Abstract

Previous research into the inflammatory cell infiltrate of chronic hyperplastic candidosis (CHC) determined that the immune response is primarily composed of T cells, the majority of which are T helper (CD4+) cells. This present investigation used immunohistochemistry to further delineate the inflammatory cell infiltrate in CHC. Cells profiled were those expressing IL-17A cytokine, EBI3 and IL-12A subunits of the IL-35 cytokine, and FoxP3+ cells. Squamous cell papilloma (with Candida infection) and oral lichen planus tissues served as comparative controls to understand the local immune responses to Candida infection. The results demonstrated that Candida-induced inflammation and immune regulation co-exist in the oral mucosa of CHC and that high prevalence of cells expressing the EBI3 cytokine subunit may play an important role in this regulation. This balance between inflammation and immune tolerance toward invading Candida in the oral mucosa may be critical in determining progress of infection.

Highlights

  • Oral candidoses are a collection of infections of the mouth caused by fungi of the genusCandida

  • Our research showed that C. albicans induces M2 macrophages to produce IL-35 (EBI3/IL-12A) and suppresses Th1 cells through inhibition of IL-12p70 [18]

  • This study used immunohistochemistry to profile cells expressing the cytokine IL-17A, the cytokine subunits of EBI3 and IL-12A, and the gene transcription protein Foxp3. This was undertaken to enhance our understanding of the host immune response involved in the control of Candida at mucosal sites. Tissue sections included those of chronic hyperplastic candidosis (CHC), and comparative control tissue sections of SqP and oral lichen planus

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Summary

Introduction

These infections occur in many people at some point during their lifetime, and they are typically superficial, there is an elevated risk of systemic candidoses in severely debilitated patients [1]. This is important, as when they occur, systemic candidoses have a high level of morbidity and mortality [2]. Oral candidoses have distinct features, relating to infection site, clinical presentation, and associated risk factors [3]. Risk factors typically change the local environment and promote microbial dysbiosis, with a corresponding increase in Candida numbers. CHC is associated with tobacco smoking [4], high frequency intake of alcohol [5], and has a higher prevalence in middle-aged men [3]

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