The Effect of IL-35 on the Expression of Nasal Epithelial-Derived Proinflammatory Cytokines

5Citations
Citations of this article
13Readers
Mendeley users who have this article in their library.
Get full text

Abstract

Background. Airway epithelium plays an important role during the development of allergic rhinitis (AR), which is characterized by production of thymic stromal lymphopoietin (TSLP), interleukin 33 (IL-33), and interleukin 25 (IL-25). IL-35, mainly expressed by Treg cells, have negative regulation in Th2, Th17, and ILC2 inflammation. However, the effect of IL-35 on human nasal epithelial cells (HNECs) especially the secretion of nasal epithelial-derived proinflammatory cytokines as well as the possible mechanism is still unclear. Methods. HNECs were cultured and stimulated by various stimulators. The expression of IL-33, IL-25, TSLP, eotaxin-1, eotaxin-2, and eotaxin-3 from supernatant was measured using real-time reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). AR mice were developed to verify the effect of IL-35 on nasal epithelial cells in vivo. Results. After Poly I:C stimulation, IL-35 inhibited the production of IL-25, and TSLP from HNECs increased significantly compared with baseline levels (P<0.05). After Dermatophagoides pteronyssinus or Aspergillus fumigatus stimulation, IL-35 inhibited the production of IL-25, IL-33, and TSLP from HNECs increased significantly compared with baseline levels (P<0.05). After Dermatophagoides pteronyssinus, IL-35 inhibited the production of eotaxin-1, eotaxin-2, and eotaxin-3 released from HNECs increased significantly compared with baseline levels (P<0.05). Similarly, IL-35-treated AR mice presented with decreased expression of IL-33, IL-25, TSLP, eotaxin-1, eotaxin-2, and eotaxin-3 in nasal lavage fluid. Conclusion. IL-35 suppressed both type 2 inflammation-inducing cytokines and eosinophil chemotactic factor from HNECs, suggesting the important role of IL-35 during the development of AR.

References Powered by Scopus

IL-33, an interleukin-1-like cytokine that signals via the IL-1 receptor-related protein ST2 and induces T helper type 2-associated cytokines

3167Citations
N/AReaders
Get full text

Innate lymphoid cells-a proposal for uniform nomenclature

2005Citations
N/AReaders
Get full text

Nuocytes represent a new innate effector leukocyte that mediates type-2 immunity

1782Citations
N/AReaders
Get full text

Cited by Powered by Scopus

New insights into the function of Interleukin-25 in disease pathogenesis

23Citations
N/AReaders
Get full text

Current Insight into the Role of IL-35 and Its Potential Involvement in the Pathogenesis and Therapy of Atopic Dermatitis

11Citations
N/AReaders
Get full text

CD19<sup>+</sup>CD24<sup>high</sup>CD27<sup>+</sup> B cell and interleukin 35 as potential biomarkers of disease activity in systemic lupus erythematosus patients

11Citations
N/AReaders
Get full text

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Cite

CITATION STYLE

APA

Nie, M., Zeng, Q., Xi, L., Tang, Y., Luo, R., & Liu, W. (2021). The Effect of IL-35 on the Expression of Nasal Epithelial-Derived Proinflammatory Cytokines. Mediators of Inflammation, 2021. https://doi.org/10.1155/2021/1110671

Readers' Seniority

Tooltip

PhD / Post grad / Masters / Doc 3

38%

Researcher 3

38%

Professor / Associate Prof. 2

25%

Readers' Discipline

Tooltip

Medicine and Dentistry 4

50%

Agricultural and Biological Sciences 2

25%

Pharmacology, Toxicology and Pharmaceut... 1

13%

Chemical Engineering 1

13%

Save time finding and organizing research with Mendeley

Sign up for free