Yersinia pestis is a Gram-negative bacterium that causes plague. After Y. pestis overcomes the skin barrier, it encounters antigen-presenting cells, such as Langerhans and dendritic cells. They transport the bacteria from the skin to the lymph nodes. However, the molecular mechanisms involved in bacterial transmission are unclear. Langerhans cells express Langerin (CD207), a calcium-dependent (C-type) lectin. Furthermore, Y. pestis possesses exposed core oligosaccharides. In this study, we show that Y. pestis invades Langerhans cells and Langerin-expressing transfectants. However, when the bacterial core oligosaccharides are shielded or truncated, Y. pestis propensity to invade Langerhans- and Langerin-expressing cells decreases. Moreover, the interaction of Y. pestis with Langerin-expressing transfectants is inhibited by purified Langerin, a DC-SIGN-like molecule, an anti-CD207 antibody, purified core oligosaccharides and several oligosaccharides. Furthermore, covering core oligosaccharides reduces the mortality associated with murine infection by adversely affecting the transmission of Y. pestis to lymph nodes. These results demonstrate that direct interaction of core oligosaccharides with Langerin facilitates the invasion of Langerhans cells by Y. pestis. Therefore, Langerin-mediated binding of Y. pestis to antigen-presenting cells may promote its dissemination and infection.

Purpose: The first case of coronavirus disease 2019 (COVID-19) was identified and confirmed in December 2019 in Wuhan, China. COVID-19 is gradually posing a serious threat to global public health. In this review the characteristics and mechanism of kidney injury caused by SARS-CoV, MERS-CoV and SARS-CoV-2 infection are summarized and contrasted. In particular, urine-oral transmission, prevention and management of the kidney injury caused by SARS-CoV-2 are emphasized. Materials and Methods: We searched PubMedÒ for English language articles published since 2003 with the keywords "SARS," "MERS," "COVID-19" or "kidney injury." ClinicalTrials.gov was queried for ongoing studies. We also used relevant data from websites, including the Centers for Disease Control and Prevention and European Centre for Disease Prevention and Control. Results: Similar to 2 other coronaviruses including SARS-CoV and MERS-CoV, SARS-CoV-2 caused severe respiratory syndrome with rapid progression and kidney injury. The infection process of SARS-CoV-2 is mediated by specifically binding to angiotensin-converting enzyme 2. Cases of COVID-19 combined with kidney impairment are associated with a higher risk of mortality than those without comorbidities. The pathological changes of the kidney are mainly due to local SARS-CoV-2 replication or indirectly by pro-inflammatory cytokine response. In addition, studies have confirmed the isolation of infectious SARS-CoV-2 in urine, raising the possibility of urine-oral transmission. Ultimately this is significant for preventing potential urine-oral transmission and improving the cure rate of acute kidney injury with COVID-19. Conclusions: Emerging evidence supports that in patients with SARS-CoV-2 infections the prevalence of kidney injury is high and usually leads to a poor prognosis. Optimal prevention and management of kidney injury will benefit patients with COVID-19.

Background Nowadays, wound is associated with a complicated repairing process and still represents a significant biomedical burden worldwide. Bone marrow mesenchymal stem cells (BMSCs) possess multidirectional differentiation potential and secretory function, emerging as potential cellular candidates in treating wounds. Ascorbic acid 2-glucoside (AA2G) is a well-known antioxidant and its function in BMSC-promoting wound healing is worth exploring. Methods The in vitro cell proliferation, migration, and angiogenesis of BMSCs and AA2G-treated BMSCs were detected by flow cytometry, EDU staining, scratch assay, transwell assay, and immunofluorescence (IF). Besides, the collagen formation effect of AA2G-treated BMSCs conditioned medium (CM) on NIH-3T3 cells was evaluated by hydroxyproline, qRT-PCR and IF staining detection. Next, in the wound healing mouse model, the histological evaluation of wound tissue in PBS, BMSCs, and AA2G-treated BMSCs group were further investigated. Lastly, western blot and ELISA were used to detect the expression levels of 5-hmc, TET2 and VEGF protein, and PI3K/AKT pathway activation in BMSCs treated with or without AA2G. Results The in vitro results indicated that AA2G-treated BMSCs exhibited stronger proliferation and improved the angiogenesis ability of vascular endothelial cells. In addition, the AA2G-treated BMSCs CM enhanced migration and collagen formation of NIH-3T3 cells. In vivo, the AA2G-treated BMSCs group had a faster wound healing rate and a higher degree of vascularization in the new wound, compared with the PBS and BMSCs group. Moreover, AA2G preconditioning might enhance the demethylation process of BMSCs by regulating TET2 and up-regulating VEGF expression by activating the PI3K/AKT pathway. Conclusions AA2G-treated BMSCs promoted wound healing by promoting angiogenesis and collagen deposition, thereby providing a feasible strategy to reinforce the biofunctionability of BMSCs in treating wounds.