Sickness behaviour is induced by a peripheral CXC-chemokine also expressed in multiple sclerosis and EAE.
Non-CNS chemokine production may contribute to previously unrecognised components of Multiple Sclerosis (MS) pathology. Here we show that IL-8, a neutrophil chemoattractant, is significantly increased in serum from individuals with MS, and that the rodent homolog of IL-8 (CXCL1) is expressed in the...
| Main Authors: | , , , , , , , , |
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| Format: | Journal article |
| Language: | English |
| Published: |
2010
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| _version_ | 1797059528334770176 |
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| author | Campbell, S Meier, U Mardiguian, S Jiang, Y Littleton, E Bristow, A Relton, J Connor, T Anthony, D |
| author_facet | Campbell, S Meier, U Mardiguian, S Jiang, Y Littleton, E Bristow, A Relton, J Connor, T Anthony, D |
| author_sort | Campbell, S |
| collection | OXFORD |
| description | Non-CNS chemokine production may contribute to previously unrecognised components of Multiple Sclerosis (MS) pathology. Here we show that IL-8, a neutrophil chemoattractant, is significantly increased in serum from individuals with MS, and that the rodent homolog of IL-8 (CXCL1) is expressed in the liver in experimental autoimmune encephalomyelitis (EAE), a rodent model of MS. The hepatic expression of CXCL1 in EAE is accompanied by neutrophil recruitment to the liver, and we show that this recruitment is a feature of post mortem liver tissue from MS patients, which is a previously unrecognised phenomenon. We speculated that the presence of peripheral CXC-chemokine expression might contribute to the sickness behaviours associated with MS, which are a significant contributor to morbidity. Peripheral, but not central, administration of CXCL1 to Wistar rats inhibited spontaneous activity in the open field and burrowing behaviour in a dose-dependent manner (5-45 microg). The expression of CXCL1 by the liver and the recruitment of neutrophils can be modelled by the intracerebral injection of IL-1beta. Here, we found that interferon-beta (IFN-beta) pretreatment significantly inhibited hepatic CXCL1 production and neutrophil recruitment to the liver induced by the microinjection of IL-1beta into the brain. Thus while the mechanism by which IFN-beta therapy suppresses disease in MS remains unclear, the data presented here suggests that the inhibition of hepatic chemokine synthesis may be a contributing factor. |
| first_indexed | 2024-03-06T20:05:34Z |
| format | Journal article |
| id | oxford-uuid:28cae585-6693-4542-af9d-d86a0666fb1c |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-06T20:05:34Z |
| publishDate | 2010 |
| record_format | dspace |
| spelling | oxford-uuid:28cae585-6693-4542-af9d-d86a0666fb1c2022-03-26T12:15:06ZSickness behaviour is induced by a peripheral CXC-chemokine also expressed in multiple sclerosis and EAE.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:28cae585-6693-4542-af9d-d86a0666fb1cEnglishSymplectic Elements at Oxford2010Campbell, SMeier, UMardiguian, SJiang, YLittleton, EBristow, ARelton, JConnor, TAnthony, DNon-CNS chemokine production may contribute to previously unrecognised components of Multiple Sclerosis (MS) pathology. Here we show that IL-8, a neutrophil chemoattractant, is significantly increased in serum from individuals with MS, and that the rodent homolog of IL-8 (CXCL1) is expressed in the liver in experimental autoimmune encephalomyelitis (EAE), a rodent model of MS. The hepatic expression of CXCL1 in EAE is accompanied by neutrophil recruitment to the liver, and we show that this recruitment is a feature of post mortem liver tissue from MS patients, which is a previously unrecognised phenomenon. We speculated that the presence of peripheral CXC-chemokine expression might contribute to the sickness behaviours associated with MS, which are a significant contributor to morbidity. Peripheral, but not central, administration of CXCL1 to Wistar rats inhibited spontaneous activity in the open field and burrowing behaviour in a dose-dependent manner (5-45 microg). The expression of CXCL1 by the liver and the recruitment of neutrophils can be modelled by the intracerebral injection of IL-1beta. Here, we found that interferon-beta (IFN-beta) pretreatment significantly inhibited hepatic CXCL1 production and neutrophil recruitment to the liver induced by the microinjection of IL-1beta into the brain. Thus while the mechanism by which IFN-beta therapy suppresses disease in MS remains unclear, the data presented here suggests that the inhibition of hepatic chemokine synthesis may be a contributing factor. |
| spellingShingle | Campbell, S Meier, U Mardiguian, S Jiang, Y Littleton, E Bristow, A Relton, J Connor, T Anthony, D Sickness behaviour is induced by a peripheral CXC-chemokine also expressed in multiple sclerosis and EAE. |
| title | Sickness behaviour is induced by a peripheral CXC-chemokine also expressed in multiple sclerosis and EAE. |
| title_full | Sickness behaviour is induced by a peripheral CXC-chemokine also expressed in multiple sclerosis and EAE. |
| title_fullStr | Sickness behaviour is induced by a peripheral CXC-chemokine also expressed in multiple sclerosis and EAE. |
| title_full_unstemmed | Sickness behaviour is induced by a peripheral CXC-chemokine also expressed in multiple sclerosis and EAE. |
| title_short | Sickness behaviour is induced by a peripheral CXC-chemokine also expressed in multiple sclerosis and EAE. |
| title_sort | sickness behaviour is induced by a peripheral cxc chemokine also expressed in multiple sclerosis and eae |
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