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2016 ; 84
(6
): 1857-1865
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Macrophage Apoptosis Triggered by IpaD from Shigella flexneri
#MMPMID27068089
Arizmendi O
; Picking WD
; Picking WL
Infect Immun
2016[Jun]; 84
(6
): 1857-1865
PMID27068089
show ga
Shigellosis, a potentially severe bacillary dysentery, is an infectious
gastrointestinal disease caused by Shigella spp. Shigella invades the human
colonic epithelium and avoids clearance by promoting apoptosis of resident immune
cells in the gut. This process is dependent on the Shigella type III secretion
system (T3SS), which injects effector proteins into target cells to alter their
normal cellular functions. Invasion plasmid antigen D (IpaD) is a structural
component that forms a complex at the tip of the T3SS apparatus needle. Recently,
IpaD has also been shown to indirectly induce apoptosis in B lymphocytes. In this
study, we explored the cytotoxicity profile during macrophage infection by
Shigella and discovered that the pathogen induces macrophage cell death
independent of caspase-1. Our results demonstrate that IpaD triggers apoptosis in
macrophages through activation of host caspases accompanied by mitochondrial
disruption. Additionally, we found that the IpaD N-terminal domain is necessary
for macrophage killing and SipD, a structural homologue from Salmonella, was
found to promote similar cytotoxicity. Together, these findings indicate that
IpaD is a contributing factor to macrophage cell death during Shigella infection.
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