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 (beta-oestradiol-17-dipropionate or E-2) and challenged with lipopolysaccharide (LPS). Oestrogen injections induced FLHS, but the incidence and severity of the condition was increased with a combination of E-2 & LPS. Hepatic mRNA levels of the genes encoding key regulators of inflammation, such as interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6) and interleukin-18 (IL-18), were evaluated. The expression of IL-6 mRNA in hepatocytes of all treated groups (E-2, LPS and E-2 & 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 3h post-treatment. The mRNA levels for IL-1 beta were better expressed at 24h post-treatments with E-2, LPS and E-2 & LPS. The expression of IL-18 mRNA in the liver tissue was lower than IL-1 beta and IL-6 mRNA in all treated birds. At 24h post-treatment, total white blood cell (WBC) counts and fibrinogen levels were elevated (P<0.05) in E-2-, LPS- and E-2- & LPS-treated hens. Histologically, livers of hens from E-2- and E-2- & 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.