New insights into the impact of neuro-inflammation in rheumatoid arthritis
Rheumatoid arthritis (RA) is considered to be, in many respects, an archetypal autoimmune disease that causes activation of pro-inflammatory pathways resulting in joint and systemic inflammation. RA remains a major clinical problem with the development of several new therapies targeted at cytokine i...
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Format: | Article |
Language: | English |
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Frontiers Media S.A.
2014-11-01
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Series: | Frontiers in Neuroscience |
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Online Access: | http://journal.frontiersin.org/Journal/10.3389/fnins.2014.00357/full |
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author | Nicholas Rubek Fuggle Franklyn eHowe Rachel Louise Allen Nidhi eSofat |
author_facet | Nicholas Rubek Fuggle Franklyn eHowe Rachel Louise Allen Nidhi eSofat |
author_sort | Nicholas Rubek Fuggle |
collection | DOAJ |
description | Rheumatoid arthritis (RA) is considered to be, in many respects, an archetypal autoimmune disease that causes activation of pro-inflammatory pathways resulting in joint and systemic inflammation. RA remains a major clinical problem with the development of several new therapies targeted at cytokine inhibition in recent years. In RA, biologic therapies targeted at inhibition of tumor necrosis factor alpha (TNFα) have been shown to reduce joint inflammation, limit erosive change, reduce disability and improve quality of life. The cytokine TNFα has a central role in systemic RA inflammation and has also been shown to have pro-inflammatory effects in the brain. Emerging data suggests there is an important bidirectional communication between the brain and immune system in inflammatory conditions like RA. Recent work has shown how TNF inhibitor therapy in people with RA is protective for Alzheimer’s disease. Functional MRI studies to measure brain activation in people with RA to stimulus by finger joint compression, have also shown that those who responded to TNF inhibition showed a significantly greater activation volume in thalamic, limbic, and associative areas of the brain than non-responders. Infections are the main risk of therapies with biologic drugs and infections have been shown to be related to disease flares in RA. Recent basic science data has also emerged suggesting that bacterial components including lipopolysaccharide induce pain by directly activating sensory neurons that modulate inflammation, a previously unsuspected role for the nervous system in host-pathogen interactions. In this review, we discuss the current evidence for neuro-inflammation as an important factor that impacts on disease persistence and pain in RA. |
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issn | 1662-453X |
language | English |
last_indexed | 2024-12-23T13:22:08Z |
publishDate | 2014-11-01 |
publisher | Frontiers Media S.A. |
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series | Frontiers in Neuroscience |
spelling | doaj.art-a99474cc147d466c87d20180f3fb5c4f2022-12-21T17:45:25ZengFrontiers Media S.A.Frontiers in Neuroscience1662-453X2014-11-01810.3389/fnins.2014.00357117393New insights into the impact of neuro-inflammation in rheumatoid arthritisNicholas Rubek Fuggle0Franklyn eHowe1Rachel Louise Allen2Nidhi eSofat3St George's, University of LondonSt George's, University of LondonSt George's, University of LondonSt George's, University of LondonRheumatoid arthritis (RA) is considered to be, in many respects, an archetypal autoimmune disease that causes activation of pro-inflammatory pathways resulting in joint and systemic inflammation. RA remains a major clinical problem with the development of several new therapies targeted at cytokine inhibition in recent years. In RA, biologic therapies targeted at inhibition of tumor necrosis factor alpha (TNFα) have been shown to reduce joint inflammation, limit erosive change, reduce disability and improve quality of life. The cytokine TNFα has a central role in systemic RA inflammation and has also been shown to have pro-inflammatory effects in the brain. Emerging data suggests there is an important bidirectional communication between the brain and immune system in inflammatory conditions like RA. Recent work has shown how TNF inhibitor therapy in people with RA is protective for Alzheimer’s disease. Functional MRI studies to measure brain activation in people with RA to stimulus by finger joint compression, have also shown that those who responded to TNF inhibition showed a significantly greater activation volume in thalamic, limbic, and associative areas of the brain than non-responders. Infections are the main risk of therapies with biologic drugs and infections have been shown to be related to disease flares in RA. Recent basic science data has also emerged suggesting that bacterial components including lipopolysaccharide induce pain by directly activating sensory neurons that modulate inflammation, a previously unsuspected role for the nervous system in host-pathogen interactions. In this review, we discuss the current evidence for neuro-inflammation as an important factor that impacts on disease persistence and pain in RA.http://journal.frontiersin.org/Journal/10.3389/fnins.2014.00357/fullInfectionNeuroimaginglipopolysaccharideRheumatoid arthritisNeuroinflammationtumor necrosis factor alpha |
spellingShingle | Nicholas Rubek Fuggle Franklyn eHowe Rachel Louise Allen Nidhi eSofat New insights into the impact of neuro-inflammation in rheumatoid arthritis Frontiers in Neuroscience Infection Neuroimaging lipopolysaccharide Rheumatoid arthritis Neuroinflammation tumor necrosis factor alpha |
title | New insights into the impact of neuro-inflammation in rheumatoid arthritis |
title_full | New insights into the impact of neuro-inflammation in rheumatoid arthritis |
title_fullStr | New insights into the impact of neuro-inflammation in rheumatoid arthritis |
title_full_unstemmed | New insights into the impact of neuro-inflammation in rheumatoid arthritis |
title_short | New insights into the impact of neuro-inflammation in rheumatoid arthritis |
title_sort | new insights into the impact of neuro inflammation in rheumatoid arthritis |
topic | Infection Neuroimaging lipopolysaccharide Rheumatoid arthritis Neuroinflammation tumor necrosis factor alpha |
url | http://journal.frontiersin.org/Journal/10.3389/fnins.2014.00357/full |
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