Abstract
Feline eosinophilic sclerosing fibroplasia (FESF) is a unique fibroproliferative disease of cats marked by eosinophilic inflammation and extensive tissue fibroplasia that affects the gastrointestinal tract predominantly. Biopsy specimens were examined from an 11-y-old, spayed female, domestic shorthair cat with a 1–2-mo history of vomiting and anorexia, abdominal lymphadenopathy, and multiple hepatic nodules. Microscopically, the liver nodules and enlarged mesenteric lymph node had profound eosinophilic inflammation and sclerosis characteristic of FESF; the stomach, duodenum, jejunum, and ileum were unremarkable. Immunohistochemistry (IHC) was performed to further characterize the cell populations. Increased intralesional mesenchymal cells, interpreted as reactive fibroblasts, were positive with antibodies against smooth muscle actin (SMA), indicating a myofibroblast phenotype. Abundant intralesional macrophages were ionized calcium–binding adapter molecule 1 (IBA1) immunolabeled. Dual IHC of SMA and IBA1 revealed several double-positive mesenchymal cells, suggesting macrophage-to-myofibroblast transition (MMT). Our findings underscore the important role of macrophages not only in chronic inflammation, but also in tissue repair and fibrosis. Our case was a unique presentation of FESF with primary liver and mesenteric lymph node involvement, and without overt gastrointestinal lesions. Additionally, to our knowledge, myofibroblast phenoconversion and MMT have not been reported previously in cats, giving new insights to the pathogenesis of this poorly understood disease entity.
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