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Updated: Jan 24, 2026

In vitro Induction of Human Dental Pulp Stem Cells Toward Pancreatic Lineages
Published on: September 25, 2021
Interleukin-17 plays a role in pulp inflammation partly by WNT5A protein induction
Mengyu Liu1, Yuan Zhao2, Chenglin Wang1
1State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Dept. of Cariology and Endodonics West China Hospital of Stomatology, Sichuan University, China.
Objective:
Our study aimed to investigate the role of interleukin (IL)-17 in dental pulp inflammation and the relationship between WNT5A and IL-17.
Methods:
Immunohistochemical staining was used to detect the expression of tumor necrosis factor-α (TNF-α), WNT5A and IL-17 in pulp tissues. Anti-IL-17 neutralizing antibody was used in rat pulpitis model and to study the role of IL-17 in pulpitis. TNF-α, WNT5A or IL-17 recombinant protein were used to treat human dental pulp cells. RT-PCR, Western blot, and Enzyme linked immunosorbent assay were used to detect the expression of mRNA and protein. Transwell assay was used to measure the migration of THP-1 cells, which is a human monocytic cell line.
Results:
IL-17 and WNT5A are co-expressed in TNF-α high-expressed region in human and rat pulpitis tissue. IL-17 mainly contributes to its positive regulatory role in inflammation through up regulate cytokines and mediated macrophages migration. Anti-IL-17 neutralizing antibody can suppress the inflammatory cell infiltration and TNF-α expression in dental pulpitis. TNF-α promotes the expression of IL-17 partly through WNT5A and WNT5A regulates IL-17 expression by mitogen-activated protein kinase (MAPK)-(P38 and ERK) pathway.
Conclusions:
IL-17 acts as an inflammatory mediator in dental pulp inflammation. The expression of IL-17 can be partially regulated by WNT5A.
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