Cheryl Burdette ND
Our understanding of immunotolerance and autoimmunity, through gut based exposure, has grown exponentially over the years. This broadened understanding of gut based immune priming elucidates new targets for immune regulation in autoimmune conditions. As our understanding of the microbiome increases, we can understand the mechanisms that skew and support immune tolerance and T-cell differentiation. A key regulator in many autoimmune conditions includes the interaction between LipoPolySaccharide (LPS), a bacterial endotoxin, and Treg cells. Although LPS is ubiquitous to Gram-negative bacteria, and created by several commensal bacterial Genera, immune regulation to LPS also involves the interaction of Gram-positive flora such as Bifidobacter. These interactions will determine programming of naïve T-cells and influence the balance of the immune response. LPS, even more so than the bacteria that make it, is uniquely able to trigger an autoimmune process by many mechanisms. LPS is associated with Toll-Like Receptor (TLR) differentiation that is pathognomonic for certain autoimmune conditions, demonstrating its pivotal relationship. LPS is also able to decrease Treg function, a hallmark of autoimmunity, thus allowing immune function to proceed stimulated and unregulated. An understanding of LPS and its activity in immune function increases our clinical understanding and management of autoimmune conditions such as Rheumatoid arthritis, and Crohn’s Disease, to name a few.