Background: Asthma is characterized by excessive bronchoconstriction and cough. Airway nerves control these reflexes. In asthma, an abundance of airway eosinophils cause airway nerve dysfunction by altering neurotransmitter content and neuronal receptor expression.

Objective: To characterize the effects of eosinophils on Transient Receptor Potential V1 (TRPV1) and substance P (SP) expression in dorsal root ganglia sensory neurons.

Methods: Dorsal root ganglia were isolated from wild-type C57BL/6 mice, IL-5 transgenic mice with airway eosinophilia driven by high IL-5 (IL5tg, NJ.1726 lineage), and transgenic eosinophil deficient (PHIL) mice. Ganglia were immersed for 24 hours at 4 degrees in Zamboni’s fixative, immunolabeled with antibodies against TRPV1 and SP, and imaged on a Zeiss laser scanning confocal microscope (LSM780). Neuronal TRPV1 and SP intensity were measured using ImageJ.

Results: In wild-type mice, 24% of dorsal root ganglia neurons expressed TRPV1 and 26% expressed SP. In contrast, in IL5tg mice, 99% of neurons expressed TRPV1 and 97% expressed SP. TRPV1 expression in eosinophil-deficient PHIL mice was similar to wild-type control with 20% of neurons expressing TRPV1. However, SP expression in eosinophil-deficient PHIL mice was increased compared to wild-type, with 73% of neurons expressing SP. In total, 39% of TRPV1-positive neurons also expressed SP in wild-type mice whereas 97% of TRPV1-positive neurons expressed SP in IL5tg mice and 90% of TRPV1-positive neurons expressed SP in PHIL mice.

Conclusions: Eosinophils increase TRPV1 and SP expression in dorsal root sensory neurons. These changes may underlie increased cough and bronchoconstriction in asthma.



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