Luke A. Pattison

This study determines the cryo-EM structure of a brain shuttle antibody bound to the transferrin receptor and shows how its binding features affect avidity, pH sensitivity, and brain delivery.

The paper shows that GPR65 internalization in fibroblast-like synoviocytes is necessary for ERK activation and cytokine release, which sensitize nociceptive neurons.

This study shows that overexpressing Prdm12 in knee-innervating neurons reduces inflammatory joint pain and neuronal hyperexcitability in mice.

This study shows that sphingomyelin 34:1 induces inflammatory pain and neuronal hyperexcitability in mice with osteoarthritis.

This study shows that activating GPR65 on fibroblast-like synoviocytes leads to inflammatory mediator release, contributing to joint pain in mice and humans.

This study investigates how inflammatory mediators affect TRPM3 channel function in mouse sensory neurons and finds that IL-1β and TNF potentiate TRPM3 without changing its expression, while pharmacological blockade does not alleviate inflammatory pain in a specific model.

This study correlates mouse digging behavior with human pain experience, showing that digging deficits reflect pain levels and that meloxicam is more effective than gabapentin in alleviating these deficits.

This study demonstrates the efficacy of a humanised chemogenetic system in silencing sensory neuron hyperexcitability and reducing pain in both mouse and human models.

This study shows TNFα sensitizes colonic nociceptors via TNFR1 and p38 MAPK, enhancing responses to capsaicin and noxious distension.

The paper maps behavioral signatures of inflammatory pain and its relief in mice using computational tools and identifies that a common anti-inflammatory drug does not fully restore pre-injury behavior.

This study uses AAV-PHP.S to deliver chemogenetic receptors to knee-innervating DRG neurons, showing that inhibitory DREADDs reduce inflammation-induced pain in mice.

This study shows that TNF-α activated fibroblast-like synoviocytes sensitize knee neurons in vitro, contributing to inflammatory pain in arthritis.

The paper identifies a genetic variant in KCNG4 associated with increased labor pain by altering KV6.4 function in uterine nociceptors.

This study shows that acute knee inflammation in mice sensitizes sensory neurons and reduces digging behavior, mediated by TRPV1 receptor upregulation.