The generalized anxiety disorder (GAD) is often a debilitating chronic condition, characterized by long-lasting anxiety that is not focused on any object or situation. Besides being clearly linked to increased susceptibility to infectious diseases, anxiety is also known to contribute to the pathogenesis of many inflammatory/autoimmune disorders. The present work aimed to explore the T cell profile following in vitro activation in cultures obtained from a group of individuals with GAD, comparing them with healthy control individuals. Our results demonstrated that cell cultures from GAD group proliferated less following T cell activation as compared with the control group. The analysis of the cytokine profile revealed Th1 and Th2 cytokine deficiencies in the anxious group, as compared with the control subjects. On the other hand, this cellular and humoral immune damage was followed by enhanced production of Th17-derived cytokines. In particular, the levels of TNF-α and IL-17 were significantly higher in cell cultures containing activated T cells from GAD individuals. Therefore, besides a deficiency on Th1 phenotype, an elevated proinflammatory status of these individuals might be related to both glucocorticoid immune resistance and lower IL-10 levels produced by activated T cells. In conclusion, our results demonstrated a T cell functional dysregulation in individuals with GAD, and can help to explain the mechanisms of immune impairment in these subjects and their relationship with increased susceptibility to infections and autoimmune diseases.
The oral cavity may act as a reservoir for several pathogens related to systemic infections. Therefore, the purpose of this study was to determine the prevalence and levels of pathogenic bacteria in the subgingival biofilm of chronic periodontitis lesions and healthy periodontal sites using the checkerboard DNA-DNA hybridization technique. 200 samples of subgingival biofilm from sites with periodontitis (probing pocket depth ≥ 4 mm and /or clinical attachment level ≥ 4 mm) and 200 samples from healthy sites of 14 patients with chronic periodontitis, as well as 200 samples from 3 periodontally healthy patients were obtained. The presence and levels of 11 pathogenic bacteria were determined using whole genomic DNA probes and the checkerboard method, computed for each site and then across sites within each subject group. Significance of differences in clinical and microbiological parameters among groups were examinated using the MannWhitney and Wilcoxon sign tests. The predominant species in all 600 samples included Corynebacterium diphtheriae, Enterococcus faecalis, Staphylococcus aureus, Acinetobacter baumannii and Escherichia coli. In general, most of the species were detected in greater prevalence and levels in sites with and without disease from patients with periodontitis in comparison to the periodontally healthy group. In particular, C. diphtheriae, E. coli, E. faecalis, Pseudomonas aeruginosa and S. aureus were significantly more prevalent and detected in higher counts in diseased sites of patients with periodontal disease compared to healthy subjects (p < 0.05). Clinical signs of disease presented a positive correlation with the species A. baumannii, Streptococcus pyogenes, E. coli, S. aureus and P. aeruginosa. In conclusion, "non-oral" pathogenic bacteria are detected in high prevalence and levels in periodontal sites of chronic periodontitis patients.
Lectins of different activities were found in the crop, midgut, and hemolymph of the insect Rhodnius prolixus. These were not specific for N-acetyl-D-mannosamine, alpha-N-acetyl-D-galactosamine, and alpha- and beta-galactose, respectively. Lectin receptors were detectable in epimastigote but not in trypomastigote forms of Trypanosoma cruzi, a protozoan parasite of the insect and of humans.
Corynebacterium diphtheriae strains expressed variation in hydrophobic characteristics dependent on the method used. Results of single assays are not a reliable representation of C. diphtheriae hydrophobicity. All 12 strains adhered to polystyrene surfaces; three showed spontaneous aggregation (SA) in Trypticase Soy Broth (TSB) medium, and eight exhibited autoagglutination in phosphate-buffered saline (PBS; AA-positive). The salt aggregation test (SAT) values =0.002 or >/=1.6 represented breakpoints for groups of strains with differing hydrophobicity. C. diphtheriae strains showed affinity towards n-hexadecane. Percentages of adhesion varied from 31% to 63% and were not directly related to morphological n-hexadecane adhesion patterns. Diffuse and localized adhesion patterns were noted predominantly among sucrose-positive and sucrose-negative strains, respectively. Strains of the sucrose-negative biotype expressed a higher degree of hydrophobicity. The choice of the growth medium influenced the hydrophobicity, not the hemagglutinating activity (HA) of C. diphtheriae. Heating bacterial suspensions at 121 degrees C decreased both HA and hydrophobicity of three strains. However, hydrophobins and hemagglutinins were trypsin and detergent resistant. The treatment of microorganisms with Clostridium perfringens neuraminidase increased the hydrophobicity but not the HA titers of strains tested. Hemagglutinins were partially responsible for hydrophobicity. Hydrophilic AA-negative strains adhered strongly to glass but expressed weak HA. Sialylglycoconjugates functioned as hydrophilins on C. diphtheriae surfaces.
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