IgG antibodies from fibromyalgia patients bind more mouse gut bacteria
Hannah Cho1,2, Carolina B. Meloto1,2, Luda Diatchenko1,2, Emerson Krock1,2
1. Faculty of Dental Medicine and Oral Health Sciences, 缅北强奸, 2. Alan Edwards Centre for Research on Pain
Introduction:
We previously found that transferring IgG from fibromyalgia (FM) patients into mice induces pain-like behaviour. The FM IgG binds satellite glial cells in the dorsal root ganglia and gliabinding IgG is elevated in FM patients with more severe pain. These findings suggest that IgG autoantibodies could drive a subset of FM. However, why FM autoantibodies develop remains unclear. The gut microbiome is altered in FM patients and is linked to pain in humans and mice. Therefore, one possibility is that FM autoantibodies develop through cross reactivity with gut microbiota. Our initial study aims to establish methodology for quantifying circulating IgG binding to gut bacteria.
Methods: IgG was purified from primary FM (n=8) and healthy control (HC) serum (n=13) using Protein G columns. Purified IgG was incubated with mouse gut bacteria and then with fluorescently
conjugated antibodies against IgG (Alexa Fluor 647) and a bacterial DNA stain (SytoBC). IgG binding was quantified using a BD LSR Fortessa flow cytometer and data was analyzed in FlowJo.
Results: FM IgG binding to mouse gut bacteria is increased compared to HC IgG (Figure 1). Moreover, IgG binding to mouse gut bacteria was positively correlated with the previously reported levels
of IgG binding to satellite glial cells (SGC).
Conclusions: IgG from FM patients has increased binding to mouse gut bacteria, suggesting that there is abnormal immune activity in the gut lumen. Future studies will identify bacteria that are cross reactive with fibromyalgia autoantibodies. Figure 1. Proportionate comparison of IgG bound bacteria (dead, live, and all) by patient groups.
