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Xu, M. X.

Publications and source records attributed to Xu, M. X..

2 recordsLinked to original sources

Exploring Porphyromonas gingivalis Pathogenesis and Antibody Pool Effect Using a Novel Mouse Reproductive Model

This study introduces a novel animal model consisting of two phases. In phase I, Balb/c mice received three intraperitoneal injections of antibodies and two subcutaneous challenges with Porphyromonas gingivalis. The mice were divided into seven groups: G1, G2, and G3 received a single monoclonal antibody targeting the major outer membrane protein RagB of P. gingivalis and infection; G4 was infected without antibody; G5 and G6 received a mixture of monoclonal antibodies and infection; and G7 served as the healthy control. In phase II, one male was paired with one female from the same group and one healthy female. Fertility was assessed using maximum body weight growth rate (MWGR) and alive pup rate (APR). Results indicated that the APR of neonatal mice in G5+G6 significantly lower than G1-G3 and G7 (P < 0.05). Similarly, the MWGR of G5+G6 significantly lower than G7 (P < 0.05). Notably, the APR and MWGR in G4, which received no antibody, were lower than in G7 but higher than in G5-G6. These findings suggest that a mixture of antibodies coexisting with P. gingivalis infection leads to more detrimental reproductive damage than infection alone. The so-called Antibody Pool Effect plays a role in the pathogenesis of P. gingivalis. Understanding the mechanisms of this immunopathological damage may provide insights into the correlation between P. gingivalis infection and systemic diseases.

immunology↗

Epidermal Eg5 promotes X-ROS dependent paclitaxel neurotoxicity

Taxanes are chemotherapeutic agents that induce microtubule modifications in cancer cells, resulting in cell cycle modifications and tumor remission. Here we show that paclitaxel, a widely used taxane, also induces microtubule modifications in healthy epidermal keratinocytes leading to chemotherapy-induced peripheral neuropathy (CIPN). Paclitaxel activates the cell cycle regulator, Kinesin-5 (Eg5), which promotes microtubule detyrosination and fasciculation (dfMT). Eg5 loss protects neurons from paclitaxel neurotoxicity, whereas keratinocyte-specific overexpression promotes axon degeneration. In vivo imaging and 3D reconstructions of dfMTs and nuclei, combined with mechanotransduction studies further show that dfMTs constrict keratinocyte nuclei, leading to nuclear Nox-dependent reactive oxygen species (X-ROS) formation upstream of MMP-13 and cutaneous sensory axon degeneration. This new insight facilitates our understanding of chemotherapy side effects and highlights the need for targeted therapies.

cell biology↗