fluid samples from septic arthritis and osteoarthritis individuals were assessed regarding IL-33 and soluble (s) ST2 levels. The IL-33 levels in samples from synovial fluid were significantly increased, whereas no sST2 levels were detected in patients with septic arthritis when compared with osteoarthritis individuals. The intra-articular injection of 1 × 107 colony-forming unity/10 μl of S. aureus American Type Culture Collection 6538 in wild-type (WT) mice induced IL-33 and sST2 production with a profile resembling the observation in the synovial fluid of septic arthritis patients. Data using WT, and ST2 deficient (−/−) and interferon-γ (IFN-γ)−/− mice showed that ST2 deficiency shifts the immune balance toward a type 1 immune response that contributes to eliminating the infection due to enhanced microbicide effect via NO production by neutrophils and macrophages. In fact, the treatment of ST2−/− bone marrow-derived macrophage cells with anti-IFN-γ abrogates the beneficial phenotype in the absence of ST2, which confirms that ST2 deficiency leads to IFN-γ expression and boosts the bacterial killing activity of macrophages against S. aureus. In agreement, WT cells achieved similar immune response to ST2 deficiency by IFN-γ treatment. The present results unveil a previously unrecognized beneficial effect of ST2 deficiency in S. aureus-induced septic arthritis.
Quantifying the spatial spread of dengue in a non-endemic Brazilian metropolis via transmission chain reconstruction
(Universidade Federal de Minas Gerais, 2018) Giorgio Guzzetta; Cecília de Almeida Marques-Toledo; Roberto Rosà; Mauro Martins Teixeira; Stefano Merler
The ongoing geographical expansion of dengue is inducing an epidemiological transition in many previously transmission-free urban areas, which are now prone to annual epidemics. To analyze the spatiotemporal dynamics of dengue in these settings, we reconstruct transmission chains in Porto Alegre, Brazil, by applying a Bayesian inference model to geo-located dengue cases from 2013 to 2016. We found that transmission clusters expand by linearly increasing their diameter with time, at an average rate of about 600 m month−1. The majority (70.4%, 95% CI: 58.2–79.8%) of individual transmission events occur within a distance of 500 m. Cluster diameter, duration, and epidemic size are proportionally smaller when control interventions were more timely and intense. The results suggest that a large proportion of cases are transmitted via short-distance human movement (<1 km) and a limited contribution of long distance commuting within the city. These results can assist the design of control policies, including insecticide spraying and strategies for active case finding.
Revisiting the Role of Eotaxin-1/CCL11 in Psychiatric Disorders
(Universidade Federal de Minas Gerais, 2018) Antonio Lúcio Teixeira; Clarissa Severino Gama; Natalia Rocha; Mauro Martins Teixeira
Eotaxin-1/CCL11 is a chemokine originally implicated in the selective recruitment of eosinophils into inflammatory sites during allergic reactions, being thoroughly investigated in asthma, allergic rhinitis, and other eosinophil-related conditions. Eotaxin-1/CCL11 is also involved with a skewed immune response toward a type-2 (Th2) profile. In addition to its role in immune response, recent studies have shown that eotaxin-1/CCL11 is associated with aging, neurogenesis and neurodegeneration, being able to influence neural progenitor cells, and microglia. Increased circulating levels of eotaxin-1/CCL11 have been described in major psychiatric disorders (schizophrenia, bipolar disorder, major depression), sometimes correlating with the severity of psychopathological and cognitive parameters. As similar findings have been reported in neurodegenerative conditions such as Alzheimer's disease, it has been hypothesized that mechanisms involving eotaxin-1/CCL11 signaling may underlie the “accelerated aging” profile commonly linked to psychiatric disorders. Future studies must determine whether eotaxin-1/CCL11 can be regarded as a prognostic biomarker and/or as therapeutic target for resistant/progressive cases.
Paradoxical Role of Matrix Metalloproteinases in Liver Injury and Regeneration after Sterile Acute Hepatic Failure
(Universidade Federal de Minas Gerais, 2018) Débora Moreira Alvarenga; Matheus Silvério Mattos; Mateus Eustáquio Lopes; Sarah Cozzer Marchesi; Alan Moreira Araújo; Brenda Naemi Nakagaki; Mônica Morais Santos; Bruna Araújo David; Viviane Aparecida De Souza; Érika Carvalho; Rafaela Vaz Sousa Pereira; Pedro Elias Marques; Kassiana Mafra; Hortência Maciel de Castro Oliveira; Camila Dutra Moreira de Miranda; Ariane Barros Diniz; Thiago Henrique Caldeira de Oliveira; Mauro Martins Teixeira; Rafael Machado Rezende; Maísa Mota Antunes; Gustavo Batista Menezes
Acetaminophen (APAP) poisoning is one of the leading causes of acute hepatic failure and liver transplantation is often the only lifesaving alternative. During the course of hepatocyte necrosis, an intense accumulation of neutrophils is often observed within the liver microenvironment. Despite the classic idea that neutrophil accumulation in tissues causes collateral tissue damage, there is a growing body of evidence showing that neutrophils can also orchestrate the resolution of inflammation. In this work, drug-induced liver injury was induced by oral administration of APAP and pharmacological intervention was made 12 h after this challenge. Liver injury and repair kinetics were evaluated by a novel combination of enzyme quantifications, ELISA, specific antagonists of neutrophil enzymes and confocal intravital microscopy. We have demonstrated that neutrophil infiltration is not only involved in injury amplification, but also in liver tissue repair after APAP-induced liver injury. In fact, while neutrophil depletion led to reduced hepatic necrosis during APAP poisoning, injury recovery was also delayed in neutropenic mice. The mechanisms underlying the neutrophil reparative role involved rapid degranulation and matrix metalloproteinases (MMPs) activity. Our data highlights the crucial role of neutrophils, in particular for MMPs, in the resolution phase of APAP-induced inflammatory response.

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