Objective To understand the correlation of enterovirus 71 (EV71), P-selectin glycoprotein ligand-1 (PSG L-1), and scavenger receptor B2 (SCARB2) and to explore the possible pathway and mechanismof EV71 infection by observing the expression of EV71, PSG L-1 and SCARB2 in tissues of infants with brain stemencephalitis. Methods T he organs and tissues of infants with EV71-VP1 positivi-ty in their brain stems were chosen. Expression and distribution of EV71-VP1, PSG L-1, and SCARB2 were detected and compared by immunohistochemistry. Results Strong staining of EV71-VP1 was ob-served in the neuron, glial cells, the inflammatory cells of perivascular cuffing, parietal cells of the gas-tric fundus gland while alveolar macrophages, intestinal gland epitheliumcells, mucosa lymphoid nodule and lymphocyte of palatine tonsil showed moderate staining and weak staining were displayed in mesen-teric lymph nodes and lymphocyte of spleen. PSG L-1 expression was detected in parietal cells of the gastric fundus gland, tonsillar crypt squamous epithelium, alveolar macrophages and leukocytes in each tissue. SCARB2 expression was observed in all the above tissues except the intestines and spleen. Con-clusion T he distribution of EV71 correlates with SCARB2 expression. SCARB2 plays an important role in virus infection and replication. Stomach may be an important site for EV71 replication.

The oral cavity harbors a diverse population of microorganisms, making it one of the most heavily colonized sites in the human body. Maintaining a balanced microecology is crucial for oral health. Ligilactobacillus salivarius as a species of Ligilactobacillus, has good oral colonization ability and potential to improve oral microecology for disease prevention and control. Currently, the application and mechanism of Ligilactobacillus salivarius in oral diseases include several aspects. First, by directly inhibiting the growth of Streptococcus mutans and downregulating the expression of its cariogenic virulence factor, gtfs, the aim is to reduce the number of adherent Streptococcus mutans on the tooth surface, thereby preventing dental caries. Second, reducing the number of keystone taxa in periodontitis, and the virulence factors of Aggregatibacter actinomycetemcomitans, including CdtB and LtxA, can alleviate local stimulation in patients with periodontitis. Additionally, directly inhibiting macrophage MAPK and NF-κB pathway activation suppresses osteoclastogenesis and reduces periodontal bone absorption. In mucosal inflammation, Ligilactobacillus salivarius competes with Candida albicans, inhibits the formation of pathogenic hyphae or germ tubes, and prevents monilial stomatitis. Ligilactobacillus salivarius can also reduce the amount of Staphylococcus aureus and mitigate the activation of the macrophage TLR/PI3K/Akt/mTOR and TLR/PI3K/Akt/IκB/NF-κB pathways induced by S. aureus infections, thus alleviating inflammation in the oral and pharyngeal regions. In vitro studies on oral tumors have revealed that Ligilactobacillus salivarius can downregulate the expression of cancer cell Akt/Cyclin D1, induce direct apoptosis of tumor cells, reduce COX-2 expression, and improve the tumor immune-suppressive microenvironment. Previous studies have revealed considerable variability in Ligilactobacillus salivarius, necessitating more detailed research to clarify its clinical effects, safety, and mechanisms. Despite the emergence of novel microbiological research techniques, their application to Ligilactobacillus salivarius remains relatively limited. One crucial direction for future research is to better utilize these methods to investigate the effects of Ligilactobacillus salivarius on oral diseases. Considering these factors, this study provides a comprehensive review of existing research studies on Ligilactobacillus salivarius in the fields of oral medicine and dentistry, with the aim to serve as a reference and guide for future studies.