dc.contributor.author |
Pretorius, Etheresia
|
|
dc.contributor.author |
Akeredolu, Oore-Ofe
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|
dc.contributor.author |
Soma, Prashilla
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dc.contributor.author |
Kell, Douglas B.
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|
dc.date.accessioned |
2018-01-16T07:52:56Z |
|
dc.date.available |
2018-01-16T07:52:56Z |
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dc.date.issued |
2017-02 |
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dc.description.abstract |
We review the evidence that infectious agents, including those that become dormant within the host, have a major role to play in much of the etiology of rheumatoid arthritis and the inflammation that is its hallmark. This occurs in particular because they can produce cross-reactive (auto-)antigens, as well as potent inflammagens such as lipopolysaccharide that can themselves catalyze further inflammagenesis, including via β-amyloid formation. A series of observables coexist in many chronic, inflammatory diseases as well as rheumatoid arthritis. They include iron dysregulation, hypercoagulability, anomalous morphologies of host erythrocytes, and microparticle formation. Iron dysregulation may be responsible for the periodic regrowth and resuscitation of the dormant bacteria, with concomitant inflammagen production. The present systems biology analysis benefits from the philosophical idea of “coherence,” that reflects the principle that if a series of ostensibly unrelated findings are brought together into a self-consistent narrative, that narrative is thereby strengthened. As such, we provide a coherent and testable narrative for the major involvement of (often dormant) bacteria in rheumatoid arthritis. |
en_ZA |
dc.description.department |
Physiology |
en_ZA |
dc.description.librarian |
hj2018 |
en_ZA |
dc.description.sponsorship |
The Manchester Centre for Synthetic Biology of Fine and Speciality Chemicals (SYNBIOCHEM) (BBSRC grant BB/M017702/1). |
en_ZA |
dc.description.uri |
http://ebm.sagepub.com |
en_ZA |
dc.identifier.citation |
Pretorius, E., Akeredolu, O.-O., Soma, P. & Kell, D.B. 2017, 'Major involvement of bacterial components in rheumatoid arthritis and its accompanying oxidative stress, systemic inflammation and hypercoagulability', Experimental Biology and Medicine, vol. 242, no. 4, pp. 355-373.
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en_ZA |
dc.identifier.issn |
1535-3702 (print) |
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dc.identifier.issn |
1535-3699 (online) |
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dc.identifier.other |
10.1177/1535370216681549 |
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dc.identifier.uri |
http://hdl.handle.net/2263/63561 |
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dc.language.iso |
en |
en_ZA |
dc.publisher |
Sage |
en_ZA |
dc.rights |
© 2016 by the Society for Experimental Biology and Medicine. This article is distributed under the terms of the Creative Commons Attribution 4.0 License (http://www.creativecommons.org/licenses/by/4.0/). |
en_ZA |
dc.subject |
Rheumatoid arthritis |
en_ZA |
dc.subject |
Dormancy |
en_ZA |
dc.subject |
Iron dysregulation |
en_ZA |
dc.subject |
Atopobiosis |
en_ZA |
dc.subject |
Infectious agents |
en_ZA |
dc.subject |
Lipopolysaccharides |
en_ZA |
dc.subject |
Proteus |
en_ZA |
dc.subject |
Inflammation |
en_ZA |
dc.subject |
Comorbidities |
en_ZA |
dc.title |
Major involvement of bacterial components in rheumatoid arthritis and its accompanying oxidative stress, systemic inflammation and hypercoagulability |
en_ZA |
dc.type |
Article |
en_ZA |