Release of cytokines by stimulated peripheral blood mononuclear cells in chronic periodontitis

Abstract

In conclusion, the results of the present study showed that E. coli LPS-stimulated PBMC from subjects with periodontitis present a different pattern of cytokine release when compared to PBMC from healthy subjects. This phenomenon could have implications locally, in periodontitis, as well as in systemic diseases.

Evaluation of cytotoxicity of different tobacco product preparations

“…IL8 is a critical signaling protein for recruitment of neutrophils and can be secreted by several cell types (Goncalves et al, 2010;Kobayashi, 2008;Larsen et al, 1989;Tomita et al, 2003). Expression and secretion of IL8 from acute exposure to the combustible tobacco preparation has been demonstrated van Leeuwen et al, 2005;Yang et al, 2006).…”

“…The chemokine IL8 mainly attracts neutrophils and lymphocytes and may result in neutrophilia (Goncalves et al, 2010;Kobayashi, 2008;Larsen et al, 1989;Tomita et al, 2003) and lymphocytosis (Jagels and Hugli, 1992;Terashima et al, 1998). In smokers, blood IL8 levels were significantly higher than those in non-smokers (Iho et al, 2003).…”

Correlation of chronic periodontitis progression with sTREM-1 and E-Cadherin salivary levels

“…/rrlm-2017 To the Editor, Chronic periodontitis is a common infectious disease in humans, caused by periodontopathic bacteria, which untreated can lead to destruction of tooth supporting tissues and eventually tooth loss (1). It is the consequence of an imbalance between the production of host inflammatory mediators, amplified by the presence of periodontal pathogens (2). In a previous study published in your journal, authors demonstrated that the salivary level of the 8-OHdG and IL-1 gene polymorphism can be used in the evaluation of the oro-dental status at patients with aggressive periodontitis (3).…”

What is the future of periodontal regeneration?

“…[5,29] In periodontitis, tissue destruction results from a combination of sustained microbial challenge and a failure of endogenous resolution of inflammation. [11,47] New data revealed that endogenous control of inflammation directly affects bone healing and regeneration. Mediators of resolution of inflammation have actions beyond control of PMN function; they exhibit receptor-mediated control of osteoclast and osteoblast function in wound healing and bone regeneration.…”