Substance P represents a novel first-line defense mechanism in the nose

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Substance P represents a novel first-line defense mechanism in the nose

Larsson, Olivia (author): Karolinska Institutet,Karolinska Institute

Tengroth, Lotta (author): Karolinska Institutet,Karolinska Institute

Xu, Yuan (author): Karolinska Institutet,Karolinska Institute

Uddman, Rolf (author): Lund University,Lunds universitet,Klinisk och experimentell allergiforskning,Laryngoesofagologi, allergi och livskvalitet,Forskargrupper vid Lunds universitet,Clinical and Experimental Allergy Research,Laryngoesophagology, Allergy and Life Quality,Lund University Research Groups,Skåne University Hospital

Kumlien Georén, Susanna (author): Karolinska Institutet,Karolinska Institute

Cardell, Lars-Olaf (author): Karolinska Institute,Karolinska University Hospital

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Elsevier BV, 2018
2018
English.
In: Journal of Allergy and Clinical Immunology. - : Elsevier BV. - 0091-6749 .- 1097-6825. ; 141:1, s. 3-136

Related links:: http://dx.doi.org/10...; show more...; http://www.jacionlin...; https://lup.lub.lu.s...; https://doi.org/10.1...; http://kipublication...; show less...

Journal article (peer-reviewed)

Abstract Subject headings

Background: Neuropeptides, such as substance P (SP), have long been seen as mediators of widespread continuous airway inflammation, a process known as neurogenic inflammation. However, this has been difficult to demonstrate clinically, suggesting an alternative role for these signaling molecules. Objectives: We sought to examine the role of SP in nasal infection by assessing the release of SP in response to viral stimulation and characterizing the effects of SP on innate immunity, with the latter reflected in changes in local Toll-like receptor (TLR) expression. Methods: The distribution of SP and TLRs in the nasal mucosa and local airway neurons was assessed with immunohistochemistry. The TLR7 agonists R-837 and R-848 were used to mimic a viral insult in the upper airways represented by primary human nasal epithelial cells (HNECs) and murine nasal epithelial cells (MNECs) and isolated murine trigeminal ganglial neurons. SP release from HNECs, MNECs, and trigeminal ganglial neurons was quantified with EIA. The effects of SP on TLR expression on HNECs were determined by using flow cytometry and confocal microscopy. Results: SP was released from the sensory neurons, MNECs, and HNECs within 15 minutes of local TLR7 stimulation. Subsequently, stimulation with SP induced upregulation of TLR expression in HNECs within 30 minutes through induction of TLR movement within HNECs. Upregulation of TLR expression was not evident when cells were treated with the neurokinin 1 receptor antagonist aprepitant before SP stimulation. Conclusions: This highlights a novel role for sensory neuropeptides as acute and local mediators of pathogen-driven inflammation, rapidly priming innate immune defenses in the airway.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Farmakologi och toxikologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Pharmacology and Toxicology (hsv//eng)
MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Immunologi inom det medicinska området (hsv//swe)
MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Immunology in the medical area (hsv//eng)

Keyword

Epithelial cells
Innate immunity
Nasal mucosa
Substance P
Toll-like receptor
Toll-like receptor 7
Viral infection

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