The immune battle against Burkholderia pseudomallei in melioidosis progression

Melioidosis, caused by Burkholderia pseudomallei , is a severe and underdiagnosed infectious disease associated with high mortality. Its complex pathogenesis is supported by its ability to survive intracellularly and evade host immune responses. This review aims to summarise important host pathogen interaction which shape the melioidosis progression with emphasis on immune modulation. Following host entry, B. pseudomallei activates innate immune responses but simultaneously disrupts them by impairing macrophage function, resisting oxidative stress, and evading neutrophil extracellular traps. Mechanisms including pyroptosis, autophagy evasion, and MNGC formation contributes to bacterial persistence. The host responses were characterised by balance between both pro and anti-inflammatory cytokines, including TNF-α, IL-1β, IL-6, IFN-γ, and IL-10, which influences disease severity and outcome. Emerging evidence also highlights the role of epigenetic reprogramming and mitophagy in immune subversion. Adaptive immunity, including T-cell activation and antibody responses, plays a critical role but is often insufficient to achieve complete clearance, contributing to chronic infection and latency. Despite recent advances, gaps remain in understanding immune evasion and relapse mechanism. Improved insights into these processes are essential for developing effective vaccines and targeted immunotherapies against melioidosis.