Abstract

Background:
The persistence of the activation of pro-inflammatory cytokines, which facilitates the pathological tissue remodeling by disrupting the extracellular matrix (ECM), has been identified as a risk factor for chronic inflammation. A disproportion in the proinflammatory cytokines and anti-inflammatory cytokines enhances tissue destruction and disease etiology.

Aim:
This study aimed to assess the role of inflammatory cytokines and tissue remodeling markers in disease progression and determine the association of these factors with systemic inflammation and structural tissue changes.

Methods:
The study was a hospital-based case-control study that was conducted between February 20 and October 15, 2024, and involved 150 participants (100 with chronic inflammatory disease involving tissue remodeling and 50 healthy controls). The clinical and laboratory diagnoses were made. Serum samples of pro-inflammatory cytokines interleukin-6 [IL-6, tumor necrosis factor (TNF) a, IL-1 b, and C-reactive protein (CRP)], regulatory cytokines interleukin-10 (IL-10, TGFB), and tissue remodeling markers matrix metalloproteinases [MMP-2, MMP-9, and Tissue metalloproteinase inhibitors (TIMP)-1] were obtained by Enzyme-Linked Immunosorbent Assay.

Results:
Age and sex were not different between patients and controls, which demonstrated demographic homogeneity. However, patients were older, smoked more, and had more diabetes, which is evidence of the presence of inflammation-facilitating risk factors. The levels of pro-inflammatory cytokines (IL-6, TNF- 02, interleukin-1 beta) and CRP were significantly high in the patients, indicating active systemic inflammation. Conversely, the levels of anti-inflammatory cytokines (IL-10, transforming growth factor-beta), on the other hand, were decreased significantly. The tissue markers of remodeling were found to be more MMP-2 and MMP-9 with less TIMP-1, indicating dysregulated ECM turnover.

Conclusion:
Excess pro-inflammatory cytokine activity and the absence of regulatory signaling are features of chronic inflammatory diseases that cause dysregulated matrix remodeling. High levels of IL-6, TNF, and MMPs stimulate the degradation of the ECM, whereas low levels of IL-10 and TIMP-1 do not balance the effects of inflammation, increasing tissue destruction and disease progression.

Key words: Inflammatory cytokines; Tissue remodeling; Disease progression; Matrix metalloproteinases; Tissue remodeling.