Activation of the Urokinase Plasminogen Activator/Urokinase Plasminogen Activator Receptor System in Periodontitis: A Case-Control Study.

Introduction: The plasminogen activating (PA) system has a multitude of functions such as wound healing, proteolytic activity, collagen degradation and cell growth, and the role of the urokinase plasminogen activator/urokinase plasminogen activator receptor (uPA/uPAR) system has been studied in many disease states. The aim of this study was to investigate salivary concentrations of uPA, uPAR and uPA activity in patients with periodontitis to identify biomarkers and novel pathogenic relationships.

Methods: Saliva samples were obtained from 169 participants, comprising patients with periodontitis (n = 103) and periodontally healthy volunteers (n = 66) and analysed for uPA and uPAR with a multiplex protein assay using proximity extension analysis in a subset of samples, followed by validation with ELISA.

Publisher Correction: Blocking elevated p38 MAPK restores efferocytosis and inflammatory resolution in the elderly.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Blocking elevated p38 MAPK restores efferocytosis and inflammatory resolution in the elderly.

Increasing age alters innate immune-mediated responses; however, the mechanisms underpinning these changes in humans are not fully understood. Using a human dermal model of acute inflammation, we found that, although inflammatory onset is similar between young and elderly individuals, the resolution phase was substantially impaired in elderly individuals. This arose from a reduction in T cell immunoglobulin mucin receptor-4 (TIM-4), a phosphatidylserine receptor expressed on macrophages that enables the engulfment of apoptotic bodies, so-called efferocytosis.

Treatment of periodontitis reduces systemic inflammation in type 2 diabetes.

Aims: To assess the impact of periodontal treatment on systemic inflammation in type 2 diabetes.

Materials And Methods: Adults with type 2 diabetes (n = 83) and without diabetes (controls, n = 75) were recruited, and participants with periodontitis received periodontal treatment and 12 months' follow-up. Biomarkers for periodontal inflammation (gingival crevicular fluid interleukin-6, tumour necrosis factor-α, interleukin-1β, interferon-γ, matrix metalloproteinase-8, matrix metalloproteinase-9, adiponectin) and serum markers of inflammation and diabetes control (glycated haemoglobin, high sensitivity C-reactive protein, interleukin-6, tumour necrosis factor-α, interleukin-1β, interferon-γ, leptin, adiponectin) were measured.

Inflammatory Resolution Triggers a Prolonged Phase of Immune Suppression through COX-1/mPGES-1-Derived Prostaglandin E.

Acute inflammation is characterized by granulocyte infiltration followed by efferocytosing mononuclear phagocytes, which pave the way for inflammatory resolution. Until now, it was believed that resolution then leads back to homeostasis, the physiological state tissues experience before inflammation occurred. However, we discovered that resolution triggered a prolonged phase of immune suppression mediated by prostanoids.