A trypsin inhibitor from Tecoma stans leaves inhibits growth and promotes ATP depletion and lipid peroxidation in Candida albicans and Candida krusei

Tecoma stans (yellow elder) has shown medicinal properties and antimicrobial activity. Previous reports on antifungal activity of T. stans preparations and presence of trypsin inhibitor activity from T. stans leaves stimulated the investigation reported here. In this work, we proceeded to the purification and characterization of a trypsin inhibitor (TesTI), which was investigated for anti-Candida activity. Finally, in order to determine the potential of TesTI as a new natural chemotherapeutic product, its cytotoxicity to human peripheral blood mononuclear cells (PBMCs) was evaluated. TesTI was isolated from saline extract by ammonium sulphate fractionation followed by ion exchange and gel filtration chromatographies. Antifungal activity was evaluated by determining the minimal inhibitory (MIC) and fungicide (MFC) concentrations using fungal cultures containing only yeast form or both yeast and hyphal forms. Candida cells treated with TesTI were evaluated for intracellular ATP levels and lipid peroxidation. Cytotoxicity of TesTI to PBMCs was evaluated by MTT assay. TesTI (39.8 kDa, pI 3.41, Ki 43 nM) inhibited similarly the growth of both C. albicans and C. krusei culture types at MIC of 100 µg/mL. The MFCs were 200 µg/mL for C. albicans and C. krusei. Time-response curves revealed that TesTI (at MIC) was more effective at inhibiting the replication of C. albicans cells. At MIC, TesTI promoted reduction of ATP levels and lipid peroxidation in the Candida cells, being not cytotoxic to PBMCs. In conclusion, TesTI is an antifungal agent against C. albicans and C. krusei, without toxicity to human cells

The Role of PPAR Gamma in Systemic Sclerosis

Fibrosis is recognized as an important feature of many chronic diseases, such as systemic sclerosis (SSc), an autoimmune disease of unknown etiology, characterized by immune dysregulation and vascular injury, followed by progressive fibrosis affecting the skin and multiple internal organs. SSc has a poor prognosis because no therapy has been shown to reverse or arrest the progression of fibrosis, representing a major unmet medical need. Recently, antifibrotic effects of PPARγ ligands have been studied in vitro and in vivo and some theories have emerged leading to new insights. Aberrant PPARγ function seems to be implicated in pathological fibrosis in the skin and lungs. This antifibrotic effect is mainly related to the inhibition of TGF-β/Smad signal transduction but other pathways can be involved. This review focused on recent studies that identified PPARγ as an important novel pathway with critical roles in regulating connective tissue homeostasis, with emphasis on skin and lung fibrosis and its role on systemic sclerosis

Single Nucleotide Polymorphisms at +191 and +292 of Galectin-3 Gene (LGALS3) Related to Lower GAL-3 Serum Levels Are Associated with Frequent Respiratory Tract Infection and Vaso-Occlusive Crisis in Children with Sickle Cell Anemia

Submitted by Adagilson Silva ([email protected]) on 2017-06-05T13:08:05Z No. of bitstreams: 1 27603703 2016 men-sin.oa.PDF: 1008770 bytes, checksum: 82f0081628ade062bc08ce6be5782a03 (MD5)Approved for entry into archive by Adagilson Silva ([email protected]) on 2017-06-05T13:08:29Z (GMT) No. of bitstreams: 1 27603703 2016 men-sin.oa.PDF: 1008770 bytes, checksum: 82f0081628ade062bc08ce6be5782a03 (MD5)Made available in DSpace on 2017-06-05T13:08:29Z (GMT). No. of bitstreams: 1 27603703 2016 men-sin.oa.PDF: 1008770 bytes, checksum: 82f0081628ade062bc08ce6be5782a03 (MD5) Previous issue date: 2016Programa de Doutorado da Rede Nordeste de Biotecnologia. Recife, PE, Brasil.Universidade de Pernambuco. Instituto de Ciências Biológicas e Faculdade de Ciências Médicas. Recife, PE, Brasil.Universidade de Pernambuco. Instituto de Ciências Biológicas e Faculdade de Ciências Médicas. Recife, PE, Brasil.Universidade Federal de Pernambuco. Laboratório de Imunomodulação e Novas Abordagens Terapêutica (LINAT). Recife, PE, Brasil.Universidade de Pernambuco. Instituto de Ciências Biológicas e Faculdade de Ciências Médicas. Recife, PE, Brasil.Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.Fundação Hematologia e Hemoterapia de Pernambuco (HEMOPE). Recife, PE, Brasil.Universidade Federal de Pernambuco. Departamento de Ciências Biológicas. Recife, PE, Brasil.Universidade Federal de Pernambuco. Laboratório de Imunomodulação e Novas Abordagens Terapêutica (LINAT). Recife, PE, Brasil.Universidade Federal de Pernambuco. Departamento de Ciências Biológicas. Recife, PE, Brasil.Fundação Hematologia e Hemoterapia de Pernambuco (HEMOPE). Recife, PE, Brasil.Universidade Federal de Pernambuco. Laboratório de Imunomodulação e Novas Abordagens Terapêutica (LINAT). Recife, PE, Brasil.Programa de Doutorado da Rede Nordeste de Biotecnologia. Recife, PE, Brasil / Universidade de Pernambuco. Instituto de Ciências Biológicas e Faculdade de Ciências Médicas. Recife, PE, Brasil.Programa de Doutorado da Rede Nordeste de Biotecnologia. Recife, PE, Brasil / Universidade de Pernambuco. Instituto de Ciências Biológicas e Faculdade de Ciências Médicas. Recife, PE, Brasil.Patients with sickle cell anemia (SCA) may present chronic hemolytic anemia, vaso-occlusion and respiratory tract infection (RTI) episodes. Galectin-3 (GAL-3) is a multifunctional protein involved in inflammation, apoptosis, adhesion and resistance to reactive oxygen species. Studies point to a dual role for GAL-3 as both a circulation damage-associated molecular pattern and a cell membrane associated pattern recognition receptor

Increased Serum Interleukin-9 Levels in Rheumatoid Arthritis and Systemic Lupus Erythematosus: Pathogenic Role or Just an Epiphenomenon?

The purpose of this paper was to evaluate the levels of IL-9 in patients with SLE and RA compared with controls and the association of IL-9 levels with clinical and laboratory parameters. IL-9 levels were assessed in 117 SLE patients, 67 RA patients, and 24 healthy controls by ELISA. Clinical and laboratory parameters were recorded. The IL-9 serum levels were significantly higher in RA patients (4,77 ± 3,618 pg/mL) and in SLE patients (12,26 ± 25,235 pg/mL) than in healthy individuals (1,22 ± 0,706 pg/mL) (p<0,001). In SLE patients, there were no statistically significant associations or correlations between the levels of IL-9 and SLEDAI or other clinical and laboratorial parameters, with the exception of disease time, which showed a statistically significant negative correlation with IL-9 levels (r=-0,1948; p=0,0378). In RA patients, no association or statistically significant correlation was observed with disease duration, DAS28, HAQ, rheumatoid factor positivity, or erosions on radiography. These data demonstrated increased serum levels of IL-9 in SLE and RA patients, but further studies are needed to clarify the precise role of this cytokine and its potential use as therapeutic target

Serum galectin-3 levels are associated with <i>LGALS3</i> +191 and +292 combined genotypes in children with SCA.

<p>Statistical analysis of <i>LGALS3</i> combined genotype related of galectin-3 levels (high, intermediate and low) in which the serum concentrations in ng/ml were compared using Kruskal-Wallis test. High vs. intermediate: <i>p =</i> 0.1687; high vs. low: <i>p =</i> 0.0002; high vs. intermediate+low: <i>p</i> = 0.0098.</p

Clinical data of children with sickle cell anemia attended in Hemope Foundation—Recife/Brazil.

<p>Clinical data of children with sickle cell anemia attended in Hemope Foundation—Recife/Brazil.</p

<i>LGALS3</i> +191 and +292 diplotype of serum levels with vaso-occlusive crisis and respiratory tract infection in children with sickle cell anemia attended in Hemope Foundation—Recife/Brazil.

<p><i>LGALS3</i> +191 and +292 diplotype of serum levels with vaso-occlusive crisis and respiratory tract infection in children with sickle cell anemia attended in Hemope Foundation—Recife/Brazil.</p