Short Communication - (2024) Volume 8, Issue 4
Received: 01-Jul-2024, Manuscript No. Jgdr-24-144414;
Editor assigned: 03-Jul-2024, Pre QC No. P-144414;
Reviewed: 17-Jul-2024, QC No. Q-144414;
Revised: 23-Jul-2024, Manuscript No. R-144414;
Published:
31-Jul-2024
, DOI: 10.37421/2684-6039.2024.08.214
Citation: Ohi, Nair. “Environmental and Genetic Factors Influencing Ankylosing Spondylitis.” J Genet DNA Res 08 (2024): 214.
Copyright: © 2024 Ohi N. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Ankylosing Spondylitis (AS) is a chronic inflammatory disease primarily affecting the spine and sacroiliac joints, leading to progressive stiffness and pain. The pathogenesis of AS involves both genetic and environmental factors, which interact to influence disease onset and progression. This minireview explores the key genetic determinants and environmental triggers associated with AS, discussing their roles in disease development and their potential implications for prevention and management strategies. Ankylosing Spondylitis (AS) is a type of spondyloarthritis characterized by inflammation of the axial skeleton, which can lead to severe functional impairment due to spinal fusion. The disease has a multifactorial etiology, involving genetic predisposition and environmental factors. Understanding these determinants is crucial for unraveling the mechanisms behind AS and developing targeted interventions. This review examines the current knowledge of genetic and environmental influences on AS, highlighting their contributions to disease susceptibility and progression.
The HLA-B27 antigen is the strongest genetic risk factor for AS, with over 90% of patients testing positive for this allele. HLA-B27 is a class I major histocompatibility complex molecule involved in immune system regulation. Although the precise mechanism is not fully understood, it is hypothesized that HLA-B27 may present self-peptides to T cells, triggering an autoimmune response. Structural abnormalities in HLA-B27 may also contribute to disease pathogenesis. Variants in genes encoding interleukin-23 receptor and interleukin-17A have been associated with AS. These cytokines play crucial roles in inflammatory pathways and are involved in the pathogenesis of AS. TNF-alpha and IL-6: Polymorphisms in genes related to tumor necrosis factoralpha and interleukin-6 are also implicated in AS, influencing inflammatory responses and disease severity. Emerging research suggests that epigenetic modifications, such as DNA methylation and histone modifications, may influence gene expression related to AS. These modifications can be affected by environmental exposures, further complicating the disease mechanisms [1].
Gut microbiome has been proposed as a potential environmental trigger for AS. Dysbiosis, or an imbalance in gut microbiota, may contribute to systemic inflammation and immune dysregulation. Certain bacterial infections, such as those caused by Klebsiella pneumoniae, have been linked to AS. Molecular mimicry between bacterial antigens and self-antigens may trigger autoimmune responses in genetically predisposed individuals. Smoking is associated with increased risk and severity of AS. It is thought to exacerbate inflammation and modify immune responses, potentially contributing to disease progression. While physical activity is generally beneficial for AS patients, it may have a complex relationship with disease onset. Some studies suggest that lack of physical activity may increase the risk of developing AS, while others emphasize the need for tailored exercise regimens to manage symptoms [2].
There is evidence suggesting that dietary factors may influence AS risk and progression. Diets high in inflammatory foods or low in anti-inflammatory nutrients may exacerbate symptoms, though more research is needed to establish definitive links. Genetic susceptibility to AS may be influenced by environmental exposures, such as infections or smoking. For example, individuals carrying the HLA-B27 allele may have an altered response to environmental triggers, increasing their risk of developing AS. Understanding gene-environment interactions is essential for developing predictive models of AS risk. Identifying high-risk individuals based on genetic and environmental factors may lead to more effective prevention and early intervention strategies. Insights into the interplay between genetic and environmental factors can inform personalized treatment approaches. Tailoring interventions based on individual genetic profiles and environmental exposures may enhance treatment efficacy and reduce disease burden. Long-term studies are needed to better understand the temporal relationships between genetic and environmental factors in AS. Such studies could elucidate how these factors interact over time to influence disease progression [3,4]
Developing comprehensive models that integrate genetic, environmental, and lifestyle factors will be crucial for advancing our understanding of AS and improving patient outcomes. Identifying modifiable environmental factors and incorporating genetic risk assessments into clinical practice can aid in the prevention and management of AS. Public health initiatives and personalized strategies should be developed based on these insights [5].
Ankylosing Spondylitis is influenced by a complex interplay of genetic and environmental factors. The strong association with HLA-B27, along with other genetic variants, underscores the genetic component of the disease. Environmental factors, including infections, smoking, and diet, also play significant roles in disease development and progression. Understanding these determinants and their interactions is essential for advancing research, improving diagnostic approaches, and developing targeted prevention and treatment strategies.
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Journal of Genetics and DNA Research received 3 citations as per Google Scholar report
