chondroitin-sulfates and Escherichia-coli-Infections

To determine the protective effects of hyaluronic acid and chondroitin sulfate in treating urinary tract infections in a rat model.. A total of 28 rats, which were induced with urinary tract infections through intravesical administration of Escherichia coli, were included in the study. By random selection, they were equally divided into four groups as control (no treatment), hyaluronic acid, chondroitin sulfate and hyaluronic acid + chondroitin sulfate. Bacteriological cultures of the urine and bladder tissue samples were carried out, and the data for each group were statistically compared.. In the urine cultures, there were significant differences in median bacterial growth rates in hyaluronic acid (5 × 10(3) cfu/mL) and chondroitin sulfate (1 × 10(4) cfu/mL) groups relative to the control group (5 × 10(4) cfu/mL). However, a significantly lower rate of bacterial colony growth was observed in the hyaluronic acid + chondroitin sulfate group (8 × 10(2) cfu/mL; P < 0.05). In the bladder tissues, statistically significant decreases in median bacterial growth rates were detected in the hyaluronic acid and hyaluronic acid + chondroitin sulfate groups (both 0 cfu/mg tissue; P < 0.05). Also, transitional epithelium damage decreased in the treatment groups. However, this effect was prominent in hyaluronic acid + chondroitin sulfate group.. Our experimental findings show that the hyaluronic acid + chondroitin sulfate combination has a potential benefit in reducing the bacterial load in urine and the thickness of the transitional epithelium.

Topics: Adjuvants, Immunologic; Administration, Intravesical; Analysis of Variance; Animals; Chondroitin Sulfates; Colony Count, Microbial; Drug Therapy, Combination; Escherichia coli; Escherichia coli Infections; Female; Hyaluronic Acid; Rats; Rats, Sprague-Dawley; Statistics, Nonparametric; Urinary Bladder; Urinary Tract Infections; Urine; Urothelium

Topics: Adjuvants, Immunologic; Animals; Chondroitin Sulfates; Escherichia coli; Escherichia coli Infections; Female; Hyaluronic Acid; Urinary Tract Infections

In rheumatoid arthritis, pannus formation resulting from synovial inflammation is a major factor in cartilage destruction. The ability of arthritic synovial cells to undergo pannus formation depends upon their initial adhesion to the partially deformed cartilage surfaces. Our recent studies using various lipid-derivatized glycosaminoglycans have revealed a preeminent inhibitory activity of phosphatidyl ethanol amine-derivatized chondroitin sulphate (CS-PE) toward cell-matrix adhesion. Here we evaluate whether CS-PE may protect articular cartilage from pannus extension in different in vitro and in vivo model systems using Escherichia coli 0:14-induced arthritis in rabbits and the articular cartilage explants, synovial tissues, and synovial cells obtained from them. These studies showed that CS-PE suppressed the in vivo pannus-like extension on cartilage surfaces, as well as the in vitro extension of the synovial cell layer on both CS-PE treated culture plates and cartilage explants. The results suggest that native chondroitin sulphate proteoglycans in the surface of normal articular cartilage play an important role in protecting the tissues from pannus extension and that the CS-PE immobilized onto partially eroded cartilage can mimic the inhibitory action of native chondroitin sulphate proteoglycans.

Topics: Animals; Arthritis, Infectious; Cartilage, Articular; Cell Movement; Cells, Cultured; Chondroitin Sulfates; Escherichia coli Infections; Exudates and Transudates; In Vitro Techniques; Microscopy, Fluorescence; Microscopy, Phase-Contrast; Phosphatidylethanolamines; Rabbits; Synovial Membrane

The timing and molecular profile of cartilage destruction in Escherichia coli and Staphylococcus aureus infectious arthritis and killed Mycobacterium butyricum adjuvant arthritis are presented. Infectious arthritis was studied for 3 weeks; cartilage samples were analyzed at 2, 10, and 21 days. At 48 h postinfection, glycosaminoglycan content was reduced by 20% (p less than 0.05) in E. coli infected knees and by 42% (p less than 0.05) in tibial plateau cartilage of S. aureus infected knees. By the 3rd week of infection, glycosaminoglycan losses amounted to as much as 73% (p less than 0.005). In comparison, collagen losses were not significant prior to the 3rd week of infection, at which time 42% (p less than 0.05) was lost. Adjuvant arthritic tibial plateau cartilage was examined at 1, 3 and 12 weeks. Glycosaminoglycans decreased by 42% the 1st week, plateauing at 62% by the 3rd and 12th weeks. Collagen degradation began at 3 weeks (28% loss, p less than 0.10) and by the 12th week was reduced by 49% (p less than 0.005). Analysis of the individual species of glycosaminoglycan showed a parallel loss of chondroitin sulfate and keratan sulfate. Fractionation of glycosaminoglycans with respect to size produced no evidence of shortened chains in cartilage from infected joints. Hyaluronic acid losses were greatest when collagen was significantly decreased. The pattern by which chondroitin and keratan sulfates are lost demonstrates that a prominent feature of infectious and noninfectious inflammatory arthritis is a rapid loss of proteoglycan subunits that precedes collagen loss.

Topics: Animals; Arthritis; Arthritis, Experimental; Arthritis, Infectious; Cartilage, Articular; Chondroitin Sulfates; Chromatography, Gel; Collagen; Escherichia coli Infections; Hyaluronic Acid; Keratan Sulfate; Mycobacterium; Rabbits; Staphylococcal Infections; Time Factors