Michael D. Burton

The paper investigates the role of cannabinoid receptor 1 (CB1R) in pain modulation by selectively reactivating it in peripheral sensory neurons, finding it contributes to chronic but not acute analgesia.

This study shows that neuronal-endothelial communication enhances blood-brain barrier resistance to Group B Streptococcus (GBS) infection by reducing bacterial adherence and invasion.

This study shows that lifelong hydroxyurea treatment reduces chronic pain in sickle cell disease mice by decreasing immune activity and reversing TRPA1 sensitization.

This study shows that TLR4+ dermal fibroblasts induce acute and transitional pain states in mice through inflammatory and calcium signaling mechanisms.

This study shows that LKB1 in sensory neurons affects female mouse fertility by altering ovarian innervation and follicular turnover.

This study shows that 12/15-Lipoxygenases contribute to neuropathic-like pain hypersensitivity in female mice, with inhibitors reversing pain symptoms.

This paper shows that ICOS agonist antibody alleviates paclitaxel-induced neuropathy in female mice via IL-10-mediated mechanisms, suggesting potential for CIPN treatment.

The paper examines the translatability of clinical pain and function assessments to preclinical models of chronic musculoskeletal pain in fibromyalgia.

The paper identifies 844 differentially expressed genes in DRGs from DPN patients, showing increased inflammation and decreased neuronal genes, suggesting intraganglionic pathology in diabetic neuropathy.

The paper profiles RNA in human DRGs from neuropathic pain patients, identifying sex-specific gene expression differences and neuro-immune pathways associated with pain.

The paper uses spatial transcriptomics to characterize human sensory neurons, comparing them to mouse and non-human primate data to identify similarities and divergences in drug targets.

This study identifies a specific subset of sensory neurons expressing PAR2 that mediate mechanical and affective pain behaviors, clarifying the cellular basis of PAR2-evoked pain.