Research

Molecular pharmacology of inflammation


J.M. Pfeilschifter

In collaboration with H. Böhles (Frankfurt, Germany); V.A. Briner (Luzern, Switzerland); PO. Bruckner (Münster, Germany); B. Brüne (Frankfurt, Germany); J. Couchman (London, England); S-E. Dahlen (Stockholm, Sweden); J. Eble (Münster, Germany); D. Fabbro (Basel, Switzerland); J. Fischer (Düsseldorf, Germany); U. Forstermann (Mainz, Germany); H. Geiger (Frankfurt, Germany); G. Geisslinger (Frankfurt, Germany); A. Görlach (München, Germany); H-J. Gröne (Heidelberg, Gernany); A. Hartner (Erlangen, Germany); R.V. Iozzo (Phildadelphia, USA): P-J. Jacobsson (Stockholm, Sweden); R. Mason (London, England); H-J. Pavenstädt (Müünster, Germany); Sader (Frankfurt, Germany); L. Sorokin (Münster, Germany); H. Steinmetz (Frankfurt, Germany); C. Thiemermann (London, England); V. Ullrich (Konstanz, Germany); M. Young (Bethesda, USA); B. Zwissler (Frankfurt, Germany)

Introduction

Our group is interested in the molecular mechanisms of inflammation that underlie the so-called cardinal symptoms of inflammation including redness, heat, swelling and pain.These symptoms are due to vasodilatation in pericapillary beds and increased vascular permeability to solutes, followed rapidly by neutrophil and other inflammatory cell infiltration. The complexity of this stage is reflected in the large number of inflammatory mediators that are synthesized and released in response to an injurious agent, such as C5a, proteases, toxic oxygen radicals, arachidonic acid metabolites, platelet activating factor and a variety of cytokines.We use renal mesangial cells as a model system to study the regulation of key enzymes and mediators under inflammatory conditions. In addition we are interested in the signalling pathways and functions of various inflammatory cytokines such as interleukin 1, interleukin 18, interleukin 22 and tumor necrosis factor. The functional relevance of these mediators is evaluated in various experimental models of glomerulonephritis, hemorrhagic shock and endotoxemia. Cutaneous wound healing prototypically reflects processes that generally occur also in kidney injury and renegeration and form a second major research topic in the Institute.

Synthesis and function of nitric oxide and reactive oxygen species in rat
glomerular mesangial cells and the redox regulation of gene expression

(AG Beck/ Pfeilschifter)

Immunopharmacology of Autoimmune Diseases
(AG Christen)

Regulation of matrix degrading enzymes and their intrinsic inhibitors in renal
inflammation and during tumorigenesis

(AG Eberhardt)

Identification of novel NO-regulated genes involved in inflammatory
processes during renal diseases and cutaneous wound healing

(AG Frank)

Role of stress-activated protein kinases and mitogen-activated protein kinases in
inflammatory responses / Role of sphingolipids in glomerular pathophysiology

(AG Huwiler/ Pfeilschifter)

Signaltransduction by sphingosine-1-phosphate (S1P), regulation of sphingosine
kinases, regulation of calciumhomoeostasis by intracellular S1P

(AG Meyer zu Heringdorf)

The biology of the immunoregulatory cytokines IFNg, IL-18, and IL-22
(AG Mühl)

Chemokines and Chronic Inflammation
(AG Radeke)

Role of extracellular matrix components in renal pathophysiology
(AG Schaefer)

 
 
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Sekretariat Prof. Dr. Josef Pfeilschifter

N.N.
Telefon: +49-69-6301-6951
Fax: +49-69-6301-7942/ -7420
Impressum
Pub Med Online
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