For the past decade, bacteria have increasingly been proposed to play a role in the autoimmune disease known as lupus. Specifically, research has shown that biofilms containing bacteria are potential triggers of this serious disease.
A new fascinating study raises the possibility that bacteria that are commonly found on humans could trigger some of the auto-antibodies found in patients with with systemic lupus erythematosus (SLE).
About 50% of patients with SLE have anti-Ro antibodies, including anti-Ro60 antibodies. These are among the most common antinuclear antibodies that can be seen even before the disease develops. These auto-antibodies are also “pathogenic” meaning the directly cause disease.
In a new study, a research team from Yale collected microbiome samples from 8 SLE patients who were positive for anti-Ro60 autoantibodies. Controls include five SLE patients who were anti-Ro60-negative, and seven healthy controls. The researchers then took samples from the mouth, sternum, and stool. They found that commensal bacteria containing orthologs to Ro60 were found commonly in all of the patient groups.
In addition, the study investigators showed that CD4 memory T-cell clones from SLE patients that were specific to Ro60 autoantigen were stimulated by Ro60-containing bacteria. Further studies in mice showed that injection of bacteria could trigger a “lupus-like” disease. The conclusion from their study was that commensal bacterial have the potential to initiate and trigger lupus. More research is needed int his important area. This data is important and adds to a large body of research already present that infections could potentially trigger lupus.
Commensal orthologs of the human autoantigen Ro60 as triggers of autoimmunity in lupus.
Greiling TM, et al. Sci Transl Med. 2018
Article orginally posted at donovanmedical.com