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Simple Summary: Mannheimia haemolytica (M. haemolytica) is a significant bacterial pathogen that causes substantial economic losses to the livestock industry by infecting ruminants. In our previous study, we successfully isolated and identified a strain of M. haemolytica from Hainan Black goats. However, the pathogenicity of this strain and the molecular mechanism underlying the interaction between M. haemolytica and animals have not been investigated. In this study, we constructed a M. haemolytica infection model in mice to analyze the histopathology of the bacterial infection and explore the immune mechanisms employed by the murine spleen to resist M. haemolytica infection. (1) Background: Mannheimia haemolytica (M. haemolytica) is an opportunistic pathogen and is mainly associated with respiratory diseases in cattle, sheep, and goats. (2) Methods: In this study, a mouse infection model was established using a M. haemolytica strain isolated from goats. Histopathological observations were conducted on various organs of the mice, and bacterial load determination and RNA-seq analysis were specifically performed on the spleens of the mice. (3) Results: The findings of this study suggest that chemokines, potentially present in the spleen of mice following a M. haemolytica challenge, may induce the migration of leukocytes to the spleen and suppress the release of pro-inflammatory factors through a negative feedback regulation mechanism. Additionally, an interesting observation was made regarding the potential of hematopoietic stem/progenitor cells congregating in the spleen to differentiate into immune cells, which could potentially collaborate with leukocytes in their efforts to counteract M. haemolytica invasion. (4) Conclusions: This study revealed the immune regulation mechanism induced by M. haemolytica in the mouse spleen, providing valuable insights into host–pathogen interactions and offering a theoretical basis for the prevention, control, and treatment of mannheimiosis. [ABSTRACT FROM AUTHOR]

• Investigate genetic diversity and unravel genomic regions potentially under selection for climatic conditions and geographic isolation in Hainan cattle. • The population structure revealed that Hainan cattle were originally from bos indicus and carried other ancestry. • The positive selection genes in Hainan cattle were mainly associated with immune pathways including bacterial invasion of epithelial cells, chemokine signaling pathway, and T cell receptor signaling pathway. The equatorial climate of Hainan Island has led to the evolution of Hainan cattle that are well adapted to the local conditions. This study aims to estimate the genetic diversity and selection signatures of Hainan cattle. After analyzing the whole-genome sequencing (WGS) data of 76 cattle from four representative populations of East Asian taurine cattle, India-Pakistan indicine cattle, Chinese indicine cattle, and Hainan locally adapted cattle, a total of 20,075,403 autosomal single nucleotide polymorphisms (SNPs) were detected. The Hainan cattle exhibited the highest level of genetic diversity (Ho=0.31, He=0.3). The increased genetic diversity observed in Hainan cattle population may be attributed to the admixture with Chinese indicine cattle population. The analysis of selective sweep, which was achieved through the utilization of Z F ST and log 2 π, indicated the detection of 92 potential loci in Hainan cattle, which encompassed 141 genes that underwent positive selection and were associated with immune pathways, including bacterial invasion of epithelial cells, the chemokine signaling pathway, and the T cell receptor signaling pathway. Mutations analysis revealed that two missense mutations in SKINT1 (c.458C>T, p.P153L and c.580G> A , p.D194N) and two missense mutations in BCAR1 (c.1765C>G, p.A589P and c.1150C>T, p.G384S) were the homozygous genotypes in Hainan cattle. This finding enhances our understanding of the polygenic basis underlying climatic adaptation in Hainan cattle and holds significant value for the preservation and utilization of these genetic resources. [ABSTRACT FROM AUTHOR]