Matsayapan Pudla1, Chanya Srisaowakarn2, Pongsak Utaisincharoen2. 1. Department of Oral Microbiology, Faculty of Dentistry, Mahidol University, Bangkok, 10400, Thailand. matsayapan.pud@mahidol.ac.th. 2. Department of Microbiology, Faculty of Science, Mahidol University, Bangkok, 10400, Thailand.
Abstract
OBJECTIVE: The aim of the present study is to investigate the participation of NLRP12 in Porphyromonas gingivalis LPS-activated mouse macrophages. METHODS: NLRP12-depleted mouse macrophages were stimulated with P. gingivalis LPS (1 μg/ml.). At indicated time points, the treated cells were lysed and the supernatant from treated cells was collected. Gene and protein expression of NLRP12 and iNOS were determined by RT-PCR and immunoblotting, respectively. The level of TNF-α production in the supernatant of the activated cells was determined by ELISA. RESULTS AND CONCLUSION: NLRP12 was upregulated in response to stimulation with P. gingivalis LPS. In addition, when NLRP12 was depleted in P. gingivalis LPS-treated macrophages, an increase in TNF-α production and iNOS expression were observed when compared to those of the control cells, indicating that NLRP12 downregulates the inflammatory cytokine and antimicrobial molecule production in the macrophages.
OBJECTIVE: The aim of the present study is to investigate the participation of NLRP12 in Porphyromonas gingivalis LPS-activated mouse macrophages. METHODS:NLRP12-depleted mouse macrophages were stimulated with P. gingivalis LPS (1 μg/ml.). At indicated time points, the treated cells were lysed and the supernatant from treated cells was collected. Gene and protein expression of NLRP12 and iNOS were determined by RT-PCR and immunoblotting, respectively. The level of TNF-α production in the supernatant of the activated cells was determined by ELISA. RESULTS AND CONCLUSION:NLRP12 was upregulated in response to stimulation with P. gingivalis LPS. In addition, when NLRP12 was depleted in P. gingivalis LPS-treated macrophages, an increase in TNF-α production and iNOS expression were observed when compared to those of the control cells, indicating that NLRP12 downregulates the inflammatory cytokine and antimicrobial molecule production in the macrophages.
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