House Dust Mite Facilitates Ovalbumin-specific Allergic Sensitization and Airway Inflammation

2005 ◽  
Vol 172 (3) ◽  
pp. 314-321 ◽  
Author(s):  
Ramzi Fattouh ◽  
Mahmoud A. Pouladi ◽  
David Alvarez ◽  
Jill R. Johnson ◽  
Tina D. Walker ◽  
...  
2020 ◽  
Vol 204 (4) ◽  
pp. 753-762 ◽  
Author(s):  
Haruka Miki ◽  
Satoko Tahara-Hanaoka ◽  
Mariana Silva Almeida ◽  
Kaori Hitomi ◽  
Shohei Shibagaki ◽  
...  

2017 ◽  
Vol 214 (10) ◽  
pp. 3037-3050 ◽  
Author(s):  
Takashi Ito ◽  
Koichi Hirose ◽  
Aiko Saku ◽  
Kenta Kono ◽  
Hiroaki Takatori ◽  
...  

Previous studies have shown that IL-22, one of the Th17 cell–related cytokines, plays multiple roles in regulating allergic airway inflammation caused by antigen-specific Th2 cells; however, the underlying mechanism remains unclear. Here, we show that allergic airway inflammation and Th2 and Th17 cytokine production upon intratracheal administration of house dust mite (HDM) extract, a representative allergen, were exacerbated in IL-22-deficient mice. We also found that IL-22 induces Reg3γ production from lung epithelial cells through STAT3 activation and that neutralization of Reg3γ significantly exacerbates HDM-induced eosinophilic airway inflammation and Th2 cytokine induction. Moreover, exostatin-like 3 (EXTL3), a functional Reg3γ binding protein, is expressed in lung epithelial cells, and intratracheal administration of recombinant Reg3γ suppresses HDM-induced thymic stromal lymphopoietin and IL-33 expression and accumulation of type 2 innate lymphoid cells in the lung. Collectively, these results suggest that IL-22 induces Reg3γ production from lung epithelial cells and inhibits the development of HDM-induced allergic airway inflammation, possibly by inhibiting cytokine production from lung epithelial cells.


2021 ◽  
Author(s):  
Sorif Uddin ◽  
Augustin Amour ◽  
David J Lewis ◽  
Chris D Edwards ◽  
Matthew G Williamson ◽  
...  

Abstract Background: Phosphoinositide-3-kinase-delta (PI3Kδ) inhibition is a promising therapeutic approach for inflammatory conditions due to its role in leucocyte proliferation, migration and activation. However, the effect of PI3Kδ inhibition on group-2-innate lymphoid cells (ILC2s) and inflammatory eosinophils remains unknown. Using a murine model exhibiting persistent airway inflammation we sought to understand the effect of PI3Kδ inhibition, montelukast and anti-IL5 antibody treatment on IL33 expression, group-2-innate lymphoid cells, inflammatory eosinophils, and goblet cell metaplasia. Results: Mice were sensitised to house dust mite and after allowing inflammation to resolve, were re-challenged with house dust mite to re-initiate airway inflammation. ILC2s were found to persist in the airways following house dust mite sensitisation and after re-challenge their numbers increased further along with accumulation of inflammatory eosinophils. In contrast to montelukast or anti-IL5 antibody treatment, PI3Kδ inhibition ablated IL33 expression and prevented group-2-innate lymphoid cell accumulation. Only PI3Kδ inhibition and IL5 neutralization reduced the infiltration of inflammatory eosinophils. Moreover, PI3Kδ inhibition reduced goblet cell metaplasia. Conclusions: Hence, we show that PI3Kδ inhibition dampens allergic inflammatory responses by ablating key cell types and cytokines involved in T-helper-2-driven inflammatory responses.


2014 ◽  
Vol 15 (1) ◽  
Author(s):  
Go Kato ◽  
Koichiro Takahashi ◽  
Hiroki Tashiro ◽  
Keigo Kurata ◽  
Hideharu Shirai ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document