Summary Lung nociceptors initiate cough and bronchoconstriction. To elucidate if these fibers also contribute to allergic airway inflammation we stimulated lung nociceptors with capsaicin and observed increased neuropeptide release and immune cell infiltration. In contrast, ablating Nav1.8+ sensory neurons or silencing them with QX-314, a charged sodium channel inhibitor that enters via large pore ion channels to specifically block nociceptors, substantially reduced ovalbumin or house dust mite-induced airway inflammation and bronchial hyperresponsiveness. We also discovered that IL-5, a cytokine produced by activated immune cells, acts directly on nociceptors to induce release of vasoactive intestinal peptide (VIP). VIP then stimulates CD4+ and resident innate lymphoid type 2 cells, creating an inflammatory signaling loop that promotes allergic inflammation. Our results indicate that nociceptors amplify pathological adaptive immune responses and that silencing these neurons with QX-314 interrupts this neuro-immune interplay, revealing a potential new therapeutic strategy for asthma.

Stroke is a common cause of patient morbidity and mortality, being the fifth leading cause of death in the United States. Positron emission tomography (PET) is a proven tool for oncology patients, and may have utility in patients with stroke. We demonstrate findings of stroke incidentally detected on oncologic PET/CTs using 18F-FDG, 11C-Choline, and 68Ga-DOTATATE radiotracers. Specifically, focal 11C-Choline or 68Ga-DOTATATE uptakes localized in areas of MRI confirmed ischemia, and paradoxically increased 18F-FDG activity was visualized surrounding a region of hemorrhage, in different patients. These cases demonstrate that PET may have utility in evaluating patients with stroke based on flow dynamics, metabolic activity, and receptor expression.

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