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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Main Authors: Nicholas Rubek Fuggle, Franklyn eHowe, Rachel Louise Allen, Nidhi eSofat
Format: Article
Language:English
Published: Frontiers Media S.A. 2014-11-01
Series:Frontiers in Neuroscience
Subjects:
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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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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AT nidhiesofat newinsightsintotheimpactofneuroinflammationinrheumatoidarthritis