牙周炎相关的口腔微生物菌群失调被认为是导致不良妊娠结局(APO)的原因。不孕症,女性生殖炎症。由于益生菌可以调节牙周炎和口腔微生物菌群失调,这项研究检查了益生菌细菌素的作用,Nisin,调节牙周炎引发的生殖微生物组和炎症。将24只8周龄BALB/cByJ雌性小鼠随机分为4个治疗组(对照组,感染,Nisin,和感染+乳酸链球菌素组),每组6只小鼠。一种多微生物(牙龈卟啉单胞菌,Denticola密螺旋体,连翘坦菌,核梭杆菌)牙周病小鼠模型用于评估该病对女性生殖系统的影响,专注于微生物组,局部炎症,和乳酸链球菌素在这种情况下的治疗潜力。此外,16sRNA测序用于评估微生物组的变化,RT-PCR用于评估炎性细胞因子的变化。在生殖器官中检测到牙周病原体DNA,在实验期结束时的心脏和主动脉中,感染组的口腔DNA尤其升高。与对照组相比,只有牙龈卟啉单胞菌在感染组的口腔和子宫中显著增高,在感染组的口腔中,连翘和带核F.感染和乳酸链球菌素治疗组牙龈卟啉单胞菌水平明显降低,T.连翘,与感染组相比,口腔中的F.由于在心脏和主动脉中也检测到牙周病原体DNA,这表明潜在的循环系统传播。多微生物感染通常会降低子宫中的微生物组多样性,已被Nisin治疗废除。多微生物感染组,与对照组相比,通常在所有生殖器官中都有较低的Firmicutes和较高的拟杆菌,类似的趋势在心脏中显现出来。然而,乳酸链球菌素治疗组和感染和乳酸链球菌素治疗组,与对照组或感染组相比,通常在生殖器官和心脏中具有较高的变形杆菌和较低的Firmicutes和拟杆菌。Nisin治疗还改变了生殖道中的微生物群落结构,使其处于不反映对照的新状态。牙周病,与对照组相比,引发了子宫和口腔中炎性细胞因子(IL-6,TNF-α)的增加,已被Nisin治疗废除。多微生物牙周病改变了生殖道的微生物分布,微生物组,和炎症状态。Nisin调节生殖道的微生物谱和微生物组,并减轻由牙周病引发的子宫炎症细胞因子升高。
Periodontitis-related oral microbial dysbiosis is thought to contribute to adverse pregnancy outcomes (APOs), infertility, and female reproductive inflammation. Since probiotics can modulate periodontitis and oral microbiome dysbiosis, this study examined the effects of a probiotic bacteriocin, nisin, in modulating the reproductive microbiome and inflammation triggered by periodontitis. A total of 24 eight-week-old BALB/cByJ female mice were randomly divided into four treatment groups (control, infection, nisin, and infection+nisin group), with 6 mice per group. A polymicrobial (Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, Fusobacterium nucleatum) mouse model of periodontal disease was used to evaluate the effects of this disease on the female reproductive system, with a focus on the microbiome, local inflammation, and nisin\'s therapeutic potential in this context. Moreover, 16s RNA sequencing was used to evaluate the changes in the microbiome and RT-PCR was used to evaluate the changes in inflammatory cytokines. Periodontal pathogen DNA was detected in the reproductive organs, and in the heart and aorta at the end of the experimental period, and the DNA was especially elevated in the oral cavity in the infection group. Compared to the control groups, only P. gingivalis was significantly higher in the oral cavity and uterus of the infection groups, and T. forsythia and F. nucleatum were significantly higher in the oral cavity of the infection groups. The infection and nisin treatment group had significantly lower levels of P. gingivalis, T. forsythia, and F. nucleatum in the oral cavity compared with the infection group. Since periodontal pathogen DNA was also detected in the heart and aorta, this suggests potential circulatory system transmission. The polymicrobial infection generally decreased the microbiome diversity in the uterus, which was abrogated by nisin treatment. The polymicrobial infection groups, compared to the control groups, generally had lower Firmicutes and higher Bacteroidota in all the reproductive organs, with similar trends revealed in the heart. However, the nisin treatment group and the infection and nisin group, compared to the control or infection groups, generally had higher Proteobacteria and lower Firmicutes and Bacteroidota in the reproductive organs and the heart. Nisin treatment also altered the microbiome community structure in the reproductive tract to a new state that did not mirror the controls. Periodontal disease, compared to the controls, triggered an increase in inflammatory cytokines (IL-6, TNF-α) in the uterus and oral cavity, which was abrogated by nisin treatment. Polymicrobial periodontal disease alters the reproductive tract\'s microbial profile, microbiome, and inflammatory status. Nisin modulates the microbial profile and microbiome of the reproductive tract and mitigates the elevated uterine inflammatory cytokines triggered by periodontal disease.