Periodontal diseases originate from a dysbiosis within the oral microbiota, which is associated with a deregulation of the host immune response. Although little is known about the initiation of dysbiosis, it has been shown that HO production is one of the main mechanisms by which some commensal bacteria suppress the outgrowth of pathobionts. Current models emphasize the critical nature of complex microbial biofilms that form unique microbial ecologies and of their change during transition from health (homeostatic) to disease (dysbiotic). However, very little is known on how this alters their virulence and host responses. The objective of this study was to determine differences in virulence gene expression by pathobionts and the inflammatory host response in homeostatic and dysbiotic biofilms originating from the same ecology. Quantitative polymerase chain reaction was performed to quantify the pathobiont outgrowth. Expression analysis of bacterial virulence and cellular inflammatory genes together with cytokine enzyme-linked immunosorbent assays were used to detect differences in bacterial virulence and to analyze potential differences in inflammatory response. An increase in pathobionts in induced dysbiotic biofilms was observed compared to homeostatic biofilms. The main virulence genes of all pathobionts were upregulated in dysbiotic biofilms. Exposure of these dysbiotic biofilms to epithelial and fibroblast cultures increased the expression of interleukin (IL)-6, IL-1β, tumor necrosis factor-α, and matrix metalloprotease 8, but especially the chemokine CXCL8 (IL-8). Conversely, homeostatic and beneficial biofilms had a minor immune response at the messenger RNA and protein level. Overall, induced dysbiotic biofilms enriched in pathobionts and virulence factors significantly increased the inflammatory response compared to homeostatic and commensal biofilms.
Objective: The main purpose of this study was to investigate the role of bacterial vaginosis (BV) in prematurity, premature rupture of membranes (PROM) and other disorders of pregnancy. Methods: High vaginal and cervical swabs were taken from pregnant women in the second and third trimesters of pregnancy and from 30 non-pregnant women. Informed consent was obtained from all potential subjects. The specimens were smeared, gram-stained and cultured on a variety of selective and non-selective media which were then incubated at the appropriate atmospheres. Vaginal pH, character of the discharge, and outcome of the amine test were noted. Ultrasound was performed to confirm gestational age and all pregnant women followed up until postpartum. Results: A total of 123 pregnant women were evaluated at the end of the study. BV was diagnosed clinically and bacteriologically in 34 women, giving a prevalence rate of 28%. BV was diagnosed in none of the 30 non-pregnant control patients. Fifty-four percent and 46% of the study population were Kuwaitis and non-Kuwaitis, respectively. The mean parity recorded was 2.24 ± 2.06. There was a positive correlation between BV and preterm labour (9/34, 27%; CI, p < 0.05), PROM (7/34, 21%: CI; p < 0.05) and preterm delivery (7/34, 21%; CI, p < 0.05). Three (9%) of the women with BV had babies with intra-uterine growth retardation compared with 1 (1%) in the 89 non-BV group (p < 0.05). Conclusion: The prevalence rate of BV among pregnant women in Kuwait is high and is significantly associated with prematurity and other disorders of pregnancy.
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