Unravelling fatty liver haemorrhagic syndrome: 2. Inflammation and pathophysiology

To study the role of inflammation in the pathophysiology of the fatty liver haemorrhagic syndrome (FLHS), mature laying hens were treated with oestrogen (β-oestradiol-17-dipropionate or E₂) and challenged with lipopolysaccharide (LPS). Oestrogen injections induced FLHS, but the incidence and severity of the condition was increased with a combination of E₂ & LPS. Hepatic mRNA levels of the genes encoding key regulators of inflammation, such as interleukin-1β (IL-1β), interleukin-6 (IL-6) and interleukin-18 (IL-18), were evaluated. The expression of IL-6 mRNA in hepatocytes of all treated groups (E₂, LPS and E₂ & LPS hens) was elevated from 6-fold to 56-fold (P < 0.01), when compared to baseline and control values, with the highest fold change at 3 h post-treatment. The mRNA levels for IL-1β were better expressed at 24 h post-treatments with E₂, LPS and E₂ & LPS. The expression of IL-18 mRNA in the liver tissue was lower than IL-1β and IL-6 mRNA in all treated birds. At 24 h post-treatment, total white blood cell (WBC) counts and fibrinogen levels were elevated (P < 0.05) in E₂-, LPS- and E₂- & LPS-treated hens. Histologically, livers of hens from E₂- and E₂- & LPS-treated groups revealed inflammatory alterations with areas showing mononuclear aggregations, vacuolar fatty degeneration of hepatocytes, and increased sinusoidal congestion and haemorrhages. It was concluded that liver lipid accumulation and injury were associated with incidences of local (hepatic) and systemic inflammation, which could have initiated liver blood vessel and capsule rupture and, subsequently, the onset of FLHS.