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Seehus, Corey

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Seehus

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Corey

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Seehus, Corey
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    Mechanistic Differences in Neuropathic Pain Modalities Revealed by Correlating Behavior with Global Expression Profiling
    (2018) Cobos, Enrique J.; Nickerson, Chelsea A.; Gao, Fuying; Chandran, Vijayendran; Bravo-Caparrós, Inmaculada; González-Cano, Rafael; Riva, Priscilla; Andrews, Nick A.; Latremoliere, Alban; Seehus, Corey; Perazzoli, Gloria; Nieto, Francisco R.; Joller, Nicole; Painter, Michio W.; Ma, Chi Him Eddie; Omura, Takao; Chesler, Elissa J.; Geschwind, Daniel H.; Coppola, Giovanni; Rangachari, Manu; Woolf, Clifford; Costigan, Michael
    SUMMARY Chronic neuropathic pain is a major morbidity of neural injury, yet its mechanisms are incompletely understood. Hypersensitivity to previously non-noxious stimuli (allodynia) is a common symptom. Here, we demonstrate that the onset of cold hypersensitivity precedes tactile allodynia in a model of partial nerve injury, and this temporal divergence was associated with major differences in global gene expression in innervating dorsal root ganglia. Transcripts whose expression change correlates with the onset of cold allodynia were nociceptor related, whereas those correlating with tactile hypersensitivity were immune cell centric. Ablation of TrpV1 lineage nociceptors resulted in mice that did not acquire cold allodynia but developed normal tactile hypersensitivity, whereas depletion of macrophages or T cells reduced neuropathic tactile allodynia but not cold hypersensitivity. We conclude that neuropathic pain incorporates reactive processes of sensory neurons and immune cells, each leading to distinct forms of hypersensitivity, potentially allowing drug development targeted to each pain type.
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    Sense and Immunity: Context-Dependent Neuro-Immune Interplay
    (Frontiers Media S.A., 2017) Foster, Simmie; Seehus, Corey; Woolf, Clifford; Talbot, Sébastien
    The sensory nervous and immune systems, historically considered autonomous, actually work in concert to promote host defense and tissue homeostasis. These systems interact with each other through a common language of cell surface G protein-coupled receptors and receptor tyrosine kinases as well as cytokines, growth factors, and neuropeptides. While this bidirectional communication is adaptive in many settings, helping protect from danger, it can also become maladaptive and contribute to disease pathophysiology. The fundamental logic of how, where, and when sensory neurons and immune cells contribute to either health or disease remains, however, unclear. Our lab and others’ have begun to explore how this neuro-immune reciprocal dialog contributes to physiological and pathological immune responses and sensory disorders. The cumulative results collected so far indicate that there is an important role for nociceptors (noxious stimulus detecting sensory neurons) in driving immune responses, but that this is highly context dependent. To illustrate this concept, we present our findings in a model of airway inflammation, in which nociceptors seem to have major involvement in type 2 but not type 1 adaptive immunity.