Effects of halichlorine and pinnaic acid structural analogues on the enhancement of phagocytosis of methicillin resistant Staphylococcus aureus (MRSA) via U937 macrophages in vitro

Abstract

Introduction: Periodontitis is a chronic inflammatory disease of multifactorial etiology. Although gram negative anaerobes are essential in initiating the disease, many other factors determine the course and progression of the periodontal destruction. Among the various risk factors, the genetic component of the host plays a major role in periodontal destruction. The microbial agents are first screened by the pattern like receptors – Toll like receptors (TLR) and the signals are processed intracellularly by Nod like receptors NLRP3. Thus, aim of the study was to analyze the association of 3’UTR polymorphisms of TLR4, NLRP3 gene and the micro RNAs regulating this region. The subjects were stratified into three groups chronic periodontitis, aggressive periodontitis and controls. The sample size was 240. DNA extraction from blood samples was done and the polymorphisms were analyzed using real time PCR. The TLR4 (rs11536889), NLRP3 (rs10802501), miR-146a (rs2910164) were analyzed in this study. Periodontitis (PD) is a typical irresistible illness in the oral pit, influencing around 20–half of the populace on the planet. The ailment starts with a bacterial attack in the periodontal tissue which actuates the enactment of invulnerable reaction and, the diligence of microorganisms and the irregularity in the host resistant reaction, lead to reformist periodontium tissue harm. Furthermore, hereditary and epigenetic factors add to the advancement of PD, for example, singular contrasts in the host resistant reaction, smoking propensities, sex, helpless oral-cleanliness, and foundational ailments as diabetes mellitus and rheumatic ailments. Hereditary variations that impact the defenselessness and the seriousness of periodontitis emerge from changes that happen in the qualities and in the organic atoms that they encode including cytokines.