Hemophagocytosis causes a consumptive anemia of inflammation

Erin E. Zoller, et al. 2011. J Exp Med. 208(6):1203-14

Speaker: Yi-Wen Yang (楊逸紋)                                       Place: Room 601

Commentator: Dr. Chiou-Feng Lin (林秋烽博士)         Time: 14:10~15:00, Oct.19, 2011

Abstract:

Hemophagocytosis describes the pathologic findings of activated macrophages engulfing blood components (1). This phenomenon is usually found with progressive hemophagocytic lymphohistiocytosis (HLH) and infectious diseases. Rapid development of cytopenia is also observed in patients with HLH or acute inflammation. Although it seems that  hemophagocytosis causes cytopenia in the acute inflammation diseases, the detailed mechanism is unclear. Previous study showed that IFN-g plays an important role in the HLH pathology and hyperinflammation (2). In this paper, the authors proved the indispensable role in consumptive anemia of inflammation (CAI) by lymphocytic choriomeningtitis virus (LCMV) and T. gondii-infected mouse models. They also noticed that systemic infusion of IFN-g could lead to anemia and hemophagocytosis. Furhermore, IFN-g acted directly on macrophages to induce hemophagocytosis and cause anemia in macrophages insensitive to IFN-g (MIIG) mouse model. The data also indicated that development of CAI was dependent on the downstream signaling of IFN-g including STAT1 and IRF-1 activation. Finally, the authors demonstrated that IFN-g-induced hemophagocytosis was a macropinocytosis process but not a receptor-mediated phagocytosis. These findings implicate a unique mechanism in macrophage-mediated pathogenic effects in acute inflammation-associated anemia.

References:

1.    David N. Fisman. Hemophagocytic syndromes and infection. Emerg Infect Dis. 2000. 6(6): 601-8.

2.    Gritta E. Janka. Hemophagocytic syndromes. Blood Rev. 2007. 21(5):245-53.