Systemic Th17 response in the presence of periodontal inflammation.

Lina J Suárez,Roger M Arce,Daniel E Vargas,Adriana Rodríguez,Nelly S Roa

doi:10.1590/1678-7757-2019-0490

Abstract

The relationship between periodontitis and the pathogenesis of other inflammatory diseases, such as diabetes, rheumatoid arthritis and obesity has been an important topic of study in recent decades. The Th17 pathway plays a significant role in how local inflammation can influence systemic inflammation in the absence of systemic pathology.Objective:To determine Th17 biased-cells in systemically healthy patients in the presence of generalized chronic periodontitis.Methodology:A total of 28 patients were recruited without systemic inflammatory pathology, which was determined by clinical history, the Health Assessment Questionnaire (HAQ) and rheumatoid factor detection. Of these patients, 13 were diagnosed as healthy/gingivitis (H/G) and 15 as generalized chronic periodontitis (GCP). Th17 (CD4+CD161+) cells and Th17IL23R+ (CD4+CD161+IL-23R+) cells were quantified by flow cytometry, based on the total cells and on the lymphocyte region, termed the “enriched population” (50,000 events for each).Results:The percentages of Th17 cells of the H/G and periodontitis groups were similar on total cells and enriched population (19 vs 21.8; p=4.134 and 19.6 vs 21.8; p=0.55). However, Th17IL23R+ cells differ significantly between periodontally healthy patients and generalized chronic periodontitis patients in both total cell (0.22% vs 0.65%; p=0.0004) and enriched populations (0.2% vs 0.75%; p=0.0266).Conclusions:GCP patients (otherwise systemically healthy) were characterized by increased Th17-proinflammatory cell phenotype positive for the IL-23 receptor in peripheral blood. The proportion of Th17 cells that are negative for the IL-23 receptor in the peripheral blood of systemically healthy patients seemed to be unaffected by the presence or absence of chronic periodontitis.

Highlights

Periodontitis, currently recognized as a chronic inflammatory disease, has been linked to many other proinflammatory pathologies
The proportion of Th17 cells that are negative for the IL-23 receptor in the peripheral blood of systemically healthy patients seemed to be unaffected by the presence or absence of chronic periodontitis
CD161, known as killer cell lectin-like receptor B1 (KLRB1), is a marker associated with the pathogenesis of inflammatory diseases2 by T-cell proliferation and induction of Th1 cytokine secretion

Summary

Introduction

Periodontitis, currently recognized as a chronic inflammatory disease, has been linked to many other proinflammatory pathologies. Naïve T helper (Th) cells are activated by recognition of a peptide antigen–class II major histocompatibility complex presented by antigenpresenting cells and their interaction with the T-cell receptor. Each type of effector cell phenotype presents different profiles of cytokine secretion eliciting unique functional characteristics during the inflammatory response. Th17 cells differentiate into subprofiles with functions determined by the cytokines in the environment and characterized by the expression of surface markers. CD161, known as killer cell lectin-like receptor B1 (KLRB1), is a marker associated with the pathogenesis of inflammatory diseases by T-cell proliferation and induction of Th1 cytokine secretion. IL-23 regulates the overexpression of IL23R directly or indirectly through TGF-b3 to increase its own signal and induce functionally mature Th17 pathogenic cells. In the absence of IL-23 signal, Th17 cells differentiate into non-pathogenic Th17-producing IL-10.5

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