Analysis of the Correlation Between the Expression of T-Helper Type 17 Cell-Related Cytokines and Valve Damage in Rheumatic Heart Disease

• Published in: Curēus (Palo Alto, CA) CA), 2024-10, Vol.16 (10), p.e72759
• Main Authors: Ahmad, Fraz, Arshed, Abdur Raheem, Mumtaz, Muhammad Habib, Amjad, Fatima, Tariq, Maryyam, Fatima, Adeeba, Qammar, Bilal, Islam, Maryyam, Ahmad, Maryam, Ali, Hassam
• Format: Article
• Language: English
• Subjects: Cardiology
• ISSN: 2168-8184; 2168-8184
• DOI: 10.7759/cureus.72759

Rheumatic heart disease (RHD) results from chronic inflammation and fibrosis of heart valves following untreated rheumatic fever, yet its immunopathology, particularly involving T helper 17 (Th17) cells and their cytokines, is not fully understood. Th17 cells are prominent drivers of inflammation and have been linked to various autoimmune diseases, suggesting their potential role in RHD-related valve damage. This study examines Th17-associated cytokines-interleukin (IL)-17, IL-6, IL-23, and IL-21-in RHD. IL-17 is known to amplify inflammation by inducing pro-inflammatory cytokines and recruiting neutrophils, likely exacerbating valve damage, while IL-6 plays a role in Th17 differentiation and may promote chronic inflammation linked to fibrosis. IL-23 sustains Th17 cells, thereby perpetuating the inflammatory cycle in RHD, and IL-21 influences Th17 cells and B cell responses, potentially linking adaptive immunity to valve pathology. Clarifying the roles of these cytokines could offer insights into novel therapeutic targets for mitigating inflammation and preventing disease progression in RHD. This study included 20 patients with RHD undergoing mitral valve replacement (Group O) and 20 patients with degenerative mitral valve prolapse (Group C) as controls. We utilized immunohistochemical staining and hematoxylin and eosin staining to assess the expression of Th17 cell-related cytokines in heart valves. To explore the relationship between cytokine expression and valve damage, Spearman correlation analysis was conducted. For inter-group comparisons, we employed the Mann-Whitney U test and Wilcoxon rank-sum test for non-parametric data, facilitating the evaluation of significant differences in cytokine levels and other relevant variables. In Group O, the percentage of IL-17-positive cells in mitral valve tissue was 51.6 ± 18.4%, with an immunohistochemistry score of 3.7 ± 2.2. IL-21-positive cells constituted 54.2 ± 16.5% with a score of 5.2 ± 1.3, IL-6-positive cells were at 29.4 ± 17.3% (score of 3.9 ± 1.5), and IL-23-positive cells accounted for 33.7 ± 17.9% (score of 4.3 ± 1.6). All these cytokine levels were significantly higher in Group O compared to Group C (P < 0.05), and the expression levels of IL-17, IL-21, IL-6, and IL-23 in valve tissue positively correlated with heart valve damage (P < 0.05). The main findings indicated that patients with RHD had significantly elevated levels of pro-inflammatory cytokines, including TNF-α, IL-6, and IL-10, compare