Current Projects

• Uptake of postprandial lipoproteins into liver 
  Submitted by Joerg Heeren  (University Mediacl Center Hamburg Eppendorf, Hamburg, Germany) 1/31/2010
  Lipoproteins are predominantly taken up by liver cells. In this project we want to analyse the contribution of Kupffer cells.



• Helicobacter alters macrophages in the intestine 
  Submitted by Sherry Fleming  (Kansas State University, Manhattan, KS, United States) 1/30/2010
  Helicobacter hepaticus induces changes in the liver and colon of mice. Recent data suggests that chronic infection also changes the inflammatory response to subsequent stimuli.



• Role of macrophages in microbial induced obesity 
  Submitted by Fredrik Bäckhed  (University of Gothenburg, Gothenburg, Sweden) 1/28/2010
  Obesity is associated with increased infiltration of macrophages into the adipose tissue. We have previously shown that germ-free mice are protected against diet-induced obesity. We will use the Clodronate liposomes to investigate whether macrophages are invovled in microbiota-induced obesity.



• Macrophages and lupus 
  Submitted by Andrea Edling  (Genzyme Corporation, Framingham, MA, United States) 1/27/2010
  role of macrophages in lupus disease models



• The mechanisms of immunosuppressive effects of mesenchymal stem cells on graft-versus-host disease in vivo 
  Submitted by Ling Weng  (Imperial College, London, United Kingdom) 1/26/2010
  To understand if macrophages are involved in the mechanisms of the immunosuppressive effect of MSC on cGvHD. Clodronate will be used to deplete macrophages in vivo in our murine cGvHD model.



• Deciphering the contribution of kupffer cells to the cytotoxic response to viral pathogens 
  Submitted by Katie White  (BHF GCRC, Glasgow, United Kingdom) 1/26/2010
  Many viral pathogens (e.g hepatitis, HSV1 and AAV) preferentially target the liver, inducing a localised inflammatory response. We would like to examine the contribution of liver macrophages to the inflammatory response by measuring serum cytokine levels in macrophage-depleted animals.



• oral resistance to bacterial infection 
  Submitted by RODRIGUE DESSEIN  (inserm, Lille, France) 1/25/2010
  Evaluate the role of monocyte.macrophage in oral resistance to bacterial infection in mice



• Role of macrophages and dendritic cells in clearance of apoptotic tumor cells 
  Submitted by Sabine Hoves  (Ludwig Maximilian University, Munich, Germany) 1/23/2010
  Role of macrophages and dendritic cells in clearance of apoptotic tumor cells



• Chemokines in cutaneous inflammation and neoplasia 
  Submitted by Xuesong Wu  (Medical College of Wisconsin, Milwaukee, United States) 1/22/2010
  Our lab is interested in the roles of chemokines, which are key factors in immune response and, recently, in tumor formation and metastasis. A transplanted mouse tumor model was established in our lab which featured inflammation-promoted cutaneous T cell lymphoma (CTCL). The roles of cytokines and chemokines are studied in the tumor microenvironment. Macrophages are a major component in the inflammatory tumor environment and also a major source for inflammatory chemokines. Depletion of macrophages would help us to identify the roles of some chemokines in cutaneous lymphoma, which may be very useful in exploring effective targets for treating human CTCL.



• The role of SHIP in macrophage-mediated inflammatory responses 
  Submitted by Nicole Voglmaier  (University of British Columbia, Vancouver, BC, Canada) 1/21/2010
  The lipid phosphatase SHIP is a critical, hematopoietic-specific negative regulator of the phosphatidylinositol 3-kinase (PI3K) pathway. Despite PI3K playing an activating role in many signaling pathways and cell processes, PI3K has been shown to be a negative regulator of toll-like receptor induced inflammatory responses. We therefore predicted that SHIP deficiency, that results in enhanced or prolonged PI3K activation, might cause reduced inflammatory responses. Indeed, we have found the SHIP-/- mice are protected during DSS-induced colitis. Our next step is to ask whether the protection seen in the SHIP-/- mice in this model is specifically due to macrophages. To this end, we would like to use chlodronate-containing liposomes to deplete macrophages during DSS treatment to ask whether we can abrogate the protection observed. This work will validate a critical genetic target and identify a critical cell type involved in inflammation.