Pasteurella multocida Toxin Aggravates Ligatured-Induced Periodontal Bone Loss and Inflammation via NOD-Like Receptor Protein 3 Inflammasome

Figure 4

PMT activates NLRP3 inflammasome in vitro. (a) Protein expression of NLRP3, pro-caspase-1, activated caspase-1, pro-IL-1β, activated IL-1β, and the internal control β-actin after stimulation of PMT for 12 h by western blot. The histogram shows the quantification of band intensities. β-Actin was used for normalization relative to the control groups. (b) Protein expression of NLRP3, pro-IL-1β, activated IL-1β in whole cell lysates and supernatants, and the internal control β-actin after stimulation of PMT with or without NLRP3 inhibitor MCC950 by western blot. The histogram shows the quantification of band intensities. β-Actin was used for normalization relative to the control groups. (c) Protein expression of activated IL-1β in whole cell lysates (WCL) and supernatants (Sup) and the internal control β-actin after stimulation of PMT with or without NLRP3 inhibitor MCC950 in a series of time by western blot. The histogram shows the quantification of band intensities. β-Actin was used for normalization relative to the control groups. (d) Diagram illustrated that PMT can not only induce inflammatory reactions and the transcription of NLRP3 via the NF-κB signaling pathway but also activate NLRP3 inflammasome with the release of activated IL-1β. NLRP3 inhibitor MCC950 can significantly reduce this effect. Values are presented as ( and ). Abbreviations: IL = interleukin; mRNA = messenger RNA; NLRP3 = NOD-like receptor family pyrin domain-containing 3; NF-κB = nuclear factor kappa light chain enhancer of B cells; PMT = Pasteurella multocida toxin.

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