Toxoplasma gondii Infection Induces High Mobility Group Box 1 Released from Mouse Macrophages

High mobility group box 1 (HMGB1) is abundantly expressed in intracellular engaged DNA binding ability. However, more importantly, it is a weapon against infection through proinflammatory response and immune regulation while released to extracellular. Toxoplasma gondii causes inflammatory pathologic...

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Main Authors: Qun Liu, Hui Wang, Muzi Li, Jing Liu, Jianhai Xu, Qian Han
Format: Article
Language:English
Published: Frontiers Media S.A. 2017-04-01
Series:Frontiers in Microbiology
Subjects:
Online Access:http://journal.frontiersin.org/article/10.3389/fmicb.2017.00658/full
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author Qun Liu
Hui Wang
Hui Wang
Muzi Li
Jing Liu
Jianhai Xu
Qian Han
author_facet Qun Liu
Hui Wang
Hui Wang
Muzi Li
Jing Liu
Jianhai Xu
Qian Han
author_sort Qun Liu
collection DOAJ
description High mobility group box 1 (HMGB1) is abundantly expressed in intracellular engaged DNA binding ability. However, more importantly, it is a weapon against infection through proinflammatory response and immune regulation while released to extracellular. Toxoplasma gondii causes inflammatory pathological changes including ileitis and encephalitis in chronic infection. To investigate whether HMGB1 contributes to the toxoplasmosis lesions, we examined HMGB1 changes during T. gondii infection. The results showed that HMGB1 transcription was down-regulated in the murine macrophage ANA1 cell line and mouse peritoneal macrophages (PMΦs) after T. gondii inoculation, but up-regulated in the IFN-γ treated macrophages and the intraperitoneal exudate cells from the T. gondii infected mice. The content of intracellular HMGB1 are basically consistent with the transcription levels in ANA1 assay, while there were no obvious changes in the mouse PMΦs. Both ANA1 and mouse PMΦs released HMGB1 after parasites infection, and no obvious HMGB1 aggregation in cytoplasm compare to the IFN-γ treatment group. Furthermore, we demonstrated that T. gondii invasion led to HMGB1 release, which was dependent on the Caspase 1 activity. These finding should promote to further investigate the functions of extracellular HMGB1 in the toxoplasmosis.
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spelling doaj.art-2cc88fa5392c44d896660f2d227357282022-12-22T01:32:31ZengFrontiers Media S.A.Frontiers in Microbiology1664-302X2017-04-01810.3389/fmicb.2017.00658250085Toxoplasma gondii Infection Induces High Mobility Group Box 1 Released from Mouse MacrophagesQun Liu0Hui Wang1Hui Wang2Muzi Li3Jing Liu4Jianhai Xu5Qian Han6National Animal Protozoa Laboratory, College of Veterinary Medicine, China Agricultural UniversityBeijing, ChinaNational Animal Protozoa Laboratory, College of Veterinary Medicine, China Agricultural UniversityBeijing, ChinaDepartment of Pathogenic Biology, Chengdu Medical CollegeChengdu, ChinaNational Animal Protozoa Laboratory, College of Veterinary Medicine, China Agricultural UniversityBeijing, ChinaNational Animal Protozoa Laboratory, College of Veterinary Medicine, China Agricultural UniversityBeijing, ChinaNational Animal Protozoa Laboratory, College of Veterinary Medicine, China Agricultural UniversityBeijing, ChinaLaboratory of Tropical Veterinary Medicine and Vector Biology, Hainan Key Laboratory of Sustainable Utilization of Tropical Bioresources, Hainan UniversityHaikou, ChinaHigh mobility group box 1 (HMGB1) is abundantly expressed in intracellular engaged DNA binding ability. However, more importantly, it is a weapon against infection through proinflammatory response and immune regulation while released to extracellular. Toxoplasma gondii causes inflammatory pathological changes including ileitis and encephalitis in chronic infection. To investigate whether HMGB1 contributes to the toxoplasmosis lesions, we examined HMGB1 changes during T. gondii infection. The results showed that HMGB1 transcription was down-regulated in the murine macrophage ANA1 cell line and mouse peritoneal macrophages (PMΦs) after T. gondii inoculation, but up-regulated in the IFN-γ treated macrophages and the intraperitoneal exudate cells from the T. gondii infected mice. The content of intracellular HMGB1 are basically consistent with the transcription levels in ANA1 assay, while there were no obvious changes in the mouse PMΦs. Both ANA1 and mouse PMΦs released HMGB1 after parasites infection, and no obvious HMGB1 aggregation in cytoplasm compare to the IFN-γ treatment group. Furthermore, we demonstrated that T. gondii invasion led to HMGB1 release, which was dependent on the Caspase 1 activity. These finding should promote to further investigate the functions of extracellular HMGB1 in the toxoplasmosis.http://journal.frontiersin.org/article/10.3389/fmicb.2017.00658/fullToxoplasma gondiiHMGB1IFN-γproinflammatory responsecaspase-1inflammasome
spellingShingle Qun Liu
Hui Wang
Hui Wang
Muzi Li
Jing Liu
Jianhai Xu
Qian Han
Toxoplasma gondii Infection Induces High Mobility Group Box 1 Released from Mouse Macrophages
Frontiers in Microbiology
Toxoplasma gondii
HMGB1
IFN-γ
proinflammatory response
caspase-1
inflammasome
title Toxoplasma gondii Infection Induces High Mobility Group Box 1 Released from Mouse Macrophages
title_full Toxoplasma gondii Infection Induces High Mobility Group Box 1 Released from Mouse Macrophages
title_fullStr Toxoplasma gondii Infection Induces High Mobility Group Box 1 Released from Mouse Macrophages
title_full_unstemmed Toxoplasma gondii Infection Induces High Mobility Group Box 1 Released from Mouse Macrophages
title_short Toxoplasma gondii Infection Induces High Mobility Group Box 1 Released from Mouse Macrophages
title_sort toxoplasma gondii infection induces high mobility group box 1 released from mouse macrophages
topic Toxoplasma gondii
HMGB1
IFN-γ
proinflammatory response
caspase-1
inflammasome
url http://journal.frontiersin.org/article/10.3389/fmicb.2017.00658/full
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