Toxoplasma gondii infection in the brain inhibits neuronal degeneration and learning and memory impairments in a murine model of Alzheimer's disease
Immunosuppression is a characteristic feature of Toxoplasma gondii-infected murine hosts. The present study aimed to determine the effect of the immunosuppression induced by T. gondii infection on the pathogenesis and progression of Alzheimer's disease (AD) in Tg2576 AD mice. Mice were infected...
Gespeichert in:
| Veröffentlicht in: | PloS one 2012-03, Vol.7 (3), p.e33312 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | |
|---|---|
| container_issue | 3 |
| container_start_page | e33312 |
| container_title | PloS one |
| container_volume | 7 |
| creator | Jung, Bong-Kwang Pyo, Kyoung-Ho Shin, Ki Young Hwang, Young Sang Lim, Hyoungsub Lee, Sung Joong Moon, Jung-Ho Lee, Sang Hyung Suh, Yoo-Hun Chai, Jong-Yil Shin, Eun-Hee |
| description | Immunosuppression is a characteristic feature of Toxoplasma gondii-infected murine hosts. The present study aimed to determine the effect of the immunosuppression induced by T. gondii infection on the pathogenesis and progression of Alzheimer's disease (AD) in Tg2576 AD mice. Mice were infected with a cyst-forming strain (ME49) of T. gondii, and levels of inflammatory mediators (IFN-γ and nitric oxide), anti-inflammatory cytokines (IL-10 and TGF-β), neuronal damage, and β-amyloid plaque deposition were examined in brain tissues and/or in BV-2 microglial cells. In addition, behavioral tests, including the water maze and Y-maze tests, were performed on T. gondii-infected and uninfected Tg2576 mice. Results revealed that whereas the level of IFN-γ was unchanged, the levels of anti-inflammatory cytokines were significantly higher in T. gondii-infected mice than in uninfected mice, and in BV-2 cells treated with T. gondii lysate antigen. Furthermore, nitrite production from primary cultured brain microglial cells and BV-2 cells was reduced by the addition of T. gondii lysate antigen (TLA), and β-amyloid plaque deposition in the cortex and hippocampus of Tg2576 mouse brains was remarkably lower in T. gondii-infected AD mice than in uninfected controls. In addition, water maze and Y-maze test results revealed retarded cognitive capacities in uninfected mice as compared with infected mice. These findings demonstrate the favorable effects of the immunosuppression induced by T. gondii infection on the pathogenesis and progression of AD in Tg2576 mice. |
| doi_str_mv | 10.1371/journal.pone.0033312 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_plos_</sourceid><recordid>TN_cdi_plos_journals_1324435190</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A477052707</galeid><doaj_id>oai_doaj_org_article_4b69555d21aa451cb3ff069ac390252e</doaj_id><sourcerecordid>A477052707</sourcerecordid><originalsourceid>FETCH-LOGICAL-c757t-139bd4a5e59ebbc82634d8a36e0eba3927626ff039984dd5e58e591b16ef799c3</originalsourceid><addsrcrecordid>eNqNk9tu1DAQhiMEoqXwBggsIVFxsYtPSdY3SKuKw0qVKkHh1prEk6wrx17sBLU8Bw-Mt91WXdQLlAsf8v3_2DOeonjJ6JyJmr2_CFP04Oab4HFOqRCC8UfFIVOCzypOxeN784PiWUoXlJZiUVVPiwPOZU2lVIfFn_NwGTYO0gCkD95YS6zvsB1t8HlGxjWSJoLdLta2sWMiHqcYcmRisEePEa5Z8IY4hOit768XAw4hXhE7bMDGAX1WZhcgwxStRzIEg46Ejizd7zXaAeNxIsYmhITPiycduIQvduNR8f3Tx_OTL7PTs8-rk-XprK3LepwxoRojocRSYdO0C14JaRYgKqTYgFC8rnjVdVQotZDGZG6RUdawCrtaqVYcFa9vfDcuJL1LaNJMcClFyRTNxOqGMAEu9CbaAeKVDmD19UaIvYY42tahlk2lyrI0nAHIkrWNyKErBa1QlJccs9eHXbSpGdC0OSUR3J7p_h9v17oPv3SuLKVSZIPjnUEMPydMox5satE58BimpFUlOS0ryjL55h_y4cvtqB7y-XPZQw7bbj31UtY1LXlN60zNH6DyZ3CwbX58nc37e4J3e4LMjHg59jClpFffvv4_e_Zjn317j10juHGdgpu2zy_tg_IGbGNIKWJ3l2NG9bZ3brOht72jd72TZa_u1-dOdNss4i_OwhYq</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1324435190</pqid></control><display><type>article</type><title>Toxoplasma gondii infection in the brain inhibits neuronal degeneration and learning and memory impairments in a murine model of Alzheimer's disease</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Public Library of Science (PLoS)</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><creator>Jung, Bong-Kwang ; Pyo, Kyoung-Ho ; Shin, Ki Young ; Hwang, Young Sang ; Lim, Hyoungsub ; Lee, Sung Joong ; Moon, Jung-Ho ; Lee, Sang Hyung ; Suh, Yoo-Hun ; Chai, Jong-Yil ; Shin, Eun-Hee</creator><contributor>Heimesaat, Markus M.</contributor><creatorcontrib>Jung, Bong-Kwang ; Pyo, Kyoung-Ho ; Shin, Ki Young ; Hwang, Young Sang ; Lim, Hyoungsub ; Lee, Sung Joong ; Moon, Jung-Ho ; Lee, Sang Hyung ; Suh, Yoo-Hun ; Chai, Jong-Yil ; Shin, Eun-Hee ; Heimesaat, Markus M.</creatorcontrib><description>Immunosuppression is a characteristic feature of Toxoplasma gondii-infected murine hosts. The present study aimed to determine the effect of the immunosuppression induced by T. gondii infection on the pathogenesis and progression of Alzheimer's disease (AD) in Tg2576 AD mice. Mice were infected with a cyst-forming strain (ME49) of T. gondii, and levels of inflammatory mediators (IFN-γ and nitric oxide), anti-inflammatory cytokines (IL-10 and TGF-β), neuronal damage, and β-amyloid plaque deposition were examined in brain tissues and/or in BV-2 microglial cells. In addition, behavioral tests, including the water maze and Y-maze tests, were performed on T. gondii-infected and uninfected Tg2576 mice. Results revealed that whereas the level of IFN-γ was unchanged, the levels of anti-inflammatory cytokines were significantly higher in T. gondii-infected mice than in uninfected mice, and in BV-2 cells treated with T. gondii lysate antigen. Furthermore, nitrite production from primary cultured brain microglial cells and BV-2 cells was reduced by the addition of T. gondii lysate antigen (TLA), and β-amyloid plaque deposition in the cortex and hippocampus of Tg2576 mouse brains was remarkably lower in T. gondii-infected AD mice than in uninfected controls. In addition, water maze and Y-maze test results revealed retarded cognitive capacities in uninfected mice as compared with infected mice. These findings demonstrate the favorable effects of the immunosuppression induced by T. gondii infection on the pathogenesis and progression of AD in Tg2576 mice.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0033312</identifier><identifier>PMID: 22470449</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Advertising executives ; Alzheimer Disease - complications ; Alzheimer Disease - pathology ; Alzheimer's disease ; Amyloid - metabolism ; Animal cognition ; Animal models ; Animal tissues ; Animals ; Antigens ; Apoptosis ; Behavior, Animal ; Biology ; Bone morphogenetic proteins ; Brain ; Brain - metabolism ; Brain damage ; Cells, Cultured ; Cerebral Cortex - metabolism ; Cognitive ability ; Cysts ; Cytokines ; Degeneration ; Dentistry ; Deposition ; Disease Models, Animal ; Hippocampus - metabolism ; Immunosuppression ; Immunotherapy ; Infection ; Infections ; Inflammation ; Interferon ; Interferon-gamma - metabolism ; Interleukin 10 ; Interleukin-10 - metabolism ; Learning ; Medical research ; Medicine ; Memory ; Memory Disorders - etiology ; Mice ; Microglia - cytology ; Microglia - metabolism ; Microglial cells ; Nerve Degeneration - etiology ; Nervous system ; Neurodegeneration ; Neurodegenerative diseases ; Neurons ; Neurosciences ; Nitric oxide ; Nitric Oxide - metabolism ; Parasites ; Pathogenesis ; Pathogens ; Pathology ; Pharmacology ; Physicians ; Physiological aspects ; Proteins ; Protozoa ; Rodents ; Toxoplasma - isolation & purification ; Toxoplasma gondii ; Toxoplasmosis, Animal - complications ; Toxoplasmosis, Animal - pathology ; Toxoplasmosis, Animal - virology ; Transforming Growth Factor beta - metabolism ; Transforming growth factors ; β-Amyloid ; γ-Interferon</subject><ispartof>PloS one, 2012-03, Vol.7 (3), p.e33312</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>2012 Jung et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Jung et al. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c757t-139bd4a5e59ebbc82634d8a36e0eba3927626ff039984dd5e58e591b16ef799c3</citedby><cites>FETCH-LOGICAL-c757t-139bd4a5e59ebbc82634d8a36e0eba3927626ff039984dd5e58e591b16ef799c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3310043/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3310043/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2095,2914,23846,27903,27904,53770,53772,79347,79348</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22470449$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Heimesaat, Markus M.</contributor><creatorcontrib>Jung, Bong-Kwang</creatorcontrib><creatorcontrib>Pyo, Kyoung-Ho</creatorcontrib><creatorcontrib>Shin, Ki Young</creatorcontrib><creatorcontrib>Hwang, Young Sang</creatorcontrib><creatorcontrib>Lim, Hyoungsub</creatorcontrib><creatorcontrib>Lee, Sung Joong</creatorcontrib><creatorcontrib>Moon, Jung-Ho</creatorcontrib><creatorcontrib>Lee, Sang Hyung</creatorcontrib><creatorcontrib>Suh, Yoo-Hun</creatorcontrib><creatorcontrib>Chai, Jong-Yil</creatorcontrib><creatorcontrib>Shin, Eun-Hee</creatorcontrib><title>Toxoplasma gondii infection in the brain inhibits neuronal degeneration and learning and memory impairments in a murine model of Alzheimer's disease</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Immunosuppression is a characteristic feature of Toxoplasma gondii-infected murine hosts. The present study aimed to determine the effect of the immunosuppression induced by T. gondii infection on the pathogenesis and progression of Alzheimer's disease (AD) in Tg2576 AD mice. Mice were infected with a cyst-forming strain (ME49) of T. gondii, and levels of inflammatory mediators (IFN-γ and nitric oxide), anti-inflammatory cytokines (IL-10 and TGF-β), neuronal damage, and β-amyloid plaque deposition were examined in brain tissues and/or in BV-2 microglial cells. In addition, behavioral tests, including the water maze and Y-maze tests, were performed on T. gondii-infected and uninfected Tg2576 mice. Results revealed that whereas the level of IFN-γ was unchanged, the levels of anti-inflammatory cytokines were significantly higher in T. gondii-infected mice than in uninfected mice, and in BV-2 cells treated with T. gondii lysate antigen. Furthermore, nitrite production from primary cultured brain microglial cells and BV-2 cells was reduced by the addition of T. gondii lysate antigen (TLA), and β-amyloid plaque deposition in the cortex and hippocampus of Tg2576 mouse brains was remarkably lower in T. gondii-infected AD mice than in uninfected controls. In addition, water maze and Y-maze test results revealed retarded cognitive capacities in uninfected mice as compared with infected mice. These findings demonstrate the favorable effects of the immunosuppression induced by T. gondii infection on the pathogenesis and progression of AD in Tg2576 mice.</description><subject>Advertising executives</subject><subject>Alzheimer Disease - complications</subject><subject>Alzheimer Disease - pathology</subject><subject>Alzheimer's disease</subject><subject>Amyloid - metabolism</subject><subject>Animal cognition</subject><subject>Animal models</subject><subject>Animal tissues</subject><subject>Animals</subject><subject>Antigens</subject><subject>Apoptosis</subject><subject>Behavior, Animal</subject><subject>Biology</subject><subject>Bone morphogenetic proteins</subject><subject>Brain</subject><subject>Brain - metabolism</subject><subject>Brain damage</subject><subject>Cells, Cultured</subject><subject>Cerebral Cortex - metabolism</subject><subject>Cognitive ability</subject><subject>Cysts</subject><subject>Cytokines</subject><subject>Degeneration</subject><subject>Dentistry</subject><subject>Deposition</subject><subject>Disease Models, Animal</subject><subject>Hippocampus - metabolism</subject><subject>Immunosuppression</subject><subject>Immunotherapy</subject><subject>Infection</subject><subject>Infections</subject><subject>Inflammation</subject><subject>Interferon</subject><subject>Interferon-gamma - metabolism</subject><subject>Interleukin 10</subject><subject>Interleukin-10 - metabolism</subject><subject>Learning</subject><subject>Medical research</subject><subject>Medicine</subject><subject>Memory</subject><subject>Memory Disorders - etiology</subject><subject>Mice</subject><subject>Microglia - cytology</subject><subject>Microglia - metabolism</subject><subject>Microglial cells</subject><subject>Nerve Degeneration - etiology</subject><subject>Nervous system</subject><subject>Neurodegeneration</subject><subject>Neurodegenerative diseases</subject><subject>Neurons</subject><subject>Neurosciences</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Parasites</subject><subject>Pathogenesis</subject><subject>Pathogens</subject><subject>Pathology</subject><subject>Pharmacology</subject><subject>Physicians</subject><subject>Physiological aspects</subject><subject>Proteins</subject><subject>Protozoa</subject><subject>Rodents</subject><subject>Toxoplasma - isolation & purification</subject><subject>Toxoplasma gondii</subject><subject>Toxoplasmosis, Animal - complications</subject><subject>Toxoplasmosis, Animal - pathology</subject><subject>Toxoplasmosis, Animal - virology</subject><subject>Transforming Growth Factor beta - metabolism</subject><subject>Transforming growth factors</subject><subject>β-Amyloid</subject><subject>γ-Interferon</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk9tu1DAQhiMEoqXwBggsIVFxsYtPSdY3SKuKw0qVKkHh1prEk6wrx17sBLU8Bw-Mt91WXdQLlAsf8v3_2DOeonjJ6JyJmr2_CFP04Oab4HFOqRCC8UfFIVOCzypOxeN784PiWUoXlJZiUVVPiwPOZU2lVIfFn_NwGTYO0gCkD95YS6zvsB1t8HlGxjWSJoLdLta2sWMiHqcYcmRisEePEa5Z8IY4hOit768XAw4hXhE7bMDGAX1WZhcgwxStRzIEg46Ejizd7zXaAeNxIsYmhITPiycduIQvduNR8f3Tx_OTL7PTs8-rk-XprK3LepwxoRojocRSYdO0C14JaRYgKqTYgFC8rnjVdVQotZDGZG6RUdawCrtaqVYcFa9vfDcuJL1LaNJMcClFyRTNxOqGMAEu9CbaAeKVDmD19UaIvYY42tahlk2lyrI0nAHIkrWNyKErBa1QlJccs9eHXbSpGdC0OSUR3J7p_h9v17oPv3SuLKVSZIPjnUEMPydMox5satE58BimpFUlOS0ryjL55h_y4cvtqB7y-XPZQw7bbj31UtY1LXlN60zNH6DyZ3CwbX58nc37e4J3e4LMjHg59jClpFffvv4_e_Zjn317j10juHGdgpu2zy_tg_IGbGNIKWJ3l2NG9bZ3brOht72jd72TZa_u1-dOdNss4i_OwhYq</recordid><startdate>20120321</startdate><enddate>20120321</enddate><creator>Jung, Bong-Kwang</creator><creator>Pyo, Kyoung-Ho</creator><creator>Shin, Ki Young</creator><creator>Hwang, Young Sang</creator><creator>Lim, Hyoungsub</creator><creator>Lee, Sung Joong</creator><creator>Moon, Jung-Ho</creator><creator>Lee, Sang Hyung</creator><creator>Suh, Yoo-Hun</creator><creator>Chai, Jong-Yil</creator><creator>Shin, Eun-Hee</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20120321</creationdate><title>Toxoplasma gondii infection in the brain inhibits neuronal degeneration and learning and memory impairments in a murine model of Alzheimer's disease</title><author>Jung, Bong-Kwang ; Pyo, Kyoung-Ho ; Shin, Ki Young ; Hwang, Young Sang ; Lim, Hyoungsub ; Lee, Sung Joong ; Moon, Jung-Ho ; Lee, Sang Hyung ; Suh, Yoo-Hun ; Chai, Jong-Yil ; Shin, Eun-Hee</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c757t-139bd4a5e59ebbc82634d8a36e0eba3927626ff039984dd5e58e591b16ef799c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Advertising executives</topic><topic>Alzheimer Disease - complications</topic><topic>Alzheimer Disease - pathology</topic><topic>Alzheimer's disease</topic><topic>Amyloid - metabolism</topic><topic>Animal cognition</topic><topic>Animal models</topic><topic>Animal tissues</topic><topic>Animals</topic><topic>Antigens</topic><topic>Apoptosis</topic><topic>Behavior, Animal</topic><topic>Biology</topic><topic>Bone morphogenetic proteins</topic><topic>Brain</topic><topic>Brain - metabolism</topic><topic>Brain damage</topic><topic>Cells, Cultured</topic><topic>Cerebral Cortex - metabolism</topic><topic>Cognitive ability</topic><topic>Cysts</topic><topic>Cytokines</topic><topic>Degeneration</topic><topic>Dentistry</topic><topic>Deposition</topic><topic>Disease Models, Animal</topic><topic>Hippocampus - metabolism</topic><topic>Immunosuppression</topic><topic>Immunotherapy</topic><topic>Infection</topic><topic>Infections</topic><topic>Inflammation</topic><topic>Interferon</topic><topic>Interferon-gamma - metabolism</topic><topic>Interleukin 10</topic><topic>Interleukin-10 - metabolism</topic><topic>Learning</topic><topic>Medical research</topic><topic>Medicine</topic><topic>Memory</topic><topic>Memory Disorders - etiology</topic><topic>Mice</topic><topic>Microglia - cytology</topic><topic>Microglia - metabolism</topic><topic>Microglial cells</topic><topic>Nerve Degeneration - etiology</topic><topic>Nervous system</topic><topic>Neurodegeneration</topic><topic>Neurodegenerative diseases</topic><topic>Neurons</topic><topic>Neurosciences</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Parasites</topic><topic>Pathogenesis</topic><topic>Pathogens</topic><topic>Pathology</topic><topic>Pharmacology</topic><topic>Physicians</topic><topic>Physiological aspects</topic><topic>Proteins</topic><topic>Protozoa</topic><topic>Rodents</topic><topic>Toxoplasma - isolation & purification</topic><topic>Toxoplasma gondii</topic><topic>Toxoplasmosis, Animal - complications</topic><topic>Toxoplasmosis, Animal - pathology</topic><topic>Toxoplasmosis, Animal - virology</topic><topic>Transforming Growth Factor beta - metabolism</topic><topic>Transforming growth factors</topic><topic>β-Amyloid</topic><topic>γ-Interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jung, Bong-Kwang</creatorcontrib><creatorcontrib>Pyo, Kyoung-Ho</creatorcontrib><creatorcontrib>Shin, Ki Young</creatorcontrib><creatorcontrib>Hwang, Young Sang</creatorcontrib><creatorcontrib>Lim, Hyoungsub</creatorcontrib><creatorcontrib>Lee, Sung Joong</creatorcontrib><creatorcontrib>Moon, Jung-Ho</creatorcontrib><creatorcontrib>Lee, Sang Hyung</creatorcontrib><creatorcontrib>Suh, Yoo-Hun</creatorcontrib><creatorcontrib>Chai, Jong-Yil</creatorcontrib><creatorcontrib>Shin, Eun-Hee</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jung, Bong-Kwang</au><au>Pyo, Kyoung-Ho</au><au>Shin, Ki Young</au><au>Hwang, Young Sang</au><au>Lim, Hyoungsub</au><au>Lee, Sung Joong</au><au>Moon, Jung-Ho</au><au>Lee, Sang Hyung</au><au>Suh, Yoo-Hun</au><au>Chai, Jong-Yil</au><au>Shin, Eun-Hee</au><au>Heimesaat, Markus M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Toxoplasma gondii infection in the brain inhibits neuronal degeneration and learning and memory impairments in a murine model of Alzheimer's disease</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-03-21</date><risdate>2012</risdate><volume>7</volume><issue>3</issue><spage>e33312</spage><pages>e33312-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Immunosuppression is a characteristic feature of Toxoplasma gondii-infected murine hosts. The present study aimed to determine the effect of the immunosuppression induced by T. gondii infection on the pathogenesis and progression of Alzheimer's disease (AD) in Tg2576 AD mice. Mice were infected with a cyst-forming strain (ME49) of T. gondii, and levels of inflammatory mediators (IFN-γ and nitric oxide), anti-inflammatory cytokines (IL-10 and TGF-β), neuronal damage, and β-amyloid plaque deposition were examined in brain tissues and/or in BV-2 microglial cells. In addition, behavioral tests, including the water maze and Y-maze tests, were performed on T. gondii-infected and uninfected Tg2576 mice. Results revealed that whereas the level of IFN-γ was unchanged, the levels of anti-inflammatory cytokines were significantly higher in T. gondii-infected mice than in uninfected mice, and in BV-2 cells treated with T. gondii lysate antigen. Furthermore, nitrite production from primary cultured brain microglial cells and BV-2 cells was reduced by the addition of T. gondii lysate antigen (TLA), and β-amyloid plaque deposition in the cortex and hippocampus of Tg2576 mouse brains was remarkably lower in T. gondii-infected AD mice than in uninfected controls. In addition, water maze and Y-maze test results revealed retarded cognitive capacities in uninfected mice as compared with infected mice. These findings demonstrate the favorable effects of the immunosuppression induced by T. gondii infection on the pathogenesis and progression of AD in Tg2576 mice.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22470449</pmid><doi>10.1371/journal.pone.0033312</doi><tpages>e33312</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2012-03, Vol.7 (3), p.e33312 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1324435190 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Advertising executives Alzheimer Disease - complications Alzheimer Disease - pathology Alzheimer's disease Amyloid - metabolism Animal cognition Animal models Animal tissues Animals Antigens Apoptosis Behavior, Animal Biology Bone morphogenetic proteins Brain Brain - metabolism Brain damage Cells, Cultured Cerebral Cortex - metabolism Cognitive ability Cysts Cytokines Degeneration Dentistry Deposition Disease Models, Animal Hippocampus - metabolism Immunosuppression Immunotherapy Infection Infections Inflammation Interferon Interferon-gamma - metabolism Interleukin 10 Interleukin-10 - metabolism Learning Medical research Medicine Memory Memory Disorders - etiology Mice Microglia - cytology Microglia - metabolism Microglial cells Nerve Degeneration - etiology Nervous system Neurodegeneration Neurodegenerative diseases Neurons Neurosciences Nitric oxide Nitric Oxide - metabolism Parasites Pathogenesis Pathogens Pathology Pharmacology Physicians Physiological aspects Proteins Protozoa Rodents Toxoplasma - isolation & purification Toxoplasma gondii Toxoplasmosis, Animal - complications Toxoplasmosis, Animal - pathology Toxoplasmosis, Animal - virology Transforming Growth Factor beta - metabolism Transforming growth factors β-Amyloid γ-Interferon |
| title | Toxoplasma gondii infection in the brain inhibits neuronal degeneration and learning and memory impairments in a murine model of Alzheimer's disease |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-23T02%3A11%3A32IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Toxoplasma%20gondii%20infection%20in%20the%20brain%20inhibits%20neuronal%20degeneration%20and%20learning%20and%20memory%20impairments%20in%20a%20murine%20model%20of%20Alzheimer's%20disease&rft.jtitle=PloS%20one&rft.au=Jung,%20Bong-Kwang&rft.date=2012-03-21&rft.volume=7&rft.issue=3&rft.spage=e33312&rft.pages=e33312-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0033312&rft_dat=%3Cgale_plos_%3EA477052707%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1324435190&rft_id=info:pmid/22470449&rft_galeid=A477052707&rft_doaj_id=oai_doaj_org_article_4b69555d21aa451cb3ff069ac390252e&rfr_iscdi=true |