Isolation, identification, molecular and pathogenicity characteristics of an infectious laryngotracheitis virus from Hubei province, China.

Multiple outbreaks of avian infectious laryngotracheitis (ILT) in chickens, both domestically and internationally, have been directly correlate to widespread vaccine use in affected countries and regions. Phylogenetic and recombination event analyses have demonstrated that avian infectious laryngotracheitis virus (ILTV) field strains are progressively evolving toward the chicken embryo-origin (CEO) vaccine strain. Even with standardized biosecurity measures and effective prevention and control strategies implemented on large-scale farms, continuous ILT outbreaks result in significant economic losses to the poultry industry worldwide. These outbreaks undoubtedly hinder efforts to control and eradicate ILTV in the future. In this study, an ILTV isolate was successfully obtained by laboratory PCR detection and virus isolation from chickens that exhibited dyspnea and depression on a broiler farm in Hubei Province, China. The isolated strain exhibited robust propagation on chorioallantoic membranes of embryonated eggs, but failed to establish effective infection in chicken hepatocellular carcinoma (LMH) cells. Phylogenetic analysis revealed a unique T441P point mutation in the gJ protein of the isolate. Animal experiments confirmed the virulence of this strain, as it induced mortality in 6-wk-old chickens. This study expands current understanding of the epidemiology, genetic variations, and pathogenicity of ILTV isolates circulating domestically, contributing to the elucidate of ILTV molecular basis of pathogenicity and development of vaccine.

Small Extracellular Vesicles from Periodontal Ligament Stem Cells Primed by Lipopolysaccharide Regulate Macrophage M1 Polarization via miR-433-3p Targeting TLR2/TLR4/NF-κB.

Lipopolysaccharide (LPS) is regarded as the main pathogenic factor of periodontitis. Mesenchymal stem cell-derived small extracellular vesicles (sEVs) play a key role in a variety of physiological and pathological processes. This study investigated the effects of sEVs derived from periodontal ligament stem cells (PDLSCs) pretreated with LPS on macrophage polarization and the underlying mechanisms. PDLSCs were treated with LPS (1 µg/mL) for 24 h, and sEVs were harvested by gradient centrifugation method. Macrophages were incubated with sEVs for 24 h, followed by examination of the expression profiles of inflammatory and anti-inflammatory cytokines, and polarization markers. Furthermore, microarray analysis, western blot test, and microRNA inhibitor transfection experiments were used to elucidate the molecular signaling pathway responsible for the process. The results showed that sEVs derived from LPS-preconditioning PDLSCs could significantly increase the expression of M1 markers and inflammatory cytokines, whereas decreased the expression of M2 markers and anti-inflammatory cytokines. Mechanistic analysis showed that TLR2/TLR4/NF-κB p65 pathway was involved in M1 polarization of macrophages, and microRNA-433-3p played a role, at least in part, in the course. Collectively, LPS could promote the macrophages into M1 status via TLR2/TLR4/NF-κB p65 signaling pathway partly by sEV-mediated microRNA-433-3p, which could be a potential therapeutic target for periodontitis.

Mechanical Force Modulates Alveolar Bone Marrow Mesenchymal Cells Characteristics for Bone Remodeling during Orthodontic Tooth Movement through Lactate Production.

Orthodontic tooth movement (OTM) relies on mechanical force-induced bone remodeling. As a metabolic intermediate of glycolysis, lactate has recently been discovered to participate in bone remodeling by serving as a signaling molecule. However, whether lactate could respond to mechanical stimulus during OTM, as well as whether lactate has an impact on the alveolar bone remodeling during orthodontics, remain to be further elucidated. In the current study, we observed physiologically elevated production of lactate along with increased osteogenic differentiation, proliferation, and migration of alveolar bone marrow mesenchymal cells (ABMMCs) under mechanical force. Inhibition of lactate, induced by cyclic mechanical stretch by GNE-140, remarkably suppressed the osteogenic differentiation, proliferation, and migration, yet enhanced apoptosis of ABMMCs. Mechanistically, these regulatory effects of lactate were mediated by histone lactylation. Taken together, our results suggest that force-induced lactate is involved in controlling bone remodeling-related cellular activities in ABMMCs and plays a vital role in the alveolar bone remodeling during OTM. Our findings indicate that lactate might be a critical modulator for alveolar bone remodeling during OTM, providing a novel therapeutic target for the purpose of more effectively controlling tooth movement and improving the stability of orthodontic results.

[Research Progress of Mesenchymal Stem Cells and Their Exosomes on Tumors].

In China, malignant tumor is the main cause of death in both urban and rural areas. Mesenchymal stem cells (MSCs) have multidirectional differentiation potential, self-renewal ability and good immunomodulatory properties. Exosomes, as important paracrine substances of MSCs, mediate information exchange and transmission between cells in tumor microenvironment and influence the occurrence and development of tumors. Recently, conflicting findings have been reported on the effects of MSCs and their exosomes on tumors. On the one hand, MSCs and their exosomes are tumorigenic and can target specific sites to inhibit tumor growth; On the other hand, there is also evidence that MSCs could affect tumor growth and migration as part of the tumor microenvironment. In this paper, we will review the relationship between MSCs and exosomes and tumorgenesis and development, as well as how MSCs and exosomes play different roles in tumorgenesis and development, in order to provide beneficial help for tumor diagnosis, prognosis and precise treatment.
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