Office:	UPMC Montefiore Hospital, NW628
	3459 Fifth Avenue
	Pittsburgh, PA 15213
Phone:	412-692-2289
Fax:	412-692-2260
E-mail:	xiongz@upmc.edu

Education
	MD, Shanxi College of Chinese Medicine, China, 1988
	MS, West China University of Medical Sciences, 1995

1. Immunosuppressive effects of red cell transfusion has long been clinically recognized, but the underlying mechanisms for this effect remain elusive. Moreover, this effect may modify the outcomes of disease in critically ill patients with infection. We are currently investigating the mechanism of immune suppression in a combined bacterial pneumonia-red cell transfusion study and examining the hypothesis that red cell microparticles that accumulate within stored transfusates elicit an immunosuppressive phenotype through the suppression of NFkB gene activation. 2. Our lab has utmost interest in the role of macrophages and neutrophils in innate immune response, especially in bacteria infections. Despite recent advances in understanding macrophage activation, little is known regarding how human alveolar macrophages in health calibrate its transcriptional response to canonical TLR4 activation. With RNA-seq technology, we examined the full spectrum of LPS activation and determined whether the transcriptomic profile of human alveolar macrophages is distinguished by a TIR-domain-containing adapter-inducing interferon-ß (TRIF)-dominant type I interferon signature. We determined whether IRF-7 and USP-18 can influence downstream macrophage effector cytokine production such as IL-10. We show that IRF-7 siRNA knockdown enhanced LPS-induced IL-10 production in human monocyte-derived macrophages, and USP-18 overexpression attenuated LPS-induced production of IL-10 in RAW264.7 cells. Quantitative PCR confirmed upregulation of USP18, USP41, IL10, and IRF7. These results suggest that IRF-7 and predicted downstream target USP18, both elements of a type I interferon gene signature identified by RNA-Seq, may serve to fine-tune early cytokine response by calibrating IL-10 production in human alveolar macrophages.

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