Tobacco-derived Lipopolysaccharide, not microbial translocation, as a potential contributor to the pathogenesis of rheumatoid arthritis

dc.contributor.authorMeyer, Pieter Willem Adriaan
dc.contributor.authorAlly, Mahmood Moosa Tar Mahomed
dc.contributor.authorTikly, Mohammed
dc.contributor.authorTintinger, Gregory Ronald
dc.contributor.authorWinchow, Lai Ling
dc.contributor.authorSteel, Helen Carolyn
dc.contributor.authorAnderson, Ronald
dc.contributor.emailpieter.meyer@up.ac.zaen_ZA
dc.date.accessioned2020-03-02T07:28:31Z
dc.date.available2020-03-02T07:28:31Z
dc.date.issued2019
dc.description.abstractMicrobial lipopolysaccharides (LPS) have been implicated in the pathogenesis of rheumatoid arthritis (RA), possibly driving a systemic inflammatory response that may trigger the development and/or exacerbation of the disease. To explore the existence of this mechanism in African RA patients, we have measured systemic levels of LPS and its surrogate, LPS-binding protein (LBP), as well as those of intestinal fatty acid-binding protein (I-FABP), pulmonary surfactant protein D (SP-D), and cotinine in serum to identify possible origins of LPS, as well as associations of these biomarkers with rheumatoid factor (RF) and anticitrullinated peptide (aCCP) autoantibodies and the DAS 28-3 clinical disease severity score. A cohort of 40 diseasemodifying antirheumatic drug-naïve, black South African RA patients rated by compound disease scores and 20 healthy subjects and 10 patients with chronic obstructive pulmonary disease (COPD) as controls were included in this study. Levels of the various biomarkers and autoantibodies were measured using a combination of ELISA and immunofluorimetric and immunoturbidometric procedures. LPS levels were lowest in the RA group compared to the healthy controls (p = 0:026) and COPD patients (p = 0:017), while LBP levels were also significantly lower in RA compared to the healthy individuals (p = 0:036). Levels of I-FABP and SP-D were comparable between all three groups. Categorisation of RA patients according to tobacco usage revealed the following significant positive correlations: LBP with C-reactive protein (p = 0:0137); a trend (p = 0:073) towards an association of LBP with the DAS 28-3 disease severity score; RF-IgG antibodies with both LPS and LBP (p = 0:033 and p = 0:041, respectively); aCCP-IgG antibodies with LPS (p = 0:044); and aCCP-IgG with RF-IgM autoantibodies (p = 0:0016). The findings of this study, several of them novel, imply that tobacco products, as opposed to microbial translocation, represent a potential source of LPS in this study cohort of RA patients, again underscoring the risks posed by tobacco usage for the development and severity of RA.en_ZA
dc.description.departmentImmunologyen_ZA
dc.description.departmentInternal Medicineen_ZA
dc.description.librarianam2020en_ZA
dc.description.sponsorshipThe research and publication of this article is funded by departmental research funds.en_ZA
dc.description.urihttps://www.hindawi.com/journals/mien_ZA
dc.identifier.citationMeyer, P.W.A., Ally, M.M.T.M., Tikly, M. 2019, 'Tobacco-derived Lipopolysaccharide, not microbial translocation, as a potential contributor to the pathogenesis of rheumatoid arthritis', Mediators of Inflammation, no. 4693870, pp. 1-7.en_ZA
dc.identifier.issn0962-9351 (print)
dc.identifier.issn1466-1861 (online)
dc.identifier.other10.1155/2019/4693870
dc.identifier.urihttp://hdl.handle.net/2263/73620
dc.language.isoenen_ZA
dc.publisherHindawi Publishingen_ZA
dc.rights© 2019 Pieter W. A. Meyer et al. This is an open access article distributed under the Creative Commons Attribution License.en_ZA
dc.subjectIntestinal fatty acid-binding proteinen_ZA
dc.subjectPatientsen_ZA
dc.subjectMicrobial lipopolysaccharides (LPS)en_ZA
dc.subjectRheumatoid arthritis (RA)en_ZA
dc.subjectLPS-binding protein (LBP)en_ZA
dc.subjectIntestinal fatty acid-binding protein (I-FABP)en_ZA
dc.subjectCotinine in serumen_ZA
dc.subjectPulmonary surfactant protein D (SP-D)en_ZA
dc.titleTobacco-derived Lipopolysaccharide, not microbial translocation, as a potential contributor to the pathogenesis of rheumatoid arthritisen_ZA
dc.typeArticleen_ZA

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