Basic ResearchAbsent in Melanoma 2 (AIM2) in Rat Dental Pulp Mediates the Inflammatory Response during Pulpitis
Section snippets
Rat Pulpitis Model
Adult male Sprague-Dawley rats, each weighing 250–350 g, were anesthetized intraperitoneally with chloral hydrate (10%, 1 mL/250 g).The mouths of the rats were opened with metal tweezers, and the right maxillary first and second molars were drilled with a high-speed handpiece and 1/4 round bar 12, 13, 14. The rats were divided into 4 groups (3-day, 5-day, 7-day, and 10-day), with each group consisting of 3 animals.
Primary Dental Pulp Cell Culture
We prepared cells from the mandibular central incisors of 2-week Sprague-Dawley
Expression of AIM2 in Rat Dental Pulp Tissues and Cells
The dental pulp tissues and stimulated dental pulp cells both expressed AIM2 (Fig. 1E and H). AIM2 was expressed in the cytoplasm of odontoblasts but not in fibroblasts from healthy pulp tissues (Fig. 1A–C). In contrast, AIM2 was strongly expressed in the inflammatory cells and fibroblasts from the inflamed dental pulp (Fig. 1D–F). The immunofluorescence staining of the dental pulp cells demonstrated the same results as those described above (Fig. 1G and H). We also performed RT-PCR and Western
Discussion
On activation, AIM2 assembles into inflammasomes, which regulate the secretion and bioactivity of cytokines belonging to the IL-1 family (IL-1β, IL-18), but the exact mechanism leading to the activation of the AIM2 inflammasome remains unclear 3, 4. AIM2 is mainly expressed in cells of the host defense system, including spleen cells, macrophages, dendritic cells, B and T lymphocytes, skin keratinocytes, peripheral blood cells, and gingival epithelial cells (19). These observations, along with a
Acknowledgments
The authors deny any conflicts of interest related to this study.
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Cited by (19)
Dysregulation of Inflammasomes in Human Dental Pulp Cells Exposed to Porphyromonas gingivalis and Fusobacterium nucleatum
2020, Journal of EndodonticsCitation Excerpt :The same group29 also monitored the role of ASC and caspase-1 and reported that up-regulation of the same inducers caused up-regulation of ASC, caspase-1, pro–IL-1β, and AIM2 in HDPCs. Wang et al30 also reported up-regulation of AIM2, caspase-1 and IL-1β levels in response to LPS and IFN-γ in rat dental pulp cells and concluded that the AIM2 inflammasome plays a role during pulpitis. In the current study, P. gingivalis + F. nucleatum + ATP infection also caused up-regulation of AIM2 and IL-1β expression levels; however, it caused down-regulation of ASC levels.
Role(s) of cytokines in pulpitis: Latest evidence and therapeutic approaches
2020, CytokineCitation Excerpt :Additionally, another important innate immune mechanism related to neutrophils is neutrophil extracellular traps (NETs) which can help trap invading bacteria and prevent their advance in the pulp tissue, as well as kill them by phagocytes [36]. Wang et al. reported that IL-1β absent in melanoma 2 (AIM2) is expressed in inflamed dental pulp tissues and participates in inflammatory responses during pulpitis [37]. It is probable that following progressive reversible pulpitis and superficial caries, innate immune responses switch to adaptive immune responses.
The effects of dimethyl fumarate on cytoplasmic LPS-induced noncanonical pyroptosis in periodontal ligament fibroblasts and dental pulp cells
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Yafei Wang and Shafei Zhai contributed equally to this work.
Supported by grant 81170946 from the National Natural Science Foundation of China.