All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.

Abstract

Glucocorticoid Resistant Asthma: The Potential Contribution of IL-17

Background: Asthma is a complex disease in which environmental and genetic factors can contribute to its development. The glucocorticoid is the main drug used to treat it. However, glucocorticoid resistant asthma is an important cause of patient morbidity, and some studies have identified a subpopulation of
TCD4+ effector cells (Th17 lymphocytes) producers of cytokines such as IL-17A and IL17-F, associated with this condition. Our aim was to investigate in literature the potential role of Th17 in the development of asthma glucocorticoid resistant.

Methods and findings: The literature search was conducted in PubMed, Web of science, Scielo, Medline and Cochrane databases to identify relevant studies published in English, from 1993 to 2015. The keywords used in this search were “glucocorticoids”, “IL-17”, “asthma” and “polymorphism”. Those studies have shown that IL-17A and IL-17F are important regulators of neutrophilic inflammation
in airways, suggesting a potential role for TH17 cells in asthma severity through upregulation of β glucocorticoid receptor. There are few studies evaluating the association of polymorphisms in IL-17 genes with different asthma phenotypes, especially with glucocorticoid resistant asthma.

Conclusion: IL-17 is an important mediator of response to glucocorticoid treatment. Further studies are necessary to elucidate the mechanism in which Th17 components interfere in glucocorticoid resistance. We believe that in the future IL-17 can be used as a biomarker to predict the glucocorticoid response in asthmatics.


Author(s):

RS Costa, MJ Silva, MBR Santana, HM Pitangueira, CR Marques, VL Carneiro, CA Figueiredo



Abstract | Full-Text | PDF

Share this  Facebook  Twitter  LinkedIn  Google+
Flyer image

Abstracted/Indexed in

  • Index Copernicus
  • Google Scholar
  • Cosmos IF
  • Directory of Research Journal Indexing (DRJI)
  • WorldCat
  • Publons
  • Geneva Foundation for Medical Education and Research
  • Secret Search Engine Labs