Aberrant levels of natural IgM antibodies in osteoarthritis and rheumatoid arthritis patients in comparison to healthy controls — The Association Specialists
  1. Schedule
  2. The 3 I's: Infection, Inflamation and Immunity
  3. Aberrant levels of natural IgM antibodies in osteoarthritis and rheumatoid arthritis patients in comparison to healthy controls

Aberrant levels of natural IgM antibodies in osteoarthritis and rheumatoid arthritis patients in comparison to healthy controls (287)

Tommie Nguyen 1 2 , Kellyy McKelvey 3 , Lyn March 4 , David Hunter 5 , Chris Jackson 4 , Jonathan Morris 2 6
  1. Autoimmunity and Immunotherapy Research, Kolling Institute of Medical Research, Sydney, NSW, Australia
  2. Division of Perinatal Research, Kolling Institute of Medical Research, Sydney, NSW, Australia
  3. Sutton Arthritis Laboratory, Kolling Institute of Medical Research, Sydney, NSW, Australia
  4. Kolling Institute of Medical Research, St Leonards, NSW, Australia
  5. Department of Rheumatology, Royal North Shore Hospital, Sydney, NSW, Australia
  6. Northern Clinical School, University of Sydney, Sydney, NSW, Australia

Background: Natural IgM antibodies (nIgM) are polyreactive autoantibodies that have diverse roles in regulation of autoimmunity, inflammation, and immune responses to oxidized low-density lipoprotein (oxLDL). Altered levels of nIgM are associated with increased risks of cardiovascular disease (CVD) and some autoimmune conditions. Mounting evidence suggests that oxLDL may contribute to the development of osteoarthritis (OA) and rheumatoid arthritis (RA). Given their roles in autoimmunity and lipid oxidation, we hypothesized that aberrant states of nIgM may exist in OA and RA.
Aim: Our study characterized and compared the levels of anti-phosphorylcholine (anti-PC), anti-double stranded DNA (anti-dsDNA) and anti-galactosyl (anti-Gal) nIgM in patients with OA (n=8), RA (n=20) and healthy controls (HC, n=20).
Methods: Plasma levels of anti-PC, anti-dsDNA, anti-Gal nIgM and systematic inflammatory markers, CRP and oxLDL, were examined by ELISA. Two-tail Mann-Whitney test and Spearman’s rank correlation was performed to compare medians and examine correlation of non-parametric data sets.
Results: Levels of anti-PC nIgM were significantly lower in OA patients compared to HC and RA patients (P<0.05 and P<0.01, respectively) and remained significant after age-adjusted analysis (P<0.05). In contrast, anti-dsDNA and anti-Gal nIgM levels were significantly higher in RA patients compared to HC and OA patients (P<0.05 and P<0.01). Anti-PC nIgM levels were significantly correlated with anti-dsDNA and anti-Gal nIgM levels in HC and RA patients (P<0.05) but not in OA patients. There was no significant correlation between the levels of anti-PC nIgM and systemic inflammatory marker CRP or oxLDL in HC, OA or RA cohorts.
Conclusion: Patients with OA display a deficiency in anti-PC nIgM levels which are implicated in homeostatic regulation of oxLDL. In contrast, RA patients exhibit elevated levels of anti-dsDNA and anti-Gal nIgM that are associated with human autoimmunity. Taken together, our study highlights the evidence of aberrant state of nIgM in both OA and RA.