Mechanically induced M2 macrophages are involved in bone remodeling of the midpalatal suture during palatal expansion.

BACKGROUND: Palatal expansion is a common way of treating maxillary transverse deficiency. Under mechanical force, the midpalatal suture is expanded, causing local immune responses. This study aimed to determine whether macrophages participate in bone remodeling of the midpalatal suture during palatal expansion and the effects on bone remodeling. METHODS: Palatal expansion model and macrophage depletion model were established. Micro-CT, histological staining, and immunohistochemical staining were used to investigate the changes in the number and phenotype of macrophages during palatal expansion as well as the effects on bone remodeling of the midpalatal suture. Additionally, the effect of mechanically induced M2 macrophages on palatal osteoblasts was also elucidated in vitro. RESULTS: The number of macrophages increased significantly and polarized toward M2 phenotype with the increase of the expansion time, which was consistent with the trend of bone remodeling. After macrophage depletion, the function of osteoblasts and bone formation at the midpalatal suture were impaired during palatal expansion. In vitro, conditioned medium derived from M2 macrophages facilitated osteogenic differentiation of osteoblasts and decreased the RANKL/OPG ratio. CONCLUSIONS: Macrophages through polarizing toward M2 phenotype participated in midpalatal suture bone remodeling during palatal expansion, which may provide a new idea for promoting bone remodeling from the perspective of regulating macrophage polarization.

A Streptococcus suis Strain Δcps/ssna-msly (P353L)-SC19 Provides Cross-Protection against Serotypes 2 and 9 Strain Challenges in a Mouse Model.

Streptococcus suis is an important zoonotic pathogen that mainly causes meningitis, septicemia, and arthritis. Due to the limited cross-protection between numerous serotypes, the existing inactive vaccines in clinical use fail to offer sufficient protection. In this study, a gene deletion-attenuated strain Δcps/ssna-msly (P353L)-SC-19 was constructed by deleting cps and ssna genes from the epidemic strain SC-19 with a mutation of SLY (P353L). The safety of Δcps/ssna-msly (P353L)-SC-19 was confirmed in both in vitro and in vivo experiments. We further demonstrated that immunization with Δcps/ssna-msly (P353L)-SC-19 induced significant cellular immunity and humoral immunity in mice and protected against infections caused by type 2 strain SC-19 (100% protection) and type 9 strain S29 (50% protection), while also preventing meningitis induced by S29. This study highlights the potential of using CPS-deficient strains to achieve cross-protection against different Streptococcus suis serotypes and develop a promising universal live vaccine.

Nerve growth factor promote osteogenic differentiation of dental pulp stem cells through MEK/ERK signalling pathways.

Nerve growth factor (NGF) and its receptor, tropomyosin receptor kinase A (TrkA), are known to play important roles in the immune and nervous system. However, the effects of NGF on the osteogenic differentiation of dental pulp stem cells (DPSCs) remain unclear. This study aimed to investigate the role of NGF on the osteogenic differentiation of DPSCs in vitro and the underlying mechanisms. DPSCs were cultured in osteogenic differentiation medium containing NGF (50 ng/mL) for 7 days. Then osteogenic-related genes and protein markers were analysed using qRT-PCR and Western blot, respectively. Furthermore, addition of NGF inhibitor and small interfering RNA (siRNA) transfection experiments were used to elucidate the molecular signalling pathway responsible for the process. NGF increased osteogenic differentiation of DPSCs significantly compared with DPSCs cultured in an osteogenic-inducing medium. The NGF inhibitor Ro 08-2750 (10 µM) and siRNA-mediated gene silencing of NGF receptor, TrkA and ERK signalling pathways inhibitor U0126 (10 µM) suppressed osteogenic-related genes and protein markers on DPSCs. Furthermore, our data revealed that NGF-upregulated osteogenic differentiation of DPSCs may be associated with the activation of MEK/ERK signalling pathways via TrkA. Collectively, NGF was capable of promoting osteogenic differentiation of DPSCs through MEK/ERK signalling pathways, which may enhance the DPSCs-mediated bone tissue regeneration.