PMID- 28913994
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 2092-7355 (Print)
IS  - 2092-7363 (Electronic)
IS  - 2092-7355 (Linking)
VI  - 9
IP  - 6
DP  - 2017 Nov
TI  - Mouse Model of IL-17-Dominant Rhinitis Using Polyinosinic-Polycytidylic Acid.
PG  - 540-549
LID - 10.4168/aair.2017.9.6.540 [doi]
AB  - Interleukin (IL)-17 plays an important role in rhinitis and the level thereof 
      correlates with the severity of disease. However, no mouse model for 
      IL-17-dominant rhinitis has yet been developed. Our objective was to establish a 
      mouse model of IL-17-dominant rhinitis via intranasal application of 
      polyinosinic-polycytidylic acid (abbreviated as Poly(I:C)). Mice were divided 
      into 6 groups (n=8 for each group); 1) 1 negative control group, 2) 1 positive 
      control group (OVA/alum model), 3) 2 Poly(I:C) groups (10 or 100 mug), and 4) 2 
      OVA/Poly(I:C) groups (10 or 100 mug). The positive control group was treated with 
      the conventional OVA/alum protocol. In the Poly(I:C) and OVA/Poly(I:C) groups, 
      phosphate-buffered saline or an OVA solution plus Poly(I:C) were administered. 
      The OVA/Poly(I:C) groups exhibited significantly greater neutrophil infiltration 
      and increased IL-17/interferon gamma expression compared with the other groups. 
      However, the levels of total immunoglobulin E (IgE), OVA-specific IgE, eosinophil 
      infiltration, IL-4, IL-5, IL-6, and IL-10 were significantly lower in the 
      OVA/Poly(I:C) groups than in mice subjected to conventional Th2-dominant OVA/alum 
      treatment (the positive control group). IL-17 and neutrophil measurement, 
      chemokine (C-X-C motif) ligand 1 immunohistochemistry, and confocal microscopy 
      revealed increased numbers of IL-17-secreting cells in the nasal mucosa of the 
      OVA/Poly(I:C) groups, which included natural killer cells, CD4 T cells, and 
      neutrophils. In conclusion, we developed a mouse model of IL-17-dominant rhinitis 
      using OVA together with Poly(I:C). This model will be useful in research on 
      neutrophil- or IL-17-dominant rhinitis.
CI  - Copyright (c) 2017 The Korean Academy of Asthma, Allergy and Clinical Immunology . 
      The Korean Academy of Pediatric Allergy and Respiratory Disease.
FAU - Bae, Jun Sang
AU  - Bae JS
AD  - Department of Premedical Course, 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
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
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
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
PT  - Journal Article
PL  - Korea (South)
TA  - Allergy Asthma Immunol Res
JT  - Allergy, asthma & immunology research
JID - 101518382
PMC - PMC5603483
OTO - NOTNLM
OT  - IL-17
OT  - Rhinitis
OT  - mouse model
OT  - neutrophil
OT  - polyinosinic-polycytidylic acid
COIS- There are no financial or other issues that might lead to conflict of interest.
EDAT- 2017/09/16 06:00
MHDA- 2017/09/16 06:01
PMCR- 2017/11/01
CRDT- 2017/09/16 06:00
PHST- 2017/04/11 00:00 [received]
PHST- 2017/05/17 00:00 [revised]
PHST- 2017/05/23 00:00 [accepted]
PHST- 2017/09/16 06:00 [entrez]
PHST- 2017/09/16 06:00 [pubmed]
PHST- 2017/09/16 06:01 [medline]
PHST- 2017/11/01 00:00 [pmc-release]
AID - 9.540 [pii]
AID - 10.4168/aair.2017.9.6.540 [doi]
PST - ppublish
SO  - Allergy Asthma Immunol Res. 2017 Nov;9(6):540-549. doi: 
      10.4168/aair.2017.9.6.540.