PMID- 34078339
OWN - NLM
STAT- MEDLINE
DCOM- 20211104
LR  - 20211104
IS  - 1471-2466 (Electronic)
IS  - 1471-2466 (Linking)
VI  - 21
IP  - 1
DP  - 2021 Jun 2
TI  - Increased expression of transient receptor potential channels and neurogenic 
      factors associates with cough severity in a guinea pig model.
PG  - 187
LID - 10.1186/s12890-021-01556-w [doi]
LID - 187
AB  - BACKGROUND: Previous studies suggest that transient receptor potential (TRP) 
      channels and neurogenic inflammation may be involved in idiopathic pulmonary 
      fibrosis (IPF)-related high cough sensitivity, although the details of mechanism 
      are largely unknown. Here, we aimed to further explore the potential mechanism 
      involved in IPF-related high cough sensitivity to capsaicin challenge in a guinea 
      pig model of pulmonary fibrosis induced by bleomycin. METHODS: Western blotting 
      and real-time quantitative polymerase chain reaction (RT-qPCR) were employed to 
      measure the expression of TRP channel subfamily A, member 1 (TRPA1) and TRP 
      vanilloid 1 (TRPV1), which may be involved in the cough reflex pathway. 
      Immunohistochemical analysis and RT-qPCR were used to detect the expression of 
      neuropeptides substance P (SP), Neurokinin-1 receptor (NK1R), and calcitonin 
      gene-related peptide (CGRP) in lung tissues. Concentrations of nerve growth 
      factor (NGF), SP, neurokinin A (NKA), neurokinin B (NKB), and brain-derived 
      neurotrophic factor (BDNF) in lung tissue homogenates were measured by ELISA. 
      RESULTS: Cough sensitivity to capsaicin was significantly higher in the model 
      group than that of the sham group. RT-qPCR and immunohistochemical analysis 
      showed that the expression of TRPA1 and TRPV1 in the jugular ganglion and nodal 
      ganglion, and SP, NK1R, and CGRP in lung tissue was significantly higher in the 
      model group than the control group. In addition, expression of TRP and neurogenic 
      factors was positively correlated with cough sensitivity of the experimental 
      animals. CONCLUSION: Up-regulated expression of TRPA1 and TRPV1 in the cough 
      reflex pathway and neurogenic inflammation might contribute to the IPF-related 
      high cough sensitivity in guinea pig model.
FAU - Guan, Mengyue
AU  - Guan M
AD  - Department of Respiratory Medicine, Beijing Hospital of Traditional Chinese 
      Medicine, Capital Medical University, No. 23rd Art Museum Backstreet, Dongcheng 
      District, Beijing, 10010, China.
FAU - Ying, Sun
AU  - Ying S
AD  - Department of Immunology, School of Basic Medical Sciences, Capital Medical 
      University, No. 10th Xitoutiao, You'anmenwai Street, Fengtai District, Beijing, 
      China.
FAU - Wang, Yuguang
AU  - Wang Y
AD  - Department of Respiratory Medicine, Beijing Hospital of Traditional Chinese 
      Medicine, Capital Medical University, No. 23rd Art Museum Backstreet, Dongcheng 
      District, Beijing, 10010, China. wygzhyiaids@126.com.
LA  - eng
PT  - Journal Article
DEP - 20210602
PL  - England
TA  - BMC Pulm Med
JT  - BMC pulmonary medicine
JID - 100968563
RN  - 0 (TRPA1 Cation Channel)
RN  - 0 (TRPV Cation Channels)
RN  - 11056-06-7 (Bleomycin)
RN  - 33507-63-0 (Substance P)
SB  - IM
MH  - Animals
MH  - Bleomycin
MH  - Cough/chemically induced/*metabolism
MH  - Disease Models, Animal
MH  - Disease Progression
MH  - Guinea Pigs
MH  - Idiopathic Pulmonary Fibrosis/*physiopathology
MH  - Lung/metabolism/*pathology
MH  - Male
MH  - Neurogenic Inflammation/chemically induced/metabolism
MH  - Substance P/adverse effects/metabolism
MH  - TRPA1 Cation Channel/genetics/*metabolism
MH  - TRPV Cation Channels/genetics/*metabolism
PMC - PMC8173754
OTO - NOTNLM
OT  - IPF-related high cough sensitivity
OT  - Jugular ganglion
OT  - Nodal ganglion TRP
OT  - TRPA1
OT  - TRPV1
COIS- The authors declare no conflicts of interest.
EDAT- 2021/06/04 06:00
MHDA- 2021/11/05 06:00
PMCR- 2021/06/02
CRDT- 2021/06/03 05:38
PHST- 2021/02/14 00:00 [received]
PHST- 2021/05/25 00:00 [accepted]
PHST- 2021/06/03 05:38 [entrez]
PHST- 2021/06/04 06:00 [pubmed]
PHST- 2021/11/05 06:00 [medline]
PHST- 2021/06/02 00:00 [pmc-release]
AID - 10.1186/s12890-021-01556-w [pii]
AID - 1556 [pii]
AID - 10.1186/s12890-021-01556-w [doi]
PST - epublish
SO  - BMC Pulm Med. 2021 Jun 2;21(1):187. doi: 10.1186/s12890-021-01556-w.