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Radiation-induced pulmonary fibrosis (RIPF) is a serious side effect of radiation therapy, but the underlying mechanisms are unknown. B10 cells, as negative B regulatory cells, play important roles in regulating inflammation and autoimmunity. However, the role of B10 cells in RIPF progression is unclear. The aim of this study was to determine the role of B10 cells in aggravating RIPF and the underlying mechanism. The role of B10 cells in RIPF was studied by constructing mouse models of RIPF and depleting B10 cells with an anti-CD22 antibody. The mechanism of B10 cells in RIPF was further explored through cocultivation of B10 cells and MLE-12 or NIH3T3 cells and administration of an interleukin (IL)-10 antibody to block IL-10. B10 cell numbers increased significantly during the early stage in the RIPF mouse models compared with the controls. In addition, depleting B10 cells with the anti-CD22 antibody attenuated the development of lung fibrosis in mice. Subsequently, we confirmed that B10 cells induced epithelial-mesenchymal transition and the transformation of myofibroblasts via activation of STAT3 signaling in vitro. After blockade of IL-10, it was verified that IL-10 secreted by B10 cells mediates the epithelial-mesenchymal transition of myofibroblasts, thereby promoting RIPF. Our study uncovers a novel role for IL-10-secreting B10 cells that could be a new target of research for relieving RIPF. [ABSTRACT FROM AUTHOR]

[Display omitted] • We study the kinematics and mechanics of mandibles of trap-jaw ants. • We analyze the trade-off between powerful clamping and efficient impact resistance. • The hollowness ratio plays an essential role in counterbalancing the trade-off. • The mandibles meet the demands of powerful clamping and efficient impact resistance. • The hollow mandible achieves a more robust balance than the solid mandible. The trap-jaw ant Odontomachus monticola manipulates its hollow mandibles to generate extremely high speed to impact various objects through a catapult mechanism, making the violent collision occur between the mandible and the impacted objects, which increases the risk of structural failure. However, how the ant balances the trade-off between the powerful clamping and impact resistance by using this hollow structure remains elusive. In this combined experimental and theoretical investigation, we revealed that the hollowness ratio of the mandible plays an essential role in counterbalancing the trade-off. Micro-CT and high-speed images suggested that the hollow mandibles facilitate a high angular acceleration to 108 rad/s2 for an enormous clamping force. However, this hollowness might challenge the structural strength while collision occurs. We found that under the same actuating energy, the von Mises stress of the object collided by the natural mandible striking can reach up to 2.9 times that generated by the entirely solid mandible. We defined the efficiency ratio of the von Mises stress on the impacted object to that on the mandible and found the hollow mandible achieves a more robust balance between powerful clamping and impact resistance compared to the solid mandible. [ABSTRACT FROM AUTHOR]

Radiation-induced pulmonary fibrosis (RIPF) is a common side effect of radiation therapy for thoracic tumors without effective prevention and treatment methods at present. The aim of this study was to explore whether glycyrrhetinic acid (GA) has a protective effect on RIPF and the underlying mechanism. A RIPF mouse model administered GA was used to determine the effect of GA on RIPF. The cocultivation of regulatory T (Treg) cells with mouse lung epithelial-12 cells or mouse embryonic fibroblasts and intervention with GA or transforming growth factor-β1 (TGF-β1) inhibitor to block TGF-β1 was conducted to study the mechanism by which GA alleviates RIPF. Furthermore, injection of Treg cells into GA-treated RIPF mice to upregulate TGF-β1 levels was performed to verify the roles of TGF-β1 and Treg cells. GA intervention improved the damage to lung tissue structure and collagen deposition and inhibited Treg cell infiltration, TGF-β1 levels, epithelial mesenchymal transition (EMT), and myofibroblast (MFB) transformation in mice after irradiation. Treg cell-induced EMT and MFB transformation in vitro were prevented by GA, as well as a TGF-β1 inhibitor, by decreasing TGF-β1. Furthermore, reinfusion of Treg cells upregulated TGF-β1 levels and exacerbated RIPF in GA-treated RIPF mice. GA can improve RIPF in mice, and the corresponding mechanisms may be related to the inhibition of TGF-β1 secreted by Treg cells to induce EMT and MFB transformation. Therefore, GA may be a promising therapeutic candidate for the clinical treatment of RIPF. [ABSTRACT FROM AUTHOR]