There are microbial communities in and on the bodies of all multicellular organisms, and this microbiota can have a significant impact on the biology of the host. Most studies have focused on the microbiome of the skin, mouth, and gut, whereas relatively little is known about the reproductive microbiome. From the perspective of the bovine reproductive tract, uterine diseases such as metritis and endometritis are traditionally viewed to result only from interactions occurring between the host animal and pathogens originating from either the environment or ascension from the vagina. This outdated opinion has been refuted by recent advanced studies that propose that, in addition to bacteria colonization through the extrinsic and ascending pathways to the vagina, bacteria can also move from the gut to the uterus, which is also associated with reproductive tract disorders. This has led to the concept of the “endogenous route hypothesis”, which has vital inferences for comprehending the etiology of metritis and endometritis. Furthermore, it has opened up the possibility of developing new prophylactic and therapeutic agents as alternatives to antimicrobial agents. In addition, the unveiling of next-generation sequencing technology makes it more convenient to perform detailed sequencing and analysis of data on the cervical, vaginal, and uterine flora and to further study uncultured bacteria in these niches—most importantly, the cervical niche, which previously was thought to have lower bacterial complexity. Research conducted to date has proven that the composition of microflora in a community varies widely between environmental sites, host niches, and health status. Furthermore, it has also been suggested that the occurrence of endometritis in the dairy and beef cattle reproductive tract is neither casual nor indirect but multifactorial. Whether disturbance in the variety of the microflora in the reproductive tract (dysbiosis) has a role in determining the sensitivity to metritis and endometritis is not yet known. This article outlines the current progress in understanding the microflora with regards to the bovine reproductive tract. The compositions of microflora in various niches of the reproductive tract are briefly elucidated. In addition, the functional role of these microflora communities in the reproductive tract is discussed, with particular emphasis on the association of bacterial flora with reproductive disorders and failures. Finally, prophylaxis and therapeutic approaches based on the new comprehension of the effects of antimicrobials, probiotics, and bacteriophages on the composition of the reproductive tract microflora are also considered.

The aim of this study was to investigate the effects of quercetin on inflammatory response and intestinal microflora in broiler chicken jejuna. A total of 120 broiler chickens were allocated into 3 groups: saline-challenged broilers fed a basal diet (CTR group), lipopolysaccharide (LPS)-challenged broilers fed a basal diet (L group) and LPS-challenged broilers fed a basal diet supplemented with 200 mg/kg quercetin (LQ group). Our results showed that LPS significantly increased expression of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-8, interferon (IFN)-γ, toll-like receptor (TLR)-4, Bax, Caspase-3 and diamine oxidase activity (DAO), and decreased expression of zona occludens-1 (ZO-1), Occludin and Bcl-2 in the jejunum, while dietary quercetin prevented the adverse effects of LPS injection. LPS injection significantly decreased the number of Actinobacteria, Armatimonadetes and Fibrobacteriae at the phylum level when compared to the CTR group. Additionally, at genus level, compared with the CTR group, the abundance of Halomonas, Micromonospora, Nitriliruptor, Peptococcus, Rubellimicrobium, Rubrobacter and Slaclda in L group was significantly decreased, while dietary quercetin restored the numbers of these bacteria. In conclusion, our results demonstrated that dietary quercetin could alleviate inflammatory responses of broiler chickens accompanied by modulating jejunum microflora.

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