TY  - JOUR
A1  - Kunz, Meik
A1  - Liang, Chunguang
A1  - Nilla, Santosh
A1  - Cecil, Alexander
A1  - Dandekar, Thomas
T1  - The drug-minded protein interaction database (DrumPID) for efficient target analysis and drug development
JF  - Database
N2  - The drug-minded protein interaction database (DrumPID) has been designed to provide fast, tailored information on drugs and their protein networks including indications, protein targets and side-targets. Starting queries include compound, target and protein interactions and organism-specific protein families. Furthermore, drug name, chemical structures and their SMILES notation, affected proteins (potential drug targets), organisms as well as diseases can be queried including various combinations and refinement of searches. Drugs and protein interactions are analyzed in detail with reference to protein structures and catalytic domains, related compound structures as well as potential targets in other organisms. DrumPID considers drug functionality, compound similarity, target structure, interactome analysis and organismic range for a compound, useful for drug development, predicting drug side-effects and structure–activity relationships.
KW  - drug-minded protein
KW  - database
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-147369
VL  - 2016
ER  - 
TY  - JOUR
A1  - Rosenbaum, Corinna
A1  - Schick, Martin Alexander
A1  - Wollborn, Jakob
A1  - Heider, Andreas
A1  - Scholz, Claus-Jürgen
A1  - Cecil, Alexander
A1  - Niesler, Beate
A1  - Hirrlinger, Johannes
A1  - Walles, Heike
A1  - Metzger, Marco
T1  - Activation of Myenteric Glia during Acute Inflammation In Vitro and In Vivo
JF  - PLoS One
N2  - Background
Enteric glial cells (EGCs) are the main constituent of the enteric nervous system and share similarities with astrocytes from the central nervous system including their reactivity to an inflammatory microenvironment. Previous studies on EGC pathophysiology have specifically focused on mucosal glia activation and its contribution to mucosal inflammatory processes observed in the gut of inflammatory bowel disease (IBD) patients. In contrast knowledge is scarce on intestinal inflammation not locally restricted to the mucosa but systemically affecting the intestine and its effect on the overall EGC network.

Methods and Results
In this study, we analyzed the biological effects of a systemic LPS-induced hyperinflammatory insult on overall EGCs in a rat model in vivo, mimicking the clinical situation of systemic inflammation response syndrome (SIRS). Tissues from small and large intestine were removed 4 hours after systemic LPS-injection and analyzed on transcript and protein level. Laser capture microdissection was performed to study plexus-specific gene expression alterations. Upon systemic LPS-injection in vivo we observed a rapid and dramatic activation of Glial Fibrillary Acidic Protein (GFAP)-expressing glia on mRNA level, locally restricted to the myenteric plexus. To study the specific role of the GFAP subpopulation, we established flow cytometry-purified primary glial cell cultures from GFAP promotor-driven EGFP reporter mice. After LPS stimulation, we analyzed cytokine secretion and global gene expression profiles, which were finally implemented in a bioinformatic comparative transcriptome analysis. Enriched GFAP+ glial cells cultured as gliospheres secreted increased levels of prominent inflammatory cytokines upon LPS stimulation. Additionally, a shift in myenteric glial gene expression profile was induced that predominantly affected genes associated with immune response.

Conclusion and Significance
Our findings identify the myenteric GFAP-expressing glial subpopulation as particularly susceptible and responsive to acute systemic inflammation of the gut wall and complement knowledge on glial involvement in mucosal inflammation of the intestine.
KW  - gene expression
KW  - gastrointestinal tract
KW  - inflammatory bowel disease
KW  - central nervous system
KW  - systemic inflammatory response syndrome
KW  - inflammation
KW  - astrocytes
KW  - cytokines
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-146544
VL  - 11
IS  - 3
ER  -