Anti-Bacterial Antibodies

Studies have shown that environmental factors, especially gut microbes and their toxins, may play a pathogenic role in autoimmune diseases such as rheumatoid arthritis (RA), inflammatory bowel diseases (IBDs), systemic lupus erythematosus (SLE) and other chronic diseases. Furthermore, increased translocation of bacteria and bacterial toxins due to high mucosal permeability and low immune function may be a major and common pathogenesis of autoimmune diseases. To facilitate research in this field, Creative Diagnostics offers several mouse antibacterial monoclonal antibodies that can be used in the development of human and mouse anti-bacterial antibody detection kits.

Background

Multiple lines of evidence have linked dysbiosis to barrier autoimmunity and beyond, particularly in the setting of IBD, rheumatoid arthritis, type I diabetes and multiple sclerosis (Fig 1). One hypothesis is that in the settings of intestinal inflammation, impairment of the gut barrier results in bacterial translocation, which then stimulates immune reactions in distant organs. Alternatively, immune cells are abnormally skewed by dysbiosis, as observed for Th17 polarization. Indeed, Th17 cells are most abundant in the lamina propria of the intestine, where they secrete the pro-inflammatory cytokines interleukin (IL)-17A, IL-17F and IL-22 to enforce gut barrier integrity and defense against pathogens. It is now widely accepted that understanding the complex interactions between the microbiome and immune system will be crucial to defining and treating or reversing the pathogenesis of chronic autoimmune diseases.

Fig 1. The proposed link between the gut microbiome and systemic autoimmune diseases

The commensal microbiome utilizes multiple pathways to shape mucosal immunity, and its impact may reach non-mucosal tissues and thus contribute to systemic autoimmunity in genetically susceptible individuals. The currently available techniques to detail the functions of the intestinal microbiome has provided more accurate information regarding the microbial changes in human autoimmune diseases. However, the scenario is complicated by the variability of the intestinal flora over short periods of time, which does not allow a historical perspective of the observed changes years after the initiation of the autoimmune process. Whether the observed changes are the cause or the consequence of the disease (or its treatment) remains enigmatic. Larger, longitudinal and well-controlled microbiome-wide studies are expected in the future field of autoimmune diseases, to better understand the potential confounders as well as the importance of the observed differences.