Hepatic encephalopathy in shelter-housed Van cats: neuropathology, cytokine immunoreactivity and concurrent hepatic lipidosis
Journal of Comparative Pathology, cilt.230, ss.40-48, 2026 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 230
- Basım Tarihi: 2026
- Doi Numarası: 10.1016/j.jcpa.2026.10.002
- Dergi Adı: Journal of Comparative Pathology
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, EMBASE, MEDLINE
- Sayfa Sayıları: ss.40-48
- Anahtar Kelimeler: Alzheimer type II astrocytes, Hepatic encephalopathy, Hepatic lipidosis, Interleukin-22, Neuroinflammation, Van cat
- Van Yüzüncü Yıl Üniversitesi Adresli: Evet
Özet
Hepatic encephalopathy (HE) is a neurological disorder associated with severe hepatic dysfunction or portosystemic shunting and is increasingly recognized to involve neuroinflammatory mechanisms. This study investigated neuropathological changes and cerebral cytokine immunolabelling in shelter-housed Van cats with naturally occurring HE. Post-mortem examinations were performed on 17 male Van cats that had been housed at the Van Cat House in Van, Turkey. Twelve cats were diagnosed with HE, while five cats without neurological signs served as negative controls. Histological examination of the affected cats revealed Alzheimer type II astrocytes, neuronal degeneration and necrosis, and spongy change. Concurrent hepatic lipidosis of varying severity was identified in all cats with HE. Brain sections were subjected to immunohistochemistry for interleukin (IL)-1β, IL-6, IL-22, tumour necrosis factor (TNF) and interferon-γ, and immunolabelling was quantified as the percentage of tissue area positive for 3,3′-diaminobenzidine. Cats with HE showed significantly greater immunoreactivities for all five cytokines compared with negative controls. Cytokine immunolabelling was predominantly localized to cells morphologically consistent with astrocytes and other glial cells. The marked increase in IL-22, together with IL-1β, IL-6 and TNF, identifies IL-22 as a potential component of the broader neuroinflammatory response associated with naturally occurring feline HE. Collectively, the concurrent hepatic lipidosis, characteristic neuropathological lesions and increased cerebral cytokine immunolabelling define the principal pathological features of HE in this shelter population. To our knowledge, this is the first study to demonstrate increased cerebral IL-22 immunolabelling in naturally occurring HE.