Unraveling ankylosing spondylitis: Exploring the genetic and immunological factors and latest treatment innovations

Abstract

Ankylosing spondylitis (AS) is a chronic inflammatory arthritis primarily affecting the spine and sacroiliac joints. Gut microbiota significantly affects ankylosing spondylitis (AS) pathophysiology. Environmental factors, like smoking, and genetic predispositions can worsen AS. Patients often have altered fecal microbiota, decreased Bacteroides and Lachnospiraceae, and increased Proteobacteria and Enterobacteriaceae. Bacteroides coprophilus and Prevotella copri are particularly enriched in AS. This condition is associated with the HLA-B27 genetic marker and involves various immunological cells and inflammatory cytokines. To develop more effective treatments, research is ongoing to identify specific signaling pathways and genetic markers associated with AS.Gender prevalence of AS is now more evenly distributed, with women experiencing longer diagnostic delays and increased disease activity. Treatment regimens and responses to medication may vary between genders. Some case studies suggest that an Ayurvedic approach, including Panchakarma treatments and specific Ayurvedic medications, may be beneficial in managing AS. HLA-B27 and non-HLA genes such as IL23R, ERAP1, and RUNX3 are linked to AS susceptibility. The Th17 lymphocyte system, associated with IL23R, plays a role in AS pathogenesis, highlighting potential treatment targets. Over 100 genes related to AS were identified in genome-wide association studies, many connected to IL-23-driven inflammation and antigen processing. AS is regulated by various immunological cells, and changes in bone structure are caused by the interaction of immune cells with bone cells. Ankylosing spondylitis (AS) involves inflammatory cytokines like IL-1β IL-17 and IL-23. The immune system plays a crucial role in the disease, with certain proteins linked to AS risk. However, further research is needed to determine the effectiveness of this approach.