Activation of Mast Cells Promote Plasmodium berghei ANKA Infection in Murine Model
Malaria, a mosquito-borne infectious disease, is a severe health problem worldwide. As reported, some anti-malarial drugs with anti-parasitic properties also block mast cells (MCs) activities. It is hypothesized that MCs activity may be correlated with the pathogenesis of malaria. Thus, the role of...
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| Format: | Article |
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Frontiers Media S.A.
2019-09-01
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| Series: | Frontiers in Cellular and Infection Microbiology |
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| Online Access: | https://www.frontiersin.org/article/10.3389/fcimb.2019.00322/full |
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| author | Bo Huang Bo Huang Shiguang Huang Xiaoyan Chen Xiao Bo Liu Qiang Wu Yongfei Wang Xiaobo Li Kunning Li Kunning Li Hongzhi Gao Shan Cen Rongtuan Lin Zhenlong Liu Xiaobao Jin |
| author_facet | Bo Huang Bo Huang Shiguang Huang Xiaoyan Chen Xiao Bo Liu Qiang Wu Yongfei Wang Xiaobo Li Kunning Li Kunning Li Hongzhi Gao Shan Cen Rongtuan Lin Zhenlong Liu Xiaobao Jin |
| author_sort | Bo Huang |
| collection | DOAJ |
| description | Malaria, a mosquito-borne infectious disease, is a severe health problem worldwide. As reported, some anti-malarial drugs with anti-parasitic properties also block mast cells (MCs) activities. It is hypothesized that MCs activity may be correlated with the pathogenesis of malaria. Thus, the role of MCs on malarial pathogenesis and the involved physiological action and pathways need to be further investigated. This study aimed to investigate the effect of MCs activation on malaria disease severity using KunMing mice with Plasmodium berghei ANKA (PbANKA) infection treated with MCs degranulator (compound 48/80, C48/80) or MCs stabilizer (disodium cromoglycate, DSCG). PbANKA infection caused a dramatic increase in MCs density and level of MCs degranulation in cervical lymph node (CLN) and skin. Compared with infected control, C48/80 treatment had shortened survival time, increased parasitemia, exacerbated liver inflammation and CLN hyperplasia, accompanied with increase in vascular leakage and leukocyte number. The infected mice with C48/80 treatment also elevated the release of CCL2, CXCL1, and MMP-9 from MCs in CLN and skin, and TNF-α, IFN-γ, CCR2, and CXCR2 mRNA expression in CLN and liver. In contrast, the infected mice treated with DSCG showed longer survival time, lower parasitemia, improved liver inflammation and CLN hyperplasia, followed by a decline of vascular leakage and leukocyte number. Decreased MCs-derived CCL2, CXCL1, and MMP-9 from CLN and skin, mRNA expression in CLN and liver (TNF-α, IFN-γ, CCR2, and CXCR2) were also observed in infected mice with DSCG treatment. Our data indicated that MCs activation may facilitate the pathogenesis of PbANKA infection. |
| first_indexed | 2024-12-21T19:25:56Z |
| format | Article |
| id | doaj.art-05a1c1ad7a194f51a76db5d7cc78a28a |
| institution | Directory Open Access Journal |
| issn | 2235-2988 |
| language | English |
| last_indexed | 2024-12-21T19:25:56Z |
| publishDate | 2019-09-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Cellular and Infection Microbiology |
| spelling | doaj.art-05a1c1ad7a194f51a76db5d7cc78a28a2022-12-21T18:52:50ZengFrontiers Media S.A.Frontiers in Cellular and Infection Microbiology2235-29882019-09-01910.3389/fcimb.2019.00322485852Activation of Mast Cells Promote Plasmodium berghei ANKA Infection in Murine ModelBo Huang0Bo Huang1Shiguang Huang2Xiaoyan Chen3Xiao Bo Liu4Qiang Wu5Yongfei Wang6Xiaobo Li7Kunning Li8Kunning Li9Hongzhi Gao10Shan Cen11Rongtuan Lin12Zhenlong Liu13Xiaobao Jin14Guangdong Provincial Key Laboratory of Pharmaceutical Bioactive Substances, School of Life Sciences and Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou, ChinaDepartment of Pathogen Biology and Immunology, School of Life Sciences and Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou, ChinaSchool of Stomatology, Jinan University, Guangzhou, ChinaGuangdong Provincial Key Laboratory of Pharmaceutical Bioactive Substances, School of Life Sciences and Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou, ChinaDepartment of Pathogen Biology and Immunology, School of Life Sciences and Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou, ChinaDepartment of Pathogen Biology and Immunology, School of Life Sciences and Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou, ChinaCollege of Life Science and Technology, Jinan University, Guangzhou, ChinaDepartment of Pathogen Biology and Immunology, School of Life Sciences and Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou, ChinaLady Davis institute for Medical Research, Jewish General Hospital, McGill University, Montreal, QC, CanadaDivision of Experimental Medicine, Department of Medicine, McGill University, Montreal, QC, CanadaDepartment of Neurosurgery, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, ChinaDepartment of Immunology, Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences, Beijing, ChinaDivision of Experimental Medicine, Department of Medicine, McGill University, Montreal, QC, CanadaDivision of Experimental Medicine, Department of Medicine, McGill University, Montreal, QC, CanadaGuangdong Provincial Key Laboratory of Pharmaceutical Bioactive Substances, School of Life Sciences and Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou, ChinaMalaria, a mosquito-borne infectious disease, is a severe health problem worldwide. As reported, some anti-malarial drugs with anti-parasitic properties also block mast cells (MCs) activities. It is hypothesized that MCs activity may be correlated with the pathogenesis of malaria. Thus, the role of MCs on malarial pathogenesis and the involved physiological action and pathways need to be further investigated. This study aimed to investigate the effect of MCs activation on malaria disease severity using KunMing mice with Plasmodium berghei ANKA (PbANKA) infection treated with MCs degranulator (compound 48/80, C48/80) or MCs stabilizer (disodium cromoglycate, DSCG). PbANKA infection caused a dramatic increase in MCs density and level of MCs degranulation in cervical lymph node (CLN) and skin. Compared with infected control, C48/80 treatment had shortened survival time, increased parasitemia, exacerbated liver inflammation and CLN hyperplasia, accompanied with increase in vascular leakage and leukocyte number. The infected mice with C48/80 treatment also elevated the release of CCL2, CXCL1, and MMP-9 from MCs in CLN and skin, and TNF-α, IFN-γ, CCR2, and CXCR2 mRNA expression in CLN and liver. In contrast, the infected mice treated with DSCG showed longer survival time, lower parasitemia, improved liver inflammation and CLN hyperplasia, followed by a decline of vascular leakage and leukocyte number. Decreased MCs-derived CCL2, CXCL1, and MMP-9 from CLN and skin, mRNA expression in CLN and liver (TNF-α, IFN-γ, CCR2, and CXCR2) were also observed in infected mice with DSCG treatment. Our data indicated that MCs activation may facilitate the pathogenesis of PbANKA infection.https://www.frontiersin.org/article/10.3389/fcimb.2019.00322/fullPlasmodium bergheimast cellsdegranulationpathogenesisimmune responsesvascular permeability |
| spellingShingle | Bo Huang Bo Huang Shiguang Huang Xiaoyan Chen Xiao Bo Liu Qiang Wu Yongfei Wang Xiaobo Li Kunning Li Kunning Li Hongzhi Gao Shan Cen Rongtuan Lin Zhenlong Liu Xiaobao Jin Activation of Mast Cells Promote Plasmodium berghei ANKA Infection in Murine Model Frontiers in Cellular and Infection Microbiology Plasmodium berghei mast cells degranulation pathogenesis immune responses vascular permeability |
| title | Activation of Mast Cells Promote Plasmodium berghei ANKA Infection in Murine Model |
| title_full | Activation of Mast Cells Promote Plasmodium berghei ANKA Infection in Murine Model |
| title_fullStr | Activation of Mast Cells Promote Plasmodium berghei ANKA Infection in Murine Model |
| title_full_unstemmed | Activation of Mast Cells Promote Plasmodium berghei ANKA Infection in Murine Model |
| title_short | Activation of Mast Cells Promote Plasmodium berghei ANKA Infection in Murine Model |
| title_sort | activation of mast cells promote plasmodium berghei anka infection in murine model |
| topic | Plasmodium berghei mast cells degranulation pathogenesis immune responses vascular permeability |
| url | https://www.frontiersin.org/article/10.3389/fcimb.2019.00322/full |
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