Transcriptomic Analysis of the Effects of Chemokine Receptor CXCR3 Deficiency on Immune Responses in the Mouse Brain during <i>Toxoplasma gondii</i> Infection

The obligate intracellular parasite <i>Toxoplasma gondii</i> infects warm-blooded animals, including humans. We previously revealed through a whole-brain transcriptome analysis that infection with <i>T. gondii</i> in mice causes immune response-associated genes to be upregula...

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Autores principales: Kousuke Umeda, Youta Goto, Kenichi Watanabe, Nanako Ushio, Ragab M. Fereig, Fumiaki Ihara, Sachi Tanaka, Yutaka Suzuki, Yoshifumi Nishikawa
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Publicado: MDPI AG 2021
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spelling oai:doaj.org-article:ce5db034c27043eeac1a4b29a5fd72d72021-11-25T18:25:16ZTranscriptomic Analysis of the Effects of Chemokine Receptor CXCR3 Deficiency on Immune Responses in the Mouse Brain during <i>Toxoplasma gondii</i> Infection10.3390/microorganisms91123402076-2607https://doaj.org/article/ce5db034c27043eeac1a4b29a5fd72d72021-11-01T00:00:00Zhttps://www.mdpi.com/2076-2607/9/11/2340https://doaj.org/toc/2076-2607The obligate intracellular parasite <i>Toxoplasma gondii</i> infects warm-blooded animals, including humans. We previously revealed through a whole-brain transcriptome analysis that infection with <i>T. gondii</i> in mice causes immune response-associated genes to be upregulated, for instance, chemokines and chemokine receptors such as CXC chemokine receptor 3 (CXCR3) and its ligand CXC chemokine ligand 10 (CXCL10). Here, we describe the effect of CXCR3 on responses against <i>T. gondii</i> infection in the mouse brain. In vivo assays using CXCR3-deficient mice showed that the absence of CXCR3 delayed the normal recovery of body weight and increased the brain parasite burden, suggesting that CXCR3 plays a role in the control of pathology in the brain, the site where chronic infection occurs. Therefore, to further analyze the function of CXCR3 in the brain, we profiled the gene expression patterns of primary astrocytes and microglia by RNA sequencing and subsequent analyses. CXCR3 deficiency impaired the normal upregulation of immune-related genes during <i>T. gondii</i> infection, in astrocytes and microglia alike. Collectively, our results suggest that the immune-related genes upregulated by CXCR3 perform a particular role in controlling pathology when the host is chronically infected with <i>T. gondii</i> in the brain.Kousuke UmedaYouta GotoKenichi WatanabeNanako UshioRagab M. FereigFumiaki IharaSachi TanakaYutaka SuzukiYoshifumi NishikawaMDPI AGarticle<i>Toxoplasma gondii</i>CXCR3transcriptomebrainastrocytemicrogliaBiology (General)QH301-705.5ENMicroorganisms, Vol 9, Iss 2340, p 2340 (2021)
institution DOAJ
collection DOAJ
language EN
topic <i>Toxoplasma gondii</i>
CXCR3
transcriptome
brain
astrocyte
microglia
Biology (General)
QH301-705.5
spellingShingle <i>Toxoplasma gondii</i>
CXCR3
transcriptome
brain
astrocyte
microglia
Biology (General)
QH301-705.5
Kousuke Umeda
Youta Goto
Kenichi Watanabe
Nanako Ushio
Ragab M. Fereig
Fumiaki Ihara
Sachi Tanaka
Yutaka Suzuki
Yoshifumi Nishikawa
Transcriptomic Analysis of the Effects of Chemokine Receptor CXCR3 Deficiency on Immune Responses in the Mouse Brain during <i>Toxoplasma gondii</i> Infection
description The obligate intracellular parasite <i>Toxoplasma gondii</i> infects warm-blooded animals, including humans. We previously revealed through a whole-brain transcriptome analysis that infection with <i>T. gondii</i> in mice causes immune response-associated genes to be upregulated, for instance, chemokines and chemokine receptors such as CXC chemokine receptor 3 (CXCR3) and its ligand CXC chemokine ligand 10 (CXCL10). Here, we describe the effect of CXCR3 on responses against <i>T. gondii</i> infection in the mouse brain. In vivo assays using CXCR3-deficient mice showed that the absence of CXCR3 delayed the normal recovery of body weight and increased the brain parasite burden, suggesting that CXCR3 plays a role in the control of pathology in the brain, the site where chronic infection occurs. Therefore, to further analyze the function of CXCR3 in the brain, we profiled the gene expression patterns of primary astrocytes and microglia by RNA sequencing and subsequent analyses. CXCR3 deficiency impaired the normal upregulation of immune-related genes during <i>T. gondii</i> infection, in astrocytes and microglia alike. Collectively, our results suggest that the immune-related genes upregulated by CXCR3 perform a particular role in controlling pathology when the host is chronically infected with <i>T. gondii</i> in the brain.
format article
author Kousuke Umeda
Youta Goto
Kenichi Watanabe
Nanako Ushio
Ragab M. Fereig
Fumiaki Ihara
Sachi Tanaka
Yutaka Suzuki
Yoshifumi Nishikawa
author_facet Kousuke Umeda
Youta Goto
Kenichi Watanabe
Nanako Ushio
Ragab M. Fereig
Fumiaki Ihara
Sachi Tanaka
Yutaka Suzuki
Yoshifumi Nishikawa
author_sort Kousuke Umeda
title Transcriptomic Analysis of the Effects of Chemokine Receptor CXCR3 Deficiency on Immune Responses in the Mouse Brain during <i>Toxoplasma gondii</i> Infection
title_short Transcriptomic Analysis of the Effects of Chemokine Receptor CXCR3 Deficiency on Immune Responses in the Mouse Brain during <i>Toxoplasma gondii</i> Infection
title_full Transcriptomic Analysis of the Effects of Chemokine Receptor CXCR3 Deficiency on Immune Responses in the Mouse Brain during <i>Toxoplasma gondii</i> Infection
title_fullStr Transcriptomic Analysis of the Effects of Chemokine Receptor CXCR3 Deficiency on Immune Responses in the Mouse Brain during <i>Toxoplasma gondii</i> Infection
title_full_unstemmed Transcriptomic Analysis of the Effects of Chemokine Receptor CXCR3 Deficiency on Immune Responses in the Mouse Brain during <i>Toxoplasma gondii</i> Infection
title_sort transcriptomic analysis of the effects of chemokine receptor cxcr3 deficiency on immune responses in the mouse brain during <i>toxoplasma gondii</i> infection
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/ce5db034c27043eeac1a4b29a5fd72d7
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