Fractalkine receptor (CX3CR1) deficiency sensitizes mice to the behavioral changes induced by lipopolysaccharide
Interactions between fractalkine (CX3CL1) and fractalkine receptor (CX3CR1) regulate microglial activation in the CNS. Recent findings indicate that age-associated impairments in CX3CL1 and CX3CR1 are directly associated with exaggerated microglial activation and an impaired recovery from sickness b...
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| Published in: | Journal of neuroinflammation Vol. 7; no. 1; p. 93 |
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| Main Authors: | , , , , , , |
| Format: | Journal Article |
| Language: | English |
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BioMed Central Ltd
17-12-2010
BioMed Central BMC |
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| Abstract | Interactions between fractalkine (CX3CL1) and fractalkine receptor (CX3CR1) regulate microglial activation in the CNS. Recent findings indicate that age-associated impairments in CX3CL1 and CX3CR1 are directly associated with exaggerated microglial activation and an impaired recovery from sickness behavior after peripheral injection of lipopolysaccharide (LPS). Therefore, the purpose of this study was to determine the extent to which an acute LPS injection causes amplified and prolonged microglial activation and behavioral deficits in CX3CR1-deficient mice (CX3CR1-/-).
CX3CR1-/- mice or control heterozygote mice (CX3CR1+/-) were injected with LPS (0.5 mg/kg i.p.) or saline and behavior (i.e., sickness and depression-like behavior), microglial activation, and markers of tryptophan metabolism were determined. All data were analyzed using Statistical Analysis Systems General Linear Model procedures and were subjected to one-, two-, or three-way ANOVA to determine significant main effects and interactions.
LPS injection caused a prolonged duration of social withdrawal in CX3CR1-/- mice compared to control mice. This extended social withdrawal was associated with enhanced mRNA expression of IL-1β, indolamine 2,3-dioxygenase (IDO) and kynurenine monooxygenase (KMO) in microglia 4 h after LPS. Moreover, elevated expression of IL-1β and CD14 was still detected in microglia of CX3CR1-/- mice 24 h after LPS. There was also increased turnover of tryptophan, serotonin, and dopamine in the brain 24 h after LPS, but these increases were independent of CX3CR1 expression. When submitted to the tail suspension test 48 and 72 h after LPS, an increased duration of immobility was evident only in CX3CR1-/- mice. This depression-like behavior in CX3CR1-/- mice was associated with a persistent activated microglial phenotype in the hippocampus and prefrontal cortex.
Taken together, these data indicate that a deficiency of CX3CR1 is permissive to protracted microglial activation and prolonged behavioral alterations in response to transient activation of the innate immune system. |
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| AbstractList | Background Interactions between fractalkine (CX.sub.3 CL1) and fractalkine receptor (CX.sub.3 CR1) regulate microglial activation in the CNS. Recent findings indicate that age-associated impairments in CX.sub.3 CL1 and CX.sub.3 CR1 are directly associated with exaggerated microglial activation and an impaired recovery from sickness behavior after peripheral injection of lipopolysaccharide (LPS). Therefore, the purpose of this study was to determine the extent to which an acute LPS injection causes amplified and prolonged microglial activation and behavioral deficits in CX.sub.3 CR1-deficient mice (CX.sub.3 CR1.sup.-/-.sup.). Methods CX.sub.3 CR1.sup.-/- .sup.mice or control heterozygote mice (CX.sub.3 CR1.sup.+/-.sup.) were injected with LPS (0.5 mg/kg i.p.) or saline and behavior (i.e., sickness and depression-like behavior), microglial activation, and markers of tryptophan metabolism were determined. All data were analyzed using Statistical Analysis Systems General Linear Model procedures and were subjected to one-, two-, or three-way ANOVA to determine significant main effects and interactions. Results LPS injection caused a prolonged duration of social withdrawal in CX.sub.3 CR1.sup.-/- .sup.mice compared to control mice. This extended social withdrawal was associated with enhanced mRNA expression of IL-1[beta], indolamine 2,3-dioxygenase (IDO) and kynurenine monooxygenase (KMO) in microglia 4 h after LPS. Moreover, elevated expression of IL-1[beta] and CD14 was still detected in microglia of CX.sub.3 CR1.sup.-/- .sup.mice 24 h after LPS. There was also increased turnover of tryptophan, serotonin, and dopamine in the brain 24 h after LPS, but these increases were independent of CX.sub.3 CR1 expression. When submitted to the tail suspension test 48 and 72 h after LPS, an increased duration of immobility was evident only in CX.sub.3 CR1.sup.-/- .sup.mice. This depression-like behavior in CX.sub.3 CR1.sup.-/- .sup.mice was associated with a persistent activated microglial phenotype in the hippocampus and prefrontal cortex. Conclusions Taken together, these data indicate that a deficiency of CX.sub.3 CR1 is permissive to protracted microglial activation and prolonged behavioral alterations in response to transient activation of the innate immune system. Abstract Background Interactions between fractalkine (CX3CL1) and fractalkine receptor (CX3CR1) regulate microglial activation in the CNS. Recent findings indicate that age-associated impairments in CX3CL1 and CX3CR1 are directly associated with exaggerated microglial activation and an impaired recovery from sickness behavior after peripheral injection of lipopolysaccharide (LPS). Therefore, the purpose of this study was to determine the extent to which an acute LPS injection causes amplified and prolonged microglial activation and behavioral deficits in CX3CR1-deficient mice (CX3CR1-/-). Methods CX3CR1-/- mice or control heterozygote mice (CX3CR1+/-) were injected with LPS (0.5 mg/kg i.p.) or saline and behavior (i.e., sickness and depression-like behavior), microglial activation, and markers of tryptophan metabolism were determined. All data were analyzed using Statistical Analysis Systems General Linear Model procedures and were subjected to one-, two-, or three-way ANOVA to determine significant main effects and interactions. Results LPS injection caused a prolonged duration of social withdrawal in CX3CR1-/- mice compared to control mice. This extended social withdrawal was associated with enhanced mRNA expression of IL-1β, indolamine 2,3-dioxygenase (IDO) and kynurenine monooxygenase (KMO) in microglia 4 h after LPS. Moreover, elevated expression of IL-1β and CD14 was still detected in microglia of CX3CR1-/- mice 24 h after LPS. There was also increased turnover of tryptophan, serotonin, and dopamine in the brain 24 h after LPS, but these increases were independent of CX3CR1 expression. When submitted to the tail suspension test 48 and 72 h after LPS, an increased duration of immobility was evident only in CX3CR1-/- mice. This depression-like behavior in CX3CR1-/- mice was associated with a persistent activated microglial phenotype in the hippocampus and prefrontal cortex. Conclusions Taken together, these data indicate that a deficiency of CX3CR1 is permissive to protracted microglial activation and prolonged behavioral alterations in response to transient activation of the innate immune system. Abstract Background: Interactions between fractalkine (CX3 CL1) and fractalkine receptor (CX3 CR1) regulate microglial activation in the CNS. Recent findings indicate that age-associated impairments in CX3 CL1 and CX3 CR1 are directly associated with exaggerated microglial activation and an impaired recovery from sickness behavior after peripheral injection of lipopolysaccharide (LPS). Therefore, the purpose of this study was to determine the extent to which an acute LPS injection causes amplified and prolonged microglial activation and behavioral deficits in CX3 CR1-deficient mice (CX3 CR1-/- ). Methods: CX3 CR1-/- mice or control heterozygote mice (CX3 CR1+/- ) were injected with LPS (0.5 mg/kg i.p.) or saline and behavior (i.e., sickness and depression-like behavior), microglial activation, and markers of tryptophan metabolism were determined. All data were analyzed using Statistical Analysis Systems General Linear Model procedures and were subjected to one-, two-, or three-way ANOVA to determine significant main effects and interactions. Results: LPS injection caused a prolonged duration of social withdrawal in CX3 CR1-/- mice compared to control mice. This extended social withdrawal was associated with enhanced mRNA expression of IL-1β, indolamine 2,3-dioxygenase (IDO) and kynurenine monooxygenase (KMO) in microglia 4 h after LPS. Moreover, elevated expression of IL-1β and CD14 was still detected in microglia of CX3 CR1-/- mice 24 h after LPS. There was also increased turnover of tryptophan, serotonin, and dopamine in the brain 24 h after LPS, but these increases were independent of CX3 CR1 expression. When submitted to the tail suspension test 48 and 72 h after LPS, an increased duration of immobility was evident only in CX3 CR1-/- mice. This depression-like behavior in CX3 CR1-/- mice was associated with a persistent activated microglial phenotype in the hippocampus and prefrontal cortex. Conclusions: Taken together, these data indicate that a deficiency of CX3 CR1 is permissive to protracted microglial activation and prolonged behavioral alterations in response to transient activation of the innate immune system. Interactions between fractalkine (CX.sub.3 CL1) and fractalkine receptor (CX.sub.3 CR1) regulate microglial activation in the CNS. Recent findings indicate that age-associated impairments in CX.sub.3 CL1 and CX.sub.3 CR1 are directly associated with exaggerated microglial activation and an impaired recovery from sickness behavior after peripheral injection of lipopolysaccharide (LPS). Therefore, the purpose of this study was to determine the extent to which an acute LPS injection causes amplified and prolonged microglial activation and behavioral deficits in CX.sub.3 CR1-deficient mice (CX.sub.3 CR1.sup.-/-.sup.). CX.sub.3 CR1.sup.-/- .sup.mice or control heterozygote mice (CX.sub.3 CR1.sup.+/-.sup.) were injected with LPS (0.5 mg/kg i.p.) or saline and behavior (i.e., sickness and depression-like behavior), microglial activation, and markers of tryptophan metabolism were determined. All data were analyzed using Statistical Analysis Systems General Linear Model procedures and were subjected to one-, two-, or three-way ANOVA to determine significant main effects and interactions. LPS injection caused a prolonged duration of social withdrawal in CX.sub.3 CR1.sup.-/- .sup.mice compared to control mice. This extended social withdrawal was associated with enhanced mRNA expression of IL-1[beta], indolamine 2,3-dioxygenase (IDO) and kynurenine monooxygenase (KMO) in microglia 4 h after LPS. Moreover, elevated expression of IL-1[beta] and CD14 was still detected in microglia of CX.sub.3 CR1.sup.-/- .sup.mice 24 h after LPS. There was also increased turnover of tryptophan, serotonin, and dopamine in the brain 24 h after LPS, but these increases were independent of CX.sub.3 CR1 expression. When submitted to the tail suspension test 48 and 72 h after LPS, an increased duration of immobility was evident only in CX.sub.3 CR1.sup.-/- .sup.mice. This depression-like behavior in CX.sub.3 CR1.sup.-/- .sup.mice was associated with a persistent activated microglial phenotype in the hippocampus and prefrontal cortex. Taken together, these data indicate that a deficiency of CX.sub.3 CR1 is permissive to protracted microglial activation and prolonged behavioral alterations in response to transient activation of the innate immune system. Interactions between fractalkine (CX3CL1) and fractalkine receptor (CX3CR1) regulate microglial activation in the CNS. Recent findings indicate that age-associated impairments in CX3CL1 and CX3CR1 are directly associated with exaggerated microglial activation and an impaired recovery from sickness behavior after peripheral injection of lipopolysaccharide (LPS). Therefore, the purpose of this study was to determine the extent to which an acute LPS injection causes amplified and prolonged microglial activation and behavioral deficits in CX3CR1-deficient mice (CX3CR1-/-). CX3CR1-/- mice or control heterozygote mice (CX3CR1+/-) were injected with LPS (0.5 mg/kg i.p.) or saline and behavior (i.e., sickness and depression-like behavior), microglial activation, and markers of tryptophan metabolism were determined. All data were analyzed using Statistical Analysis Systems General Linear Model procedures and were subjected to one-, two-, or three-way ANOVA to determine significant main effects and interactions. LPS injection caused a prolonged duration of social withdrawal in CX3CR1-/- mice compared to control mice. This extended social withdrawal was associated with enhanced mRNA expression of IL-1β, indolamine 2,3-dioxygenase (IDO) and kynurenine monooxygenase (KMO) in microglia 4 h after LPS. Moreover, elevated expression of IL-1β and CD14 was still detected in microglia of CX3CR1-/- mice 24 h after LPS. There was also increased turnover of tryptophan, serotonin, and dopamine in the brain 24 h after LPS, but these increases were independent of CX3CR1 expression. When submitted to the tail suspension test 48 and 72 h after LPS, an increased duration of immobility was evident only in CX3CR1-/- mice. This depression-like behavior in CX3CR1-/- mice was associated with a persistent activated microglial phenotype in the hippocampus and prefrontal cortex. Taken together, these data indicate that a deficiency of CX3CR1 is permissive to protracted microglial activation and prolonged behavioral alterations in response to transient activation of the innate immune system. BACKGROUND: Interactions between fractalkine (CX3CL1) and fractalkine receptor (CX3CR1) regulate microglial activation in the CNS. Recent findings indicate that age-associated impairments in CX3CL1 and CX3CR1 are directly associated with exaggerated microglial activation and an impaired recovery from sickness behavior after peripheral injection of lipopolysaccharide (LPS). Therefore, the purpose of this study was to determine the extent to which an acute LPS injection causes amplified and prolonged microglial activation and behavioral deficits in CX3CR1-deficient mice (CX3CR1-/-). METHODS: CX3CR1-/- mice or control heterozygote mice (CX3CR1+/-) were injected with LPS (0.5 mg/kg i.p.) or saline and behavior (i.e., sickness and depression-like behavior), microglial activation, and markers of tryptophan metabolism were determined. All data were analyzed using Statistical Analysis Systems General Linear Model procedures and were subjected to one-, two-, or three-way ANOVA to determine significant main effects and interactions. RESULTS: LPS injection caused a prolonged duration of social withdrawal in CX3CR1-/- mice compared to control mice. This extended social withdrawal was associated with enhanced mRNA expression of IL-1β, indolamine 2,3-dioxygenase (IDO) and kynurenine monooxygenase (KMO) in microglia 4 h after LPS. Moreover, elevated expression of IL-1β and CD14 was still detected in microglia of CX3CR1-/- mice 24 h after LPS. There was also increased turnover of tryptophan, serotonin, and dopamine in the brain 24 h after LPS, but these increases were independent of CX3CR1 expression. When submitted to the tail suspension test 48 and 72 h after LPS, an increased duration of immobility was evident only in CX3CR1-/- mice. This depression-like behavior in CX3CR1-/- mice was associated with a persistent activated microglial phenotype in the hippocampus and prefrontal cortex. CONCLUSIONS: Taken together, these data indicate that a deficiency of CX3CR1 is permissive to protracted microglial activation and prolonged behavioral alterations in response to transient activation of the innate immune system. |
| Audience | Academic |
| Author | Huang, Yan Dantzer, Robert Godbout, Jonathan P Corona, Angela W O'Connor, Jason C Kelley, Keith W Popovich, Phillip G |
| AuthorAffiliation | 2 Department of Animal Science, University of Illinois, 1201 W. Gregory Drive, 250B Edward R. Madigan Laboratory, Urbana, IL 61820, USA 6 Department of Pharmacology, University of Texas Health Science Center, 7703 Floyd Curl Dr., San Antonio, TX 78229, USA 1 Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University, 333 W. 10th Ave, Columbus, OH 43210, USA 3 Institute for Behavioral Medicine Research, The Ohio State University, 460 Medical Center Dr., Columbus, OH 43210, USA 5 Department of Neuroscience, The Ohio State University, 333 W. 10th Ave, Columbus, OH 43210, USA 4 Center for Brain and Spinal Cord Repair, The Ohio State University, 460 W. 12th Ave, Columbus, OH 43210, USA |
| AuthorAffiliation_xml | – name: 3 Institute for Behavioral Medicine Research, The Ohio State University, 460 Medical Center Dr., Columbus, OH 43210, USA – name: 5 Department of Neuroscience, The Ohio State University, 333 W. 10th Ave, Columbus, OH 43210, USA – name: 4 Center for Brain and Spinal Cord Repair, The Ohio State University, 460 W. 12th Ave, Columbus, OH 43210, USA – name: 1 Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University, 333 W. 10th Ave, Columbus, OH 43210, USA – name: 6 Department of Pharmacology, University of Texas Health Science Center, 7703 Floyd Curl Dr., San Antonio, TX 78229, USA – name: 2 Department of Animal Science, University of Illinois, 1201 W. Gregory Drive, 250B Edward R. Madigan Laboratory, Urbana, IL 61820, USA |
| Author_xml | – sequence: 1 givenname: Angela W surname: Corona fullname: Corona, Angela W email: Angela.Wynne@osumc.edu organization: Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University, 333 W. 10th Ave., Columbus, OH 43210, USA. Angela.Wynne@osumc.edu – sequence: 2 givenname: Yan surname: Huang fullname: Huang, Yan – sequence: 3 givenname: Jason C surname: O'Connor fullname: O'Connor, Jason C – sequence: 4 givenname: Robert surname: Dantzer fullname: Dantzer, Robert – sequence: 5 givenname: Keith W surname: Kelley fullname: Kelley, Keith W – sequence: 6 givenname: Phillip G surname: Popovich fullname: Popovich, Phillip G – sequence: 7 givenname: Jonathan P surname: Godbout fullname: Godbout, Jonathan P |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21167054$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | COPYRIGHT 2010 BioMed Central Ltd. 2010 Corona et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Copyright ©2010 Corona et al.; licensee BioMed Central Ltd. 2010 Corona et al.; licensee BioMed Central Ltd. |
| Copyright_xml | – notice: COPYRIGHT 2010 BioMed Central Ltd. – notice: 2010 Corona et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. – notice: Copyright ©2010 Corona et al.; licensee BioMed Central Ltd. 2010 Corona et al.; licensee BioMed Central Ltd. |
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| DOI | 10.1186/1742-2094-7-93 |
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| Snippet | Interactions between fractalkine (CX3CL1) and fractalkine receptor (CX3CR1) regulate microglial activation in the CNS. Recent findings indicate that... Background Interactions between fractalkine (CX.sub.3 CL1) and fractalkine receptor (CX.sub.3 CR1) regulate microglial activation in the CNS. Recent findings... Interactions between fractalkine (CX.sub.3 CL1) and fractalkine receptor (CX.sub.3 CR1) regulate microglial activation in the CNS. Recent findings indicate... Abstract Background: Interactions between fractalkine (CX3 CL1) and fractalkine receptor (CX3 CR1) regulate microglial activation in the CNS. Recent findings... BACKGROUND: Interactions between fractalkine (CX3CL1) and fractalkine receptor (CX3CR1) regulate microglial activation in the CNS. Recent findings indicate... Abstract Background Interactions between fractalkine (CX3CL1) and fractalkine receptor (CX3CR1) regulate microglial activation in the CNS. Recent findings... |
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| SubjectTerms | Animals Behavior, Animal - drug effects Brain Chemokine CX3CL1 - immunology Colleges & universities CX3C Chemokine Receptor 1 Depression - immunology Humans Immunity, Innate - immunology Interleukin-1beta - genetics Interleukin-1beta - metabolism Laboratory animals Lipopolysaccharides Lipopolysaccharides - immunology Lipopolysaccharides - pharmacology Medical research Mice Mice, Inbred C57BL Mice, Knockout Microglia - cytology Microglia - drug effects Microglia - immunology Microglia - physiology Motor Activity - drug effects Neurosciences Oxygenases - genetics Oxygenases - metabolism Physiological aspects Receptors, Chemokine - deficiency Receptors, Chemokine - genetics Receptors, Chemokine - immunology Rodents Social Behavior Social research Statistical analysis Tryptophan Tryptophan - metabolism |
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| Title | Fractalkine receptor (CX3CR1) deficiency sensitizes mice to the behavioral changes induced by lipopolysaccharide |
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