06/05/2023
Oral microbiom and autoimmune diseases ,friend or foe ?
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🌐 The human microbiome might be a major player in autoimmunity . Growing evidence has demonstrated that oral microbiota dysbiosis is actively involved in regulating the initiation and progression of an array of autoimmune diseases.
🌐 Oral microbiota is linked to a group of autoimmune diseases, namely Sjogren's syndrome (SS), systemic lupus erythematosus (SLE), Crohn's disease (CD), and rheumatoid arthritis (RA).
🌐 Mechanisms of autoimmunity triggered by dysbiotic changes and dysregulation of the immune system mediated by altered microbiome-host relationships.
🌐 The host-microbiome interaction may be influenced by several ecological changes (eating habits, aging, infection, among others) that may generate dysbiosis with the consequent activation of different local or systemic autoimmune mechanisms.
🌐 The dysregulation in the oral microbiome plays a crucial role in triggering and promoting autoimmune diseases via several mechanisms, including:⬇️⬇️ 👉🛑please see figure A
1️⃣ Autoantigens overproduction : the result of the breakdown of the extracellular matrix creating "remnant epitopes" that act as autoantigens or because of enzymatic modification of antigens (citrullination).
2️⃣ Microbial translocation : bacteria, their products or even products of immune activation against them, can migrate through the bloodstream to different organs leading to an alteration of the local inflammatory response and the production of autoantibodies.
3️⃣ Molecular mimicry : cross immune response against self-antigens induced by microbial epitopes similar in composition or structure.
4️⃣ Superantigens : Self or non-self-superantigens interact with the Vβ variable region of the TCR activating and causing T cell expansion. This is a low specificity recognition, which generates low-affinity antibodies that easily end up activating autoimmune mechanisms.
5️⃣ Dysregulation of checkpoints: alteration of the CTLA4 and PD-1 autoreactivity checkpoints in T cells, resulting in the loss of physiological modulation or regulation of the autoimmune response.
🌐 However, dysbiosis/infection and chronic inflammation could trigger autoimmunity by several mechanisms including bystander activation, dysregulation of toll-like receptors, amplification of autoimmunity by cytokines, epitope spreading, autoantigens complementarity, autoantigens overproduction, microbial translocation, molecular mimicry, superantigens, and activation,
or inhibition of receptors related to autoimmunity by microorganisms.
🌐 Thus, a comprehensive understanding of the relationship between oral microbiota dysbiosis and autoimmune diseases is critical for providing novel insights into the development of oral microbiota-based therapeutic approaches for combating these refractory diseases.
