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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Language: | English |
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Frontiers Media S.A.
2017-04-01
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Series: | Frontiers in Microbiology |
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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. |
first_indexed | 2024-12-10T21:40:34Z |
format | Article |
id | doaj.art-2cc88fa5392c44d896660f2d22735728 |
institution | Directory Open Access Journal |
issn | 1664-302X |
language | English |
last_indexed | 2024-12-10T21:40:34Z |
publishDate | 2017-04-01 |
publisher | Frontiers Media S.A. |
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series | Frontiers in Microbiology |
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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