Literature DB >> 30357493

Activations of group 2 innate lymphoid cells depend on endotypes of chronic rhinosinusitis.

Lin Lin1, Jinjin Wei2, Zheng Chen2, Xinyue Tang2, Fei Dai2, Guangbin Sun2.   

Abstract

OBJECTIVE: Chronic rhinosinusitis (CRS) is a complicated disease with several variants caused by different cellular and molecular mechanisms. The characterization of this heterogeneity supports the definition that the disease consists of many endotypes, such as eosinophilic and neutrophilic CRS, and so on. This study aimed to explore group 2 innate lymphoid cells (ILC2s) in neutrophilic CRS without nasal polyps (CRSsNP) and with nasal polyps (CRSwNP), and evaluate ILC2s across characteristics of the disease.
METHODS: Nasal biopsy samples were obtained from normal subjects or subjects with CRSsNP or CRSwNP during surgery. ILC2s were sorted and purified as CD45+Lin-CD127+CD4-CD8-CRTH2+CD161+ cells through flow cytometry, and were compared among three groups of subjects. Then, these samples were cultured in vitro, and inflammatory factors were assessed in tissue cultures. After that, human recombinant (rm) interleukin (IL)-33 or IL-17 were administered into the cultures, and we again examined relevant inflammatory substances.
RESULTS: ILC2s were upregulated in neutrophilic CRSsNP and CRSwNP patients, and there were no statistical differences between them. Eosinophil cation protein (ECP), myeloperoxidase (MPO), IL-25, IL-33, IL-5, IL-13, interferon (IFN)-γ and IL-17 were increased in the cultures, however, only concentrations of MPO, IFN-γ and IL-17 were enhanced in CRSwNP tissues compared to CRSsNP ones. After administration of rmIL-33, ECP, IL-5 and IL-13 were all increased in tissues from CRSsNP and CRSwNP patients, however, there were no significant differences between them. Finally, we evaluated concentrations of several above inflammatory factors after the treatment of rmIL-17, and found that MPO and IFN-γ were enhanced in these two phenotypes of patients, and were elevated significantly in CRSwNP tissue cultures.
CONCLUSION: These findings show that ILC2s might be inactivated in neutrophilic CRSsNP and CRSwNP based on this pilot study.

Entities:  

Keywords:  Chronic rhinosinusitis; Group 2 innate lymphoid cell; Human; Nasal polyp; Neutrophil; Tissue

Mesh:

Substances:

Year:  2018        PMID: 30357493     DOI: 10.1007/s00405-018-5180-4

Source DB:  PubMed          Journal:  Eur Arch Otorhinolaryngol        ISSN: 0937-4477            Impact factor:   2.503


  37 in total

1.  IL-33-responsive innate lymphoid cells are an important source of IL-13 in chronic rhinosinusitis with nasal polyps.

Authors:  Joanne L Shaw; Samer Fakhri; Martin J Citardi; Paul C Porter; David B Corry; Farrah Kheradmand; Yong-Jun Liu; Amber Luong
Journal:  Am J Respir Crit Care Med       Date:  2013-08-15       Impact factor: 21.405

2.  Remodeling and inflammation in Chinese versus white patients with chronic rhinosinusitis.

Authors:  Nan Zhang; Shixi Liu; Ping Lin; Xiaoyuan Li; Nicholas van Bruaene; Jie Zhang; Thibaut van Zele; Claus Bachert
Journal:  J Allergy Clin Immunol       Date:  2010-01-12       Impact factor: 10.793

3.  Increased ILC2s in the eosinophilic nasal polyp endotype are associated with corticosteroid responsiveness.

Authors:  Hannah H Walford; Sean J Lund; Rachel E Baum; Andrew A White; Christopher M Bergeron; Jacob Husseman; Kelly J Bethel; David R Scott; Naseem Khorram; Marina Miller; David H Broide; Taylor A Doherty
Journal:  Clin Immunol       Date:  2014-09-16       Impact factor: 3.969

4.  Group 2 innate lymphoid cells (ILC2s) are increased in chronic rhinosinusitis with nasal polyps or eosinophilia.

Authors:  J Ho; M Bailey; J Zaunders; N Mrad; R Sacks; W Sewell; R J Harvey
Journal:  Clin Exp Allergy       Date:  2015-02       Impact factor: 5.018

5.  European Position Paper on Rhinosinusitis and Nasal Polyps 2012.

Authors:  Wytske J Fokkens; Valerie J Lund; Joachim Mullol; Claus Bachert; Isam Alobid; Fuad Baroody; Noam Cohen; Anders Cervin; Richard Douglas; Philippe Gevaert; Christos Georgalas; Herman Goossens; Richard Harvey; Peter Hellings; Claire Hopkins; Nick Jones; Guy Joos; Livije Kalogjera; Bob Kern; Marek Kowalski; David Price; Herbert Riechelmann; Rodney Schlosser; Brent Senior; Mike Thomas; Elina Toskala; Richard Voegels; De Yun Wang; Peter John Wormald
Journal:  Rhinol Suppl       Date:  2012-03

6.  IL-17A as a regulator of neutrophil survival in nasal polyp disease of patients with and without cystic fibrosis.

Authors:  L Derycke; N Zhang; G Holtappels; T Dutré; C Bachert
Journal:  J Cyst Fibros       Date:  2011-12-16       Impact factor: 5.482

Review 7.  Perspectives on the etiology of chronic rhinosinusitis.

Authors:  Bruce K Tan; Robert P Schleimer; Robert C Kern
Journal:  Curr Opin Otolaryngol Head Neck Surg       Date:  2010-02       Impact factor: 2.064

8.  Innate lymphoid cells responding to IL-33 mediate airway hyperreactivity independently of adaptive immunity.

Authors:  Hye Young Kim; Ya-Jen Chang; Srividya Subramanian; Hyun-Hee Lee; Lee A Albacker; Ponpan Matangkasombut; Paul B Savage; Andrew N J McKenzie; Dirk E Smith; James B Rottman; Rosemarie H DeKruyff; Dale T Umetsu
Journal:  J Allergy Clin Immunol       Date:  2011-11-25       Impact factor: 10.793

9.  Mixed T helper cell signatures in chronic rhinosinusitis with and without polyps.

Authors:  Lara Derycke; Stefanie Eyerich; Koen Van Crombruggen; Claudina Pérez-Novo; Gabriele Holtappels; Natalie Deruyck; Philippe Gevaert; Claus Bachert
Journal:  PLoS One       Date:  2014-06-09       Impact factor: 3.240

10.  T-cell phenotypes in chronic rhinosinusitis with nasal polyps in Japanese patients.

Authors:  Shintaro Baba; Ryoji Kagoya; Kenji Kondo; Maho Suzukawa; Ken Ohta; Tatsuya Yamasoba
Journal:  Allergy Asthma Clin Immunol       Date:  2015-11-19       Impact factor: 3.406

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