Abstract
Periodontitis is defined as inflammation affecting the supporting tissue of teeth. Periodontal pathogens initiate the disease and induce inflammatory host response. Hypoxia may accelerate the process by producing pro-inflammatory factors. The aim of this study is to investigate the effect of Porphyromonas gingivalis (P. gingivalis) lipopolysaccharides (LPS) and Escherichia coli (E. coli) LPS in inducing caspase-1 activation in normoxic or hypoxic phases. The results showed that healthy gingiva was in a normoxic phase (HIF-1α negative). However, hypoxia appeared in periodontitis, in which NLRP3, cleaved-caspase-1, interleukin 1 beta (IL-1β) and caspase-1-induced cell death was enhanced in periodontitis specimens. The in vitro experiment showed that P. gingivalis LPS slightly decreased the level of NLRP3 and IL-1β in gingival fibroblasts under normoxia. Surprisingly, hypoxia reversed the effects of P. gingivalis LPS, highly promoted caspase-1 activation and IL-1β maturation. E. coli LPS, a kind of pathogen-associated molecular pattern (PAMP) was chosen to simulate the effect of Gram-negative microbiota. Different from P. gingivalis LPS, E. coli LPS enhanced IL-1β maturation both in normoxia and hypoxia. Moreover, E. coli LPS turned normoxia into hypoxia phase in experimental periodontitis model, which may subsequently propel the inflammatory effect of P. gingivalis LPS. It was concluded that E. coli LPS induced a hypoxic phase, which is a combing pathological factor of P. gingivalis LPS in caspase-1 activating and IL-1β maturation in periodontal inflammation.
Highlights
Periodontitis is defined as chronic inflammation of tooth supporting tissues
We found hypoxia to be common in human periodontitis afflicted gingival tissues, as evidence by the expression of the transcription factor, HIF-1α (Ng et al, 2011; Figure 1A)
In response to bacterial infection, the NLRP3 inflammasome would be assembled for the caspase-1 activation
Summary
Periodontitis is defined as chronic inflammation of tooth supporting tissues. Imbalanced host-microbe interaction lead to disease initiation and progression (Cheng et al, 2015b). Pathological bacteria are significant inflammatory stimulus that triggers various cell types (epithelial cells, periodontal ligament fibroblasts, leukocytes, osteoblasts) to release pro-inflammatory factors, e.g., IL-1β, IL-6, tumor necrosis factor α (TNF-α), proteases, matrix metalloproteinases, prostaglandins (PGE), and so on Trindade et al (2014). These inflammatory molecules lead to the breakdown of connective tissue and bone (Di Benedetto et al, 2013)
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