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Severe odontogenic infections remain an important public health concern and a significant economic burden to public health care facilities. Despite this, several aspects of the disease, such as its immune response profile, remain poorly understood. The aim of this study was to search for an association between mRNA levels of the cytokines interferon-γ, interleukin (IL)-1β, tumor necrosis factor-α, IL-17A, IL-10, and transforming growth factor-β and the chemokines IL-8, CCL2/MCP-1, and CCL5 and odontogenic infection.The case group was composed of 12 patients hospitalized in consequence of severe odontogenic infection, and our control group included 12 individuals with healthy periapical tissues. Clinical samples were taken from the case (drainage site) and control (periapical interstitial fluid) groups with the aid of paper points. Total RNA was extracted, complementary DNA was synthesized, and mRNA levels were determined by quantitative polymerase chain reaction. Data analysis was performed by using SPSS, and the Wilcoxon signed rank test was used to determine statistical significance (P < .05).Data generated showed a significantly increased expression of proinflammatory cytokines (interferon-γ, IL-1β, tumor necrosis factor-α, and IL-17A), IL-8, and CCL2/MCP-1 in odontogenic infection patients. The mRNA levels of IL-10, transforming growth factor-β, and CCL5 were similar in both study groups.In general, individuals presenting with odontogenic infections exhibited extraordinary proinflammatory cytokine profiles paralleled with unaltered expression of regulatory mediators.Severe odontogenic infections are still challenging healthcare authorities.Immune response profile associated with the disease is still unknown.IFN-g, IL-1β, TNF-α, IL-17A, IL-8, and CCL2/MCP-1 mRNA levels were higher in the case group.The levels of mRNA of IL-10, TGF-β, and CCL5 were similar in case and control groups.Odontogenic infection leads to an extraordinary pro-inflammatory cytokine profile.The disease displays no alteration in regulatory mediators expression.