Secretory leukocyte protease inhibitor reduces inflammation and alveolar bone resorption in LPS-induced periodontitis in rats and in MC3T3-E1 preosteoblasts

Abstract

In periodontitis, alveolar bone resorption is induced by excessive host immune and inflammatory response against bacterial infection. Secretory leukocyte protease inhibitor (SLPI) has antibacterial and anti-inflammatory activity in inflammatory responses. SLPI inhibits joint inflammation and bone destruction, but the function of SLPI in periodontitis is unclear. Therefore, this study investigated whether SLPI inhibits the inflammatory response and alveolar bone resorption in LPS-induced periodontitis of rats. Micro-computed tomography and histological analysis showed that SLPI inhibited alveolar bone resorption by LPS-induced periodontitis. Immunohistochemistry revealed that SLPI decreased tumor necrosis factor-α (TNFα) and interleukine-1β (IL-1β) expression in periodontitis tissue, and decreased mRNA and protein expression of TNF-α and IL-1β in LPS-stimulated MC3T3-E1 cells. The results indicated that SLPI reduced alveolar bone resorption in LPS-induced periodontitis and inhibited inflammatory cytokine, such as TNF-α and IL-1β, expression in LPS-stimulated MC3T3-E1 preosteoblasts. Therefore, SLPI could be a regulatory molecule by inhibiting alveolar bone resorption through the reduction of inflammatory cytokines, and inducing osteoblast activation for bone formation. ARTICLE HISTORY

The cardioprotective effects of secretory leukocyte protease inhibitor against myocardial ischemia/reperfusion injury

“…The treatment of monocytes with exogenous SLPI inhibited the TNF-α-induced caspase-3 activation and the DNA degradation associated with apoptosis in monocytes ( 28 ). The results of other studies investigating different types of cells suggest that treatment with rhSLPI induces similar anti-inflammatory and anti-apoptotic effects ( 29 – 31 ).…”

Inhibitory Effects on Oral Microbial Activity and Production of Lipopolysaccharides-Induced Pro-Inflammatory Mediators in Raw264.7 Macrophages of Ethanol Extract of Perilla flutescens (L.) Britton

“…S. mutans plays an important role in the formation of dental plaque which is the basis for colonization of pathogenic bacteria that can cause oral disease and induce dental caries 12,13) . Periodontal tissues, including the cementum, periodontal ligaments, and alveolar bone surrounding the tooth root, are plagued by bacterial infection as acute and chronic periodontal diseases 17) . If periodontal disease is left untreated, excessive inflammatory reactions and alveolar bone resorption progress, leading to tooth loss 17) .…”

“…Periodontal tissues, including the cementum, periodontal ligaments, and alveolar bone surrounding the tooth root, are plagued by bacterial infection as acute and chronic periodontal diseases 17) . If periodontal disease is left untreated, excessive inflammatory reactions and alveolar bone resorption progress, leading to tooth loss 17) . Periodontal disease is initiated by the overgrowth of special gramnegative anaerobic bacteria such as A. actinomycetemcomitans, Porphyromonas gingivalis and Fusobacterium nucleatum, and the number increases significantly during the inflammatory conditions of periodontal tissues 15) .…”

“…LPS from gram-negative oral bacteria is an important component of the outer membrane of bacteria 17) , and induces the up-regulation and secretion of pro-inflammatory enzymes, such as nitric oxide synthase (NOS) and cyclooxygenase (COX) from immune cells (monocytes, macrophages and neutrophils) 17,18) . iNOS and COX-2, as inflammatory inducers, induce the secretion of large amounts of inflammatory mediators, such as NO and PGE2, and inflammatory cytokines such as tumor necrosis factor alpha and interleukin 1 beta, respectively 18,19) .…”

Anti-Oral Microbial Activity and Anti-Inflammatory Effects of Rosmarinic Acid in Lipopolysaccharide-Stimulated MC3T3-E1 Osteoblastic Cells on a Titanium Surface

“…TNF- and IL-1 are both osteoclastogenic factors and bone resorption factors 29) . TNF- and IL-1, produced through NF-B signaling inhibit osteoblastic bone formation and induce an increase in the expression of the receptor activator of NF-B ligand (RANKL), and the secreted RANKL induces the formation of osteoclasts and plays an important role in the initiation and acceleration of alveolar bone resorption and periodontal disease 23,24) .…”