Possible involvement of eosinophil Etosis in hepatic injury associated with hypereosinophilic syndrome

Abstract

Hypereosinophilic syndrome (HES) is a rare disorder characterised by persistent eosinophilia and multi-organ damage. While hepatic involvement is an uncommon complication, the underlying pathological mechanism driving tissue injury remains poorly understood, as conventional evidence of eosinophil degranulation is often difficult to ascertain in collagen-rich organs like the liver. We report a case of HES-associated liver injury that implicates eosinophil ETosis (EETosis)-an active cytolytic cell death-in the pathogenic process. A patient presented with marked eosinophilia and elevated liver enzymes. Liver biopsy revealed dense eosinophilic infiltration. Critically, double immunostaining for galectin-10 and major basic protein yielded the direct pathological evidence of EETosis within the liver tissue of an HES patient. Furthermore, the patient's peripheral blood eosinophils exhibited significant spontaneous ETosis in vitro, suggesting an inherent predisposition to tissue damage. This case demonstrates that eosinophil ETosis is a key pathogenic mechanism in HES-related hepatic injury. Our findings underscore the utility of combined galectin-10 and major basic protein staining for the pathological diagnosis of eosinophil-mediated damage and suggest that spontaneous ETosis may serve as a novel biomarker for identifying HES patients at high risk of organ involvement, providing a rationale for targeting eosinophil ETosis in therapeutic strategies.

Keywords: ETosis; Hypereosinophilic syndrome (HES); galectin-10; liver injury; major basic protein (MBP).