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1.
Braz J Microbiol ; 51(2): 637-645, 2020 Jun.
Article in English | MEDLINE | ID: mdl-31993990

ABSTRACT

The human T cell lymphotropic virus (HTLV) has a worldwide distribution. HTLV is endemic in some states in the northeastern region of Brazil. This study investigated the prevalence of HTLV-1/2 in 713 pregnant women attended at the Central Laboratory of Public Health of Maranhão (LACEN-MA) between February 2015 and May 2017. Serological screening was performed by chemiluminescent microparticle immunoassay (CMIA), and reactive sera were subsequently confirmed by Western blot (WB) analysis. Five samples were determined to be HTLV-1/2-reactive by CMIA analysis, while in the WB analysis, three sera were positive for HTLV-1, and two were indeterminate. The polymerase chain reaction (PCR) analysis used to detect HTLV-1 proviral DNA showed a specific 336 base pair fragment for HTLV-1 in all CMIA-reactive serum samples. PCR products were purified and sequenced. We observed a 0.7% molecular prevalence of HTLV-1 infection. The average age of the HTLV-1-positive pregnant women was 25.6 ± 8.2 years, and the average age of the HTLV-1-negative pregnant women was 24.3 ± 6.2 (p = 0.60). We observed that there was no association of HTLV-1 infection with age, ethnicity, marital status, educational level, family income, age of first sexual intercourse, previous pregnancy, breastfeeding, intravenous drug use by partner, history of blood transfusions, or use of condoms. The prevalence of HTLV-1 observed in pregnant women demonstrated the need to implement public health policies for the screening of HTLV-1/2 in prenatal care and counseling to avoid breastfeeding by infected women; this approach could control vertical transmission and reduce the spread of this virus in the population.


Subject(s)
HTLV-I Infections/diagnosis , Human T-lymphotropic virus 1/genetics , Adolescent , Adult , Brazil/epidemiology , Cross-Sectional Studies , DNA, Viral/genetics , Female , HTLV-I Infections/epidemiology , Human T-lymphotropic virus 1/isolation & purification , Humans , Pregnancy , Prevalence , Young Adult
2.
Sci Rep ; 9(1): 18159, 2019 12 03.
Article in English | MEDLINE | ID: mdl-31796807

ABSTRACT

Staphylococcus aureus is recognized as an important pathogen causing a wide spectrum of diseases. Here we examined the antimicrobial effects of the lectin isolated from leaves of Schinus terebinthifolia Raddi (SteLL) against S. aureus using in vitro assays and an infection model based on Galleria mellonella larvae. The actions of SteLL on mice macrophages and S. aureus-infected macrophages were also evaluated. SteLL at 16 µg/mL (8 × MIC) increased cell mass and DNA content of S. aureus in relation to untreated bacteria, suggesting that SteLL impairs cell division. Unlike ciprofloxacin, SteLL did not induce the expression of recA, crucial for DNA repair through SOS response. The antimicrobial action of SteLL was partially inhibited by 50 mM N-acetylglucosamine. SteLL reduced staphyloxathin production and increased ciprofloxacin activity towards S. aureus. This lectin also improved the survival of G. mellonella larvae infected with S. aureus. Furthermore, SteLL induced the release of cytokines (IL-6, IL-10, IL-17A, and TNF-α), nitric oxide and superoxide anion by macrophagens. The lectin improved the bactericidal action of macrophages towards S. aureus; while the expression of IL-17A and IFN-γ was downregulated in infected macrophages. These evidences suggest SteLL as important lead molecule in the development of anti-infective agents against S. aureus.


Subject(s)
Anacardiaceae/chemistry , Anti-Infective Agents/pharmacology , Lectins/pharmacology , Macrophages/microbiology , Plant Leaves/chemistry , Staphylococcal Infections/drug therapy , Staphylococcus aureus/drug effects , Animals , Ciprofloxacin/pharmacology , Cytokines/metabolism , Female , Macrophages/metabolism , Male , Mice , Mice, Inbred C57BL , Nitric Oxide/metabolism , Staphylococcal Infections/metabolism , Superoxides/metabolism
3.
Molecules ; 24(9)2019 May 07.
Article in English | MEDLINE | ID: mdl-31067626

ABSTRACT

The occurrence of damage on bacterial DNA (mediated by antibiotics, for example) is intimately associated with the activation of the SOS system. This pathway is related to the development of mutations that might result in the acquisition and spread of resistance and virulence factors. The inhibition of the SOS response has been highlighted as an emerging resource, in order to reduce the emergence of drug resistance and tolerance. Herein, we evaluated the ability of betulinic acid (BA), a plant-derived triterpenoid, to reduce the activation of the SOS response and its associated phenotypic alterations, induced by ciprofloxacin in Staphylococcus aureus. BA did not show antimicrobial activity against S. aureus (MIC > 5000 µg/mL), however, it (at 100 and 200 µg/mL) was able to reduce the expression of recA induced by ciprofloxacin. This effect was accompanied by an enhancement of the ciprofloxacin antimicrobial action and reduction of S. aureus cell volume (as seen by flow cytometry and fluorescence microscopy). BA could also increase the hyperpolarization of the S. aureus membrane, related to the ciprofloxacin action. Furthermore, BA inhibited the progress of tolerance and the mutagenesis induced by this drug. Taken together, these findings indicate that the betulinic acid is a promising lead molecule in the development helper drugs. These compounds may be able to reduce the S. aureus mutagenicity associated with antibiotic therapies.


Subject(s)
Drug Resistance, Bacterial/drug effects , Rec A Recombinases/genetics , Staphylococcus aureus/genetics , Triterpenes/pharmacology , Ciprofloxacin/adverse effects , Ciprofloxacin/pharmacology , DNA, Bacterial/drug effects , Gene Expression Regulation, Bacterial/drug effects , Humans , Mutagenesis/drug effects , Mutagenesis/genetics , Pentacyclic Triterpenes , SOS Response, Genetics/drug effects , SOS Response, Genetics/genetics , Staphylococcus aureus/drug effects , Staphylococcus aureus/pathogenicity , Virulence Factors/genetics , Betulinic Acid
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