P83 | INFLAMMATORY PROFILE IN SKIN, LUNG, AND KIDNEY OF A HOCL-INDUCED MURINE MODEL OF SYSTEMIC SCLEROSIS: AN IMMUNOHISTOCHEMICAL STUDY

G. Vermiglio¹, J. Freni¹, F. Nicita¹, A. Centofanti¹, D. Labellarte¹, E. Rizzuto¹, A. Favaloro¹, M. Runci Anastasi², G.P. Anastasi¹, G. Cutroneo¹ | ¹Department of Biomedical, Dental Sciences and Morphofunctional Imaging, University of Messina, Messina, Italy; ²Department of Maxillo-Facial Surgery, University of Rome, La Sapienza, Italy

Systemic sclerosis (SSc) is a complex autoimmune disease characterized by widespread microvascular damage, inflammation, and fibrosis^1,2. While inflammation is a recognized early event in disease pathogenesis, its distribution and intensity across different organs remain incompletely understood. This study investigates the inflammatory signature in skin, lung, and kidney of a murine model of SSc induced by daily subcutaneous injections of hypochlorous acid (HOCl) for six weeks. Tissue samples were collected and processed for histology (Hematoxylin and Eosin) and immunohistochemistry. We focused on macrophage infiltration (CD68, F4/80) and activation of the inflammasome pathway (NLRP3, Caspase-1, IL-1β). The skin displayed intense perivascular and interstitial infiltration by macrophages, along with marked NLRP3 and IL-1β expression. In the lung, inflammatory cells accumulated around bronchi and vessels, with strong upregulation of inflammasome markers. The kidney showed both glomerular and interstitial immune activation, suggesting early involvement despite minimal fibrotic remodeling.Our findings demonstrate a widespread activation of innate immune responses, particularly the NLRP3 inflammasome, in cutaneous and visceral tissues of SSc mice. These results highlight the key role of inflammation in systemic sclerosis and reinforce the importance of organ-specific histochemical profiling in understanding disease mechanisms and guiding therapeutic strategies.