PMID- 32141263
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200928
IS  - 2092-7355 (Print)
IS  - 2092-7363 (Electronic)
IS  - 2092-7355 (Linking)
VI  - 12
IP  - 3
DP  - 2020 May
TI  - Role of IL-17A in Chronic Rhinosinusitis With Nasal Polyp.
PG  - 507-522
LID - 10.4168/aair.2020.12.3.507 [doi]
AB  - PURPOSE: Th17-associated inflammation is increased in chronic rhinosinusitis with 
      nasal polyp (CRSwNP), and is associated with disease severity and steroid 
      resistance. Overexpressed interleukin (IL)-17A affects CRSwNP by tissue 
      remodeling, eosinophilic accumulation, and neutrophilic infiltration. We aimed to 
      identify the role of IL-17A in CRSwNP and to evaluate the effects of anti-IL-17A 
      blocking antibody on nasal polyp (NP) formation using a murine NP model. 
      Moreover, we sought to investigate whether the inhibition of mechanistic target 
      of the rapamycin (mTOR) signal pathway could suppress IL-17A expression and NP 
      formation. METHODS: Human sinonasal tissues from control subjects and patients 
      with chronic rhinosinusitis (CRS) were analyzed using immunohistochemistry (IHC) 
      and immunofluorescence staining. The effects of IL-17A neutralizing antibody and 
      rapamycin were evaluated in a murine NP model. Mouse samples were analyzed using 
      IHC, quantitative real-time polymerase chain reaction, and enzyme-linked 
      immunosorbent assay. RESULTS: IL-17A(+) inflammatory cells were significantly 
      increased in number in NP from patients with CRSwNP compared to that in uncinate 
      process tissues from control subjects and patients with CRS without NP or CRSwNP. 
      CD68(+) M1 macrophages dominantly expressed IL-17A, followed by neutrophils and T 
      helper cells, in NP tissues. Neutralization of IL-17A effectively reduced the 
      number of NPs, inflammatory cytokines, and IL-17A-producing cells, including M1 
      macrophages. Inhibition of IL-17A via the mTOR pathway using rapamycin also 
      attenuated NP formation and inflammation in the murine NP model. CONCLUSIONS: 
      IL-17A possibly plays a role in the pathogenesis of CRSwNP, the major cellular 
      source being M1 macrophage in NP tissues. Targeting IL-17A directly or indirectly 
      may be an effective therapeutic strategy for CRSwNP.
CI  - Copyright (c) 2020 The Korean Academy of Asthma, Allergy and Clinical Immunology . 
      The Korean Academy of Pediatric Allergy and Respiratory Disease.
FAU - Ryu, Gwanghui
AU  - Ryu G
AUID- ORCID: 0000-0002-3251-399X
AD  - Department of Otorhinolaryngology-Head and Neck Surgery, Soonchunhyang University 
      College of Medicine, Cheonan, Korea.
FAU - Bae, Jun Sang
AU  - Bae JS
AUID- ORCID: 0000-0003-2589-797X
AD  - Department of Otorhinolaryngology, Dankook University College of Medicine, 
      Cheonan, Korea.
AD  - Beckman Laser Institute Korea, Dankook University College of Medicine, Cheonan, 
      Korea.
FAU - Kim, Ji Hye
AU  - Kim JH
AUID- ORCID: 0000-0003-2516-774X
AD  - Department of Otorhinolaryngology, Dankook University College of Medicine, 
      Cheonan, Korea.
AD  - Beckman Laser Institute Korea, Dankook University College of Medicine, Cheonan, 
      Korea.
FAU - Kim, Eun Hee
AU  - Kim EH
AUID- ORCID: 0000-0002-9539-9928
AD  - Department of Otorhinolaryngology, Dankook University College of Medicine, 
      Cheonan, Korea.
AD  - Beckman Laser Institute Korea, Dankook University College of Medicine, Cheonan, 
      Korea.
FAU - Lyu, Lele
AU  - Lyu L
AUID- ORCID: 0000-0003-1600-0817
AD  - Department of Otorhinolaryngology, Dankook University College of Medicine, 
      Cheonan, Korea.
AD  - Beckman Laser Institute Korea, Dankook University College of Medicine, Cheonan, 
      Korea.
FAU - Chung, Young Jun
AU  - Chung YJ
AUID- ORCID: 0000-0002-3789-3485
AD  - Department of Otorhinolaryngology, Dankook University College of Medicine, 
      Cheonan, Korea.
AD  - Beckman Laser Institute Korea, Dankook University College of Medicine, Cheonan, 
      Korea.
FAU - Mo, Ji Hun
AU  - Mo JH
AUID- ORCID: 0000-0003-1331-364X
AD  - Department of Otorhinolaryngology, Dankook University College of Medicine, 
      Cheonan, Korea.
AD  - Beckman Laser Institute Korea, Dankook University College of Medicine, Cheonan, 
      Korea. jihunmo@gmail.com.
LA  - eng
GR  - NRF-2016R1A2B4010407/NRF/National Research Foundation of Korea/Korea
GR  - NRF-2019R1H1A2080182/NRF/National Research Foundation of Korea/Korea
GR  - NRF-2018R1D1A3B07048683/NRF/National Research Foundation of Korea/Korea
PT  - Journal Article
PL  - Korea (South)
TA  - Allergy Asthma Immunol Res
JT  - Allergy, asthma & immunology research
JID - 101518382
PMC - PMC7061155
OTO - NOTNLM
OT  - IL-17A
OT  - Sinusitis
OT  - TNF-alpha
OT  - immunohistochemistry
OT  - mice
OT  - nasal polyps
OT  - rapamycin
OT  - real-time polymerase chain reaction
COIS- There are no financial or other issues that might lead to conflict of interest.
EDAT- 2020/03/07 06:00
MHDA- 2020/03/07 06:01
PMCR- 2020/05/01
CRDT- 2020/03/07 06:00
PHST- 2019/11/08 00:00 [received]
PHST- 2020/01/19 00:00 [revised]
PHST- 2020/01/22 00:00 [accepted]
PHST- 2020/03/07 06:00 [entrez]
PHST- 2020/03/07 06:00 [pubmed]
PHST- 2020/03/07 06:01 [medline]
PHST- 2020/05/01 00:00 [pmc-release]
AID - 12.507 [pii]
AID - 10.4168/aair.2020.12.3.507 [doi]
PST - ppublish
SO  - Allergy Asthma Immunol Res. 2020 May;12(3):507-522. doi: 
      10.4168/aair.2020.12.3.507.