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IL-32 exacerbates adenoid hypertrophy via activating NLRP3-mediated cell pyroptosis, which promotes inflammation

  • Authors:
    • Junmei Zhang
    • Xuyuan Sun
    • Lingling Zhong
    • Bei Shen
  • View Affiliations / Copyright

    Affiliations: Department of Otolaryngology, Tianjin Children's Hospital, Tianjin 300134, P.R. China
    Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 226
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    Published online on: January 24, 2021
       https://doi.org/10.3892/mmr.2021.11865
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Abstract

Adenoid hypertrophy (AH) is a common pediatric disease caused by inflammatory stimulation. The pro-inflammatory cytokine IL-32 has been reported to promote airway inflammation and also be involved in the pyroptosis pathway. However, whether IL-32 can contribute to AH by mediating pyroptosis remains to be elucidated. The present study aimed to investigate the role of IL-32 in AH and determine the potential underlying mechanisms. Adenoid tissues were collected from healthy children and children with AH, and the expression of IL-32, NACHT LRR and PYD domains-containing protein 3 (NLRP3) and IL-1β in normal and hypertrophic tissues were measured. Human nasal epithelial cells (HNEpCs) were exposed to a series of IL-32 concentrations. HNEpCs with or without IL-32 silencing were stimulated with lipopolysaccharide (LPS), and cell proliferation, cell apoptosis, gasdermin D (GSDMD) activation, production of inflammatory cytokines and the expression levels of proteins related to the potential mechanisms were evaluated by Cell Counting Kit-8, flow cytometry, immunofluorescence staining, ELISA and western blot assays, respectively. The results showed that IL-32, NLRP3 and IL-1β exhibited higher expression in adenoid tissues with AH compared with normal tissues. In HNEpC cells, treatment with IL-32 (2 and 10 ng/ml) promoted cell proliferation, while 50 ng/ml IL-32 inhibited cell proliferation at 12, 24 and 48 h post-treatment. IL-32 (2, 10 and 50 ng/ml) also resulted in differing degrees of apoptosis, GSDMD activation, release of IL-1β, IL-6 and TNF-α, and increased protein expression levels of NLRP3, cleaved-caspase-1, activated GSDMD, nucleotide-binding oligomerization domain-containing protein (NOD) 1/2 and Toll-like receptor (TLR)4 in a concentration-dependent manner. In addition, compared with the LPS group, IL-32 knockdown significantly inhibited LPS-induced enhancement of cell proliferation, cell apoptosis, GSDMD activation and production of inflammatory cytokines, and reversed the increased protein expression of NLRP3, cleaved-caspase-1, activated GSDMD, NOD1/2 and TLR4. In conclusion, IL-32 may play a role in the progression of AH via promoting inflammation, and the potential mechanism may involve the activation of NLRP3-mediated pyroptosis.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang J, Sun X, Zhong L and Shen B: IL-32 exacerbates adenoid hypertrophy via activating NLRP3-mediated cell pyroptosis, which promotes inflammation. Mol Med Rep 23: 226, 2021.
APA
Zhang, J., Sun, X., Zhong, L., & Shen, B. (2021). IL-32 exacerbates adenoid hypertrophy via activating NLRP3-mediated cell pyroptosis, which promotes inflammation. Molecular Medicine Reports, 23, 226. https://doi.org/10.3892/mmr.2021.11865
MLA
Zhang, J., Sun, X., Zhong, L., Shen, B."IL-32 exacerbates adenoid hypertrophy via activating NLRP3-mediated cell pyroptosis, which promotes inflammation". Molecular Medicine Reports 23.3 (2021): 226.
Chicago
Zhang, J., Sun, X., Zhong, L., Shen, B."IL-32 exacerbates adenoid hypertrophy via activating NLRP3-mediated cell pyroptosis, which promotes inflammation". Molecular Medicine Reports 23, no. 3 (2021): 226. https://doi.org/10.3892/mmr.2021.11865
Copy and paste a formatted citation
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Spandidos Publications style
Zhang J, Sun X, Zhong L and Shen B: IL-32 exacerbates adenoid hypertrophy via activating NLRP3-mediated cell pyroptosis, which promotes inflammation. Mol Med Rep 23: 226, 2021.
APA
Zhang, J., Sun, X., Zhong, L., & Shen, B. (2021). IL-32 exacerbates adenoid hypertrophy via activating NLRP3-mediated cell pyroptosis, which promotes inflammation. Molecular Medicine Reports, 23, 226. https://doi.org/10.3892/mmr.2021.11865
MLA
Zhang, J., Sun, X., Zhong, L., Shen, B."IL-32 exacerbates adenoid hypertrophy via activating NLRP3-mediated cell pyroptosis, which promotes inflammation". Molecular Medicine Reports 23.3 (2021): 226.
Chicago
Zhang, J., Sun, X., Zhong, L., Shen, B."IL-32 exacerbates adenoid hypertrophy via activating NLRP3-mediated cell pyroptosis, which promotes inflammation". Molecular Medicine Reports 23, no. 3 (2021): 226. https://doi.org/10.3892/mmr.2021.11865
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