A novel accessory role of neutrophils in concanavalin A-induced hepatitis

Dietary fish oil exacerbates concanavalin A induced hepatitis through promoting hepatocyte apoptosis and altering immune cell populations

“…Neutrophil-depleted mice failed to produce inflammatory IFN-γ, and hardly caused liver injury after Con A administration (Hatada et al, 2005). This neutrophil infiltration and its associated hepatocyte death were depended on purinergic P2Y2 receptors on bone marrow-derived cells (Ayata et al, 2012).…”

Immune cell-mediated liver injury

“…Searching for these immune cell subsets responsible for ConA-induced liver damage, it was demonstrated that NK T cell-deficient mice (CD1d −/− and Vα14 −/− mice) were resistant to this form of liver disease, suggesting that uncontrolled activation of these unconventional T cells, present in large numbers in the liver, plays a central role in the development of liver damage. However, not only NK T cells are essential in the development of liver disease but also several other cell subsets of the innate immune system, i.e., Kupffer cells, neutrophils, and eosinophils, have been shown to participate in the development of ConA-induced liver damage [9][10][11][12]. The exact mechanism how these different cell subsets interplay with each other in the development of liver injury is still not exactly known.…”

Over-expression of Roquin aggravates T cell mediated hepatitis in transgenic mice using T cell specific promoter

“…Con A-induced liver injury is partly driven by up-regulation of cytokines, including TNF-a, IFN-c, and IL-6 [5,6]. Recent studies of Con A-induced hepatitis have reported that neutrophils infiltrate the liver [7,8] and regulate CD4 + T cell recruitment and production of TNF-a, IFN-c, and IL-4 [3,9]. In vitro experiments have shown that Kupffer cells also contribute to the production of various cytokines by lymph nodes, including TNF-a, IFN-c, and IL-4, in response to Con A treatment [10].…”