Trypanosoma brucei Lipophosphoglycan Induces the Formation of Neutrophil Extracellular Traps and Reactive Oxygen Species Burst via Toll-Like Receptor 2, Toll-Like Receptor 4, and c-Jun N-Terminal Kinase Activation

• DOI: 10.3389/fmicb.2021.713531
• Publication Date: 2021-07-28T06:56:37Z
• Authors: Kai Zhang; Ning Jiang; Xiaoyu Sang; Ying Feng; Ran Chen; Qijun Chen
• Keywords: Lipophosphoglycan; Neutrophil Extracellular Traps; Sphingosine Kinase; Respiratory burst

Trypanosoma brucei is the causative agent of African animal trypanosomosis, which mainly parasitizes blood host. Lipophosphoglycan (LPG), a polymer anchored to surface parasites, activates host immune response. In this study, we revealed that T. LPG stimulated neutrophils form neutrophil extracellular traps (NETs) and release reactive oxygen species (ROS). We further analyzed involvement toll-like receptor 2 (TLR2) 4 (TLR4) explored activation signaling pathway enzymes in response stimulation. During stimulation by LPG, blockade using anti-TLR2 anti-TLR4 antibodies reduced phosphorylation c-Jun N-terminal kinase (JNK), DNA from NETs, burst ROS. Moreover, addition JNK inhibitor nicotinamide adenine dinucleotide phosphate (NADPH) oxidase exhibited similar effects. Our data suggest through TLR2 TLR4 recognition, causes formation NETs