IFN-β is a macrophage-derived effector cytokine facilitating the resolution of bacterial inflammation

Senthil Kumaran Satyanarayanan, Driss El Kebir, Soaad Soboh, Sergei Butenko, Meriem Sekheri, Janan Saadi, Neta Peled, Simaan Assi, Amira Othman, Sagie Schif-Zuck, Yonatan Feuermann, Dalit Barkan, Noa Sher, János G. Filep () and Amiram Ariel ()
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Senthil Kumaran Satyanarayanan: University of Haifa
Driss El Kebir: University of Montreal, and Research Center, Maisonneuve-Rosemont Hospital
Soaad Soboh: University of Haifa
Sergei Butenko: University of Haifa
Meriem Sekheri: University of Montreal, and Research Center, Maisonneuve-Rosemont Hospital
Janan Saadi: University of Haifa
Neta Peled: University of Haifa
Simaan Assi: University of Haifa
Amira Othman: University of Montreal, and Research Center, Maisonneuve-Rosemont Hospital
Sagie Schif-Zuck: University of Haifa
Yonatan Feuermann: ResCure Pharma
Dalit Barkan: University of Haifa
Noa Sher: University of Haifa
János G. Filep: University of Montreal, and Research Center, Maisonneuve-Rosemont Hospital
Amiram Ariel: University of Haifa

Nature Communications, 2019, vol. 10, issue 1, 1-16

Abstract: Abstract The uptake of apoptotic polymorphonuclear cells (PMN) by macrophages is critical for timely resolution of inflammation. High-burden uptake of apoptotic cells is associated with loss of phagocytosis in resolution phase macrophages. Here, using a transcriptomic analysis of macrophage subsets, we show that non-phagocytic resolution phase macrophages express a distinct IFN-β-related gene signature in mice. We also report elevated levels of IFN-β in peritoneal and broncho-alveolar exudates in mice during the resolution of peritonitis and pneumonia, respectively. Elimination of endogenous IFN-β impairs, whereas treatment with exogenous IFN-β enhances, bacterial clearance, PMN apoptosis, efferocytosis and macrophage reprogramming. STAT3 signalling in response to IFN-β promotes apoptosis of human PMNs. Finally, uptake of apoptotic cells promotes loss of phagocytic capacity in macrophages alongside decreased surface expression of efferocytic receptors in vivo. Collectively, these results identify IFN-β produced by resolution phase macrophages as an effector cytokine in resolving bacterial inflammation.

Date: 2019
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DOI: 10.1038/s41467-019-10903-9

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