Abstract

This review provides a snapshot of chronic bacterial infections through the lens of Burkholderia pseudomallei and detailing its ability to establish multi-nucleated giant cells (MNGC) within the host, potentially leading to the formation of pyogranulomatous lesions. We explore the role of MNGC in melioidosis disease progression and pathology by comparing the similarities and differences of melioidosis to tuberculosis, outline the concerted events in pathogenesis that lead to MNGC formation, discuss the factors that influence MNGC formation, and consider how they fit into clinical findings reported in chronic cases. Finally, we speculate about future models and techniques that can be used to delineate the mechanisms of MNGC formation and function.

Highlights

  • Melioidosis is a severe disease caused by the Gram-negative pathogen Burkholderia pseudomallei (Bpm)

  • The aim of this mini review is to provide an overview of Bpm induced multi-nucleated giant cells (MNGC) formation, to discuss factors that influence their development, to consider the role of these lesions in disease, and to highlight the features of Bpm-induced MNGCs to MNGCs in chronic tuberculosis (TB) infections

  • These MNGC are macrophages that became polyploid through interrupted cell division, not cell-to-cell fusion events like Bpm-induced MNGC

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Summary

Introduction

Melioidosis is a severe disease caused by the Gram-negative pathogen Burkholderia pseudomallei (Bpm). The severity of the abscess seems to correlate with the number of bacteria taking refuge within the lesion, and have a bias for the spleen and lung; liver abscesses have been observed [4] These abscesses have been clinically identified as granuloma-like lesions and often are confused with extrapulmonary tuberculosis. It has been postulated that Bpm uses MNGCs as a mechanism to spread from cell-to-cell to evade the external immune system, without fully understanding the host–pathogen-mediated mechanisms of formation The aim of this mini review is to provide an overview of Bpm induced MNGC formation, to discuss factors that influence their development, to consider the role of these lesions in disease, and to highlight the features of Bpm-induced MNGCs to MNGCs in chronic tuberculosis (TB) infections. We discuss future studies to understand the biological relevance of MNGCs in melioidosis

Bpm Pathogenesis Process Leading to MNGC Formation
Similarities and Differences between Melioidosis and Tuberculosis
Role of MNGCs in Disease
Final Remarks
Full Text
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