Search

Pseudomonas aeruginosa (P. aeruginosa) is an opportunistic bacterium, which could aggressively infect immunocompromised patients and thus, cause high mortality rate. In addition, P. aeruginosa in oropharynx could be aspirated and cause ventilator associated pneumonia. Royal jelly is one of bee’s products that has been used for therapeutic needs including antibacteria. Adherence factor of P. aeruginosa were flagelum, pili and lectin. The aim of the study was to determine the effect of royal jelly to P. aeruginosa adhesion. Suspension of P. aeruginosa (ATCC® 27853) was incubated at 37 °C for 18 h. Treatment groups were exposed to royal jelly with several concentrations, 2%, 4%, 6%; while distilled water was being used as negative control. Bacterial adhesion test was determined using spectrophotometer λ = 600 nm to measure optical density values of adhered bacterial suspension in tubes. The result of one-way ANOVA showed significant differences (p

Background: Pseudomonas aeruginosa, a multidrug-resistant Gram-negative bacterium, produces pyocyanin, a virulence factor associated with antibiotic tolerance. High concentrations of royal jelly have an antibacterial effect, which may potentially overcome antibacterial resistance. However, in some cases, antibiotic tolerance can occur due to prolonged stress of low-dose antibacterial agents. This study aimed to investigate the effect of subinhibitory concentrations of royal jelly on bacterial growth, pyocyanin production, and biofilm formation of P. aeruginosa. Methods: Pseudomonas aeruginosa ATCC 10145 and clinical isolates were cultured in a royal jelly-containing medium to test the antibacterial activity. Pyocyanin production was observed by measuring the absorbance at 690 nm after 36 h culture and determined using extinction coefficient 4310 M-1 cm-1. Static microtiter plate biofilm assay performed to detect the biofilm formation, followed by scanning electron microscopy. Results: Royal jelly effectively inhibited the viability of both strains from a concentration of 25%. The highest production of pyocyanin was observed in the subinhibitory concentration group 6.25%, which gradually decreased along with the decrease of royal jelly concentration. Results of one-way ANOVA tests differed significantly in pyocyanin production of the two strains between the royal jelly groups. Tukey HSD test showed concentrations of 12.5%, 6.25%, and 3.125% significantly increased pyocyanin production of ATCC 10145, and the concentrations of 12.5% and 6.25% significantly increased production of the clinical isolates. Concentrations of 12.5% and 6.125% significantly induced biofilm formation of P. aeruginosa ATCC 10145, in line with the results of the SEM analysis. Conclusions: The royal jelly concentration of 25% or higher inhibits bacterial growth; however, the subinhibitory concentration increases pyocyanin production and biofilm formation in P. aeruginosa. It is advisable to determine the appropriate concentration of royal jelly to obtain beneficial virulence inhibiting activity.

Red onion skin (Allium cepa var ascalonicum) contains various ingredients that may function as antibacterial agents against microorganisms, as well as anti-inflammatory and immunomodulator agents for host cells, such as macrophages. Pseudomonas aeruginosa found in the oral cavity is commensal bacteria that may turn into opportunistic pathogen by utilizing its virulence factors such as motility and adhesion to the host cell. The purpose of this study was to investigate the effect of red-onion-skin ethanolic extract towards P. aeruginosa ATCC 9027 on the motility and adhesion ability, furthermore, to know its effect on the macrophage phagocytosis. The research was conducted into three parts of experiment using red-onion-skin ethanolic extract. Extract-induced bacterial motility test was carried out on semi-solid media, stained using 0.1% crystal violet, then the radial length of the bacterial movement was measured. The bacterial adhesion index to buccal cells was calculated after incubated for two hours and stained with Gram stain. Phagocytic activity of the host cells on P. aeruginosa was done by exposing the extract to the mouse peritoneal macrophages, then the phagocytosed bacteria were counted after Giemsa staining. Statistical test results from the three experiments showed significant differences between the test groups compared to the control groups (p

Background: Hairdresser is one of the fastest growing occupations in today’s society. Hairdresser help styling, cutting, colouring, perming, curling, straightening hair and various treatment to customer. Somehow, hairdresser are constantly exposed to chemical substances such as aromatic amines, hydrogen peroxide, thioglycolic acid, formaldehyde in hair products which can cause damage to human’s genome. Micronucleus is one of the effective biomarker for processes associated with the induction of DNA damage. Purpose: The aim of this study was to determine the micronucleus frequencies in buccal mucosa epithelial cells of hairdresser who were exposed to chemical of hair products. Method: This study was conducted on twenty female subjects, who were divided into 2 groups: exposed and non-exposed (control) group. All subjects recruited were working in the same beauty salon. Buccal cells were obtained from each individual by using cytobrush. The cells were stained with modified Feulgen-Ronssenback method and counting of micronucleus per 1000 cell was done under light microscope. The data were analyzed using independent t-test and one-way Anova (pResult: The result showed a significant difference in micronucleus frequency between 2 groups. There were a significantly increase of micronucleus frequency in hairdressers and increase of micronucleus frequency with the longer duration of exposure. Conclusion: It concluded that the chemical substances of hair products had affected the micronucleus frequency ofthe epithelial cells in buccal mucosa of hairdressers.

Porphyromonas gingivalis and Escherichia coli lipopolysaccharide (LPS) have been shown to induce alveolar bone resorption in the rat. The progress and distribution of bone resorption associated with periodontal disease is modified by local and systemic factors. The aim of this study was to determine the effect of a site specific, local application of P. gingivalis and E. coli LPS on alveolar bone in the rat. It appears that the injection of P. gingivalis and E. coli LPS has both a local and systemic effect on alveolar bone activity in the rat. Loss of alveolar bone height and an increase in osteoclast cell numbers were observed on both the injected and non-injected sides of the maxilla in animals injected with P. gingivalis and E. coli LPS at the dosages and time intervals examined.

OBJECTIVE: To determine whether treatments with high-density lipoprotein (HDL) may alter the lipopolysaccharide (LPS)-induced alveolar bone resorption in rats. MATERIALS AND METHODS: Rats were injected with 500 μg of LPS from Escherichia coli at the alveolar mucosa of lower right first molar once every 2 days for 8 days. The negative and positive control were injected with phosphate buffered saline (PBS) and LPS alone, respectively. In HDL-treated animals various concentration of HDL were injected immediately before, after the third or the final LPS injection. The bone sections were stained with tartrate-resistant acid phosphatase (TRAP) and the numbers of both osteoclasts and preosteoclasts and the levels of alveolar bone resorption were assessed. RESULTS: The numbers of both osteoclasts and preosteoclasts and the levels of alveolar bone resorption in animals treated with HDL before or during LPS injections were lower than those in the positive control, but higher than those in the negative control, regardless of HDL doses. Similar results were also observed in animals treated with 250 and 500 μg of HDL after the final LPS injection. Only treatments with 1000 μg of HDL after LPS injections completely reduced the number of both osteoclasts and preosteoclasts, but only partially decreased the alveolar bone resorption. CONCLUSION: HDL treatments partially reduced the LPS-induced alveolar bone resorption in vivo in rats, suggesting that HDL may neutralize the ability of LPS to induce alveolar bone resorption.

– The aim of this study was to determine whether treatment with fish oil may alter the periapical bone resorption following pulp exposure in rats. Untreated and pulp-exposed animals served as the negative and positive control, respectively. Other pulp-exposed animals were orally treated with fish oil at different concentrations and frequencies. Periapical tissue sections were stained with tartrate-resistant acid phosphatase (TRAP), and then the numbers of both periapical osteoclasts and preosteoclasts were determined. The levels of bone resorption were assessed using the osteoclast–bone interface (OBI) index. The results showed that no differences between the numbers of both osteoclasts and preosteoclasts in the fish oil-treated animals and the negative control at day 14 could be found. Similarly, the periapical bone resorption in the animals treated with fish oil for 14 days significantly reduced to the levels of that in the negative control. The results of the present study, therefore, suggest that oral treatment with fish oil may inhibit bone resorption following pulp exposure in rats and hence, may have a therapeutic modality for inflamed periradicular tissue.

The aims of this study were to determine how Prostaglandin E-2 (PGE(2)) locally applied affected the immunodistribution of latent transforming growth factor-beta 1 (TGF-beta 1), and how the eicosanoid modified TGF-beta 1 release and TGF-beta receptors gene expression in Cultured osteoblasts. PGE(2) locally delivered on the rat mandible at doses of 0.1 and 0.05 mg/day, but not 0.025 mg/ day, over 20 days significantly increased latent TGF-beta 1 immunodistribution (P < 0.001), comparing with a placebo-treated group. Cultured osteoblasts stimulated with 10(-5) or 10(-7) M PGE(2) significantly varied the level of activated TGF-beta 1 released into supernatants at different experimental periods compared with negative and positive controls. TGF-beta receptor type I gene expression was significantly increased in osteoblasts (P < 0.01) after 10 days of treatment with 10(-5) and 10(-7) M PGE(2), whereas 10(-3) M PGE(2) produced the opposite effect. It is Concluded that PGE(2) may stimulate bone deposition by affecting TGF-beta pathway. This effect on the pathway appears to be dose-dependent. (c) 2006 Elsevier Ltd. All rights reserved.