Genomic selection (GS) approaches, in combination with reproductive technologies, are revolutionizing the design and implementation of breeding programs in livestock species, particularly in cattle. GS leverages genomic readouts to provide estimates of breeding value early in the life of animals. However, the capacity of these approaches for improving genetic gain in breeding programs is limited by generation interval, the average age of an animal when replacement progeny are born. Here, we present a cost-effective approach that combines GS with reproductive technologies to reduce generation interval by rapidly producing high genetic merit calves.

The immune dysregulation induced by periodontal bacteria has important roles in the development of periodontitis. However, the role of key periodontal bacteria in local and systemic immunity has not been comprehensively studied. Herein, to explore immunoregulation maps of key periodontal bacteria, a mono-colonized germ-free mice model with P. gingivalis, F. nucleatum, and T. denticola for two weeks was designed in this study. The alveolar bone loss was determined by micro-CT. A total of 14 types of innate and adaptive immune cells of the gingiva, spleen, and colon were detected by multi-color flow cytometry. P. gingivalis induced the strongest innate immune response in gingiva and mononuclear phagocytes (MNPs) changed most significantly, compared to F. nucleatum and T. denticola. Immune dysregulation of the colon was widely induced by F. nucleatum. T. denticola mainly induced immune disorder in spleen. ILC3s, Tregs, CD11B+ dendritic cells s, MNPs, macrophages, and plasmacytoid dendritic cells were the main types in response to key periodontal bacteria. However, the alveolar bone loss was not induced by key periodontal bacteria. In conclusion, the overall immunoregulation of monomicrobial stimuli to decipher the complexities of periodontitis was provided in this study. P. gingivalis, F. nucleatum, and T. denticola have different effects on local and systemic immunity in gingiva, colon, and spleen of germ-free mice.

A two-way relationship between diabetes and periodontitis has been discussed recently. Periodontitis microbiota might affect the immune homeostasis of diabetes, but the molecular mechanism of their interactions is still not clear. The aims of this study were to clarify the possible immune regulatory effects of periodontitis microbiota on diabetes and the correlation between immunomodulation and ectopic colonization. A model of germ-free mice with streptozotocin-induced type 1 diabetes mellitus (T1D), which was orally inoculated with mixed saliva samples for 2 weeks, was used in this study. Those mice were randomly divided into two groups, namely, SP (where the T1D mice were orally inoculated with mixed saliva samples from periodontitis patients) and SH (where the T1D mice were orally inoculated with mixed saliva samples from healthy subjects). Ectopic colonization of saliva microbiota was assessed using culture-dependent method and Sanger sequencing, and the composition of gut microbiota was analyzed using 16S rRNA gene sequencing. Changes in 15 types of immune cells and six cytokines either from the small intestine or spleen were detected by multicolor flow cytometry. The correlation between gut microbiota and immune cells was evaluated by redundancy analysis. Although periodontitis microbiota minorly colonized the lungs, spleens, and blood system, they predominantly colonized the gut, which was mainly invaded by Klebsiella. SH and SP differed in beta diversity of the gut bacterial community. Compared to SH, microbial alteration in small intestine occurred with an increase of Lacticaseibacillus, Bacillus, Agathobacter, Bacteroides, and a decrease of Raoultella in SP. More types of immune cells were disordered in the spleen than in the small intestine by periodontitis microbiota, mainly with a dramatical increase in the proportion of macrophages, plasmacytoid dendritic cells (pDCs), monocytes, group 3 innate lymphoid cells, CD4-CD8- T cells and Th17 cells, as well as a decline of αβT cells in SP. Cytokines of IFNγ, IL17, and IL22 produced by CD4 + T cells as well as IL22 produced by ILCs of small intestine rose in numbers, and the intestinal and splenic pDCs were positively regulated by gut bacterial community in SP. In conclusion, periodontitis microbiota invasion leads to ectopic colonization of the extra-oral sites and immune cells infiltration, which might cause local or systemic inflammation. Those cells are considered to act as a “bridge” between T1D and periodontitis.