Poster

A seminar by Prof. Scott I. Simon was held on Thursday, September 24.

【ABSTRACT】
The most frequent cause of non-healing skin wounds is due to Staphylococcus aureus (SA) infections. Polymorphonuclear (PMN) leukocytes are critical in the innate immune response against pathogens. In particular, PMN recruitment and abscess formation is a hallmark of these infections and is required for bacterial clearance. Recent published data from our laboratory indicates that strategic manipulation of the inflammatory response of polymorphonuclear leukocytes (PMN) at the site of a cutaneous wound can suppress infection and improve the efficiency of non-scar healing. These studies employed non-invasive whole animal fluorescence imaging of genetically tagged EGFP-PMN mice, which provides a real-time readout of the dynamic changes in PMN recruitment and lifetime, SA burden, and wound closure. We propose to investigate three distinct mechanisms that act in concert to recruit PMN for host defense in SA-infected tissue, including:(1) a robust and sustained mobilization of PMN from the bone marrow, (2) a prolonged in vivo survival of PMN within the abscess, and (3) trafficking of ckit+ hematopoietic stem and progenitor cells (HSPC) that proliferate ckit+ and differentiate into mature PMN within the wound in a TLR2 dependent manner. In this presentation I will discuss host innate immune strategies that appear to tune PMN number and antibacterial activity to defeat antibiotic resistant SA infections of the skin.

Date	Thursday, September 24, 2015 2:00pm - 3:00pm
Speaker	Prof. Scott I. Simon／Biomedical Engineering, University of California Davis, USA
Title	"Engineering the innate immune response to cutaneous Staph-aureus infection"
Venue	Meeting Room#1, IFReC Research Building 2F
Host	Mikaël Martino（Host Defense）