TY - JOUR
T1 - Disruption of the Sensory System Affects Sterile Cutaneous Inflammation In Vivo
AU - La Russa, Federica
AU - Lopes, Douglas M.
AU - Hobbs, Carl
AU - Argunhan, Fulye
AU - Brain, Susan
AU - Bevan, Stuart
AU - Bennett, David L.H.
AU - McMahon, Stephen B.
PY - 2019/9
Y1 - 2019/9
N2 -
Increasing evidence suggests that nerve fibers responding to noxious stimuli (nociceptors) modulate immunity in a variety of tissues, including the skin. Yet, the role of nociceptors in regulating sterile cutaneous inflammation remains unexplored. To address this question, we have developed a detailed description of the sterile inflammation caused by overexposure to UVB irradiation (i.e., sunburn) in the mouse plantar skin. Using this model, we observed that chemical depletion of nociceptor terminals did not alter the early phase of the inflammatory response to UVB, but it caused a significant increase in the number of dendritic cells and αβ
+
T cells as well as enhanced extravasation during the later stages of inflammation. Finally, we showed that such regulation was driven by the nociceptive neuropeptide calcitonin gene–related peptide. In conclusion, we propose that nociceptors not only play a crucial role in inflammation through avoidance reflexes and behaviors, but can also regulate sterile cutaneous immunity in vivo.
AB -
Increasing evidence suggests that nerve fibers responding to noxious stimuli (nociceptors) modulate immunity in a variety of tissues, including the skin. Yet, the role of nociceptors in regulating sterile cutaneous inflammation remains unexplored. To address this question, we have developed a detailed description of the sterile inflammation caused by overexposure to UVB irradiation (i.e., sunburn) in the mouse plantar skin. Using this model, we observed that chemical depletion of nociceptor terminals did not alter the early phase of the inflammatory response to UVB, but it caused a significant increase in the number of dendritic cells and αβ
+
T cells as well as enhanced extravasation during the later stages of inflammation. Finally, we showed that such regulation was driven by the nociceptive neuropeptide calcitonin gene–related peptide. In conclusion, we propose that nociceptors not only play a crucial role in inflammation through avoidance reflexes and behaviors, but can also regulate sterile cutaneous immunity in vivo.
UR - http://www.scopus.com/inward/record.url?scp=85065627744&partnerID=8YFLogxK
U2 - 10.1016/j.jid.2019.01.037
DO - 10.1016/j.jid.2019.01.037
M3 - Article
C2 - 30974165
AN - SCOPUS:85065627744
SN - 0022-202X
VL - 139
SP - 1936-1945.e3
JO - Journal of Investigative Dermatology
JF - Journal of Investigative Dermatology
IS - 9
ER -