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1.
Odontology ; 108(1): 25-33, 2020 Jan.
Article in English | MEDLINE | ID: mdl-31214897

ABSTRACT

Periodontitis is modulated by a complex dysbiotic microbiota, these species stimulate upward the production of pro-inflammatory cytokines such as TNF-α, which, in turn, upregulates the production of bone resorption molecules. Enzymes such as MMP-8 and 9 have been associated with the destructive disease. This study evaluated the composition of periodontal microbiota with the checkerboard hybridization technique and its correlation with TNF-α, MMP-8, and MMP-9 evaluated with ELISA, of 80 patients (45 healthy, and 35 with chronic periodontitis). The frequency of the 18 species evaluated was higher in patients with bone loss compared with control group. TNF-α in gingival crevicular fluid was significantly higher in bone loss group (p < 0.01); MMP-8 (p = 0.34) by MMP-9 (p < 0.05) in bone loss group obtained lower values than in control group. Positive correlation of TNF-α was obtained with Aggregatibacter actinomycetemcomitans (rho = 0.38; p < 0.01), Fusobacterium nucleatum (rho = 0.25; p < 0.05) and Porphyromonas gingivalis (rho = 0.26; p < 0.05); negative correlation of MMP-8 with A. actinomycetemcomitans (rho = 0.26; p < 0.01), Capnocytophaga sputigena (rho = 0.33; p < 0.01), and F. nucleatum (rho = 0.21; p < 0.05); also negative correlation of MMP-9 with F. nucleatum (rho = 0.23; p < 0.05), P. gingivalis (rho = 0.23; p < 0.05), and Tannerella forsythia (rho = 0.26; p < 0.01). TNF-α increased due to the increase in each count of A. actinomycetemcomitans (ß = 0.57; p = 0.00). The presence of A. actinomycetemcomitans (ß = 1.88; p = 0.00), Campylobacter rectus (ß = 0.78; p = 0.01), F. nucleatum (ß = 0.65; p = 0.04), and P. gingivalis (ß = 0.65; p = 0.04) significantly increases TNF-α levels. TNF-α in gingival crevicular fluid, despite the minimal amounts collected, is a good biomarker of periodontal disease; since levels of TNF-α increases with the increase of the most harmful species to the periodontium.


Subject(s)
Gingival Crevicular Fluid , Microbiota , Humans , Matrix Metalloproteinase 8 , Matrix Metalloproteinase 9 , Porphyromonas gingivalis , Prevotella intermedia , Tumor Necrosis Factor-alpha
2.
Clin Exp Med ; 19(1): 105-113, 2019 Feb.
Article in English | MEDLINE | ID: mdl-30220001

ABSTRACT

Escherichia coli is the main etiological agent of urinary tract infections. Its virulence factors are important during the initial interaction stage with the host as they enable colonization of urinary tract tissues. The genetic markers evidencing susceptibility to develop recurrent infections have been previously described. Toll-like receptors are critical sensors of microbial attacks, and they are also effectors of the individual's innate defense for elimination of pathogens. The aim of this study was to evaluate the association between functional polymorphisms (896 A>G, 1196 C>T, - 2570 A>G, - 2081 G>A) and susceptibility to develop urinary tract infections as well as E. coli virulence factors. This study includes 100 samples from patients diagnosed with UTI and 100 samples from uninfected subjects. A conventional urine culture was performed and the isolates were identified by using the Vitek automated system. TLR4 gene polymorphisms were identified by the PCR-RFLP technique. The hlyA, fimH, papC, iutA and cnf1 virulence factors as well as the E. coli phylogenetic group were assessed by PCR. In this study, it was observed that the presence of the - 2570 polymorphism represents a risk of UTI (p < 0.01), whereas - 2081 confers protection (p < 0.01). The 896A>G and 1196C>T polymorphisms were associated with the E. coli virulence factors fimH and hlyA, respectively (p < 0.05). The B2 group was the most frequent in clinical isolates (51%), and it displayed more virulence factors regarding other phylogenetic groups (p ≤ 0.05). An interesting finding was that strains considered as commensals, belonging to groups A and B1, can cause UTI and present virulence factors. Polymorphisms occurring in the TLR4 promoter region are correlated with susceptibility or risk of UTI, whereas structural polymorphisms are associated with the recognition of virulence factors displayed by E. coli.


Subject(s)
Escherichia coli Infections/genetics , Genetic Predisposition to Disease , Polymorphism, Single Nucleotide , Toll-Like Receptor 4/genetics , Urinary Tract Infections/genetics , Uropathogenic Escherichia coli/pathogenicity , Virulence Factors/genetics , Adolescent , Adult , Aged , Aged, 80 and over , Bacteriological Techniques , Child , Child, Preschool , Escherichia coli Infections/microbiology , Female , Humans , Male , Middle Aged , Polymerase Chain Reaction , Polymorphism, Restriction Fragment Length , Pregnancy , Toll-Like Receptor 4/metabolism , Urinary Tract Infections/microbiology , Uropathogenic Escherichia coli/genetics , Young Adult
3.
EJIFCC ; 29(1): 26-35, 2018 Apr.
Article in English | MEDLINE | ID: mdl-29765284

ABSTRACT

OBJECTIVE: The aim of the present study was to evaluate the possible association between the Q223R Leptin receptor (LEPR) polymorphism (A>G; rs1137101) and leptin levels in patients with rheumatoid arthritis (RA) from Western Mexico. METHODS: A cross-sectional study was performed with 70 RA patients and 74 controls subject (CS). Disease activity was evaluated using DAS28 score, the Q223R LEPR polymorphism was determined by the Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) and serum leptin levels, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and rheumatoid factor (RF) were quantified. RESULTS: RA patients had significant high serum leptin levels compared with CS; leptin levels correlated strongly with body composition measures, but not with inflammatory markers, disease evolution, and activity. The genotype and allele frequencies of the Q223R LEPR polymorphism were not associated with RA. Similarly, leptin levels did not differ between Q223R LEPR genotypes. CONCLUSION: The LEPR Q223R polymorphism was not associated with RA risk in patients from Mexican population, even though high levels of serum leptin were present and these could explain the low weight observed in RA patients when they were compared to control subjects. However, the serum leptin levels did not correlate with inflammatory markers, severity and disease evolution.

4.
Hum Immunol ; 78(9): 553-558, 2017 Sep.
Article in English | MEDLINE | ID: mdl-28551357

ABSTRACT

Rheumatoid arthritis (RA) is a common autoimmune disease with a complex genetic background. The peptidyl arginine deiminase type IV (PADI4) gene has been associated with RA susceptibility in several populations. We addressed the relationship between three exonic PADI4 gene single nucleotide polymorphisms (SNPs) PADI4_89 (rs11203366), PADI4_90 (rs11203367) and PADI4_92 (rs874881) and related haplotypes with RA in a population from Southern México. This study included 200 RA patients and 200 control subjects. The SNPs were evaluated using the polymerase chain reaction-restriction fragment-length polymorphism (PCR-RFLP) technique, and antibodies to cyclic citrullinated peptides (anti-CCP) were measured by enzyme-linked immunosorbent assay (ELISA). In this population, the minor alleles of PADI4_89∗G, PADI4_90∗T and PADI4_92∗G gene polymorphisms were associated with RA susceptibility (OR=1.34, p=0.04; OR=1.35, p=0.03; OR=1.34, p=0.04; respectively). The GTG haplotype was also significantly associated with RA (OR=2.27 95%CI=1.18-4.41; p=0.008), but did not show association with levels of anti-CCP antibodies and clinical parameters. In conclusion, our replication study in a Southern Mexican population suggests that PADI4 individual polymorphisms and the related susceptibility haplotype (GTG) are also genetic risk markers for RA.


Subject(s)
Arthritis, Rheumatoid/genetics , Genetic Markers/genetics , Genotype , Protein-Arginine Deiminases/genetics , Adult , Aged , Anti-Citrullinated Protein Antibodies/blood , Case-Control Studies , Female , Gene Frequency , Genetic Association Studies , Genetic Predisposition to Disease , Haplotypes , Humans , Male , Mexico , Middle Aged , Polymorphism, Single Nucleotide , Protein-Arginine Deiminase Type 4
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