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| Home > Zentren > Zentrum für Diagnostik > Institut für Medizinische Mikrobiologie, Virologie und Hygiene > Arbeitsgruppe Hentschke

Group Hentschke

Subversion, manipulation and exploitation of the host cell signalling machinery by pathogens is a common phenomenon during infection and the ability of pathogens to do so often largely defines their virulence and their ability to survive within the host. A well studied example of a pathogen, which affects host cell signalling at multiple levels in a sequential and highly complex way, is the gram-negative bacterium Yersinia, which includes the species Y. enterocolitica, Y. pseudotuberculosis and Y. pestis. Essential for virulence of all Yersiniae is an approximately 70 kb plasmid (pYV) carrying genes which encode components of a protein secretion system called Type III secretion system (TTSS) and six effectors YopE, YopT, YopO/YdkA, YopH, YopP and YopM. The TTSS is a highly complex needle-like multiprotein assembly, which enables Yersiniae to pierce through the plasma membrane of contacting host cells, most often cells of the innate immune system, and to inject the preformed Yops into the cytosol. The injected Yops immediately interfere heavily with several normal host cell signalling pathways to counteract infection, which ultimately prevents phagocytosis and cytokine production. This enables Yersiniae to remain extracellularly and replicate in lymphoid tissue.
This research group characterizes the intracellular activities of several Yops of Yersinia enterocolitica and their impact on innate immunity. Furthermore, novel interaction partners have been identified and are being characterized functionally and structurally.

Another focus of our research group is the identification of bacterial resistance against novel antibiotics with yet uncharacterized or poorly understood resistance mechanisms in clinical isolates. Resistance against multiple antibiotics simultaneously in gram-positive and gram-negative bacteria is a rapidly emerging problem. In recent years several new antibiotics have been brought on the market and serve as reserve antibiotics against these multiresistant strains. Unfortunately, as with all antibiotics so far resistance against these substances is emerging as they are used more frequently in the clinics. We collect clinical isolates, which exhibit unusual phenotypes for further analysis to understand the molecular basis, emergence and dissemination of resistance against diverse recently introduced antibiotics.

Funding

Our research group is supported by grants to Moritz Hentschke from the following funding organisations:
Deutsche Forschungsgemeinschaft
ARGUS-Stiftung
Werner Otto-Stiftung
 

Staff

Projects

	Characterization of YopM Identification of novel interaction partners and analysis of manipulated signaling pathways.
	Antibiotic resistance Characterization of bacterial resistance against novel or reserve antibiotics in clinical isolates.

Recent publications

Hentschke M, Berneking L, Belmar Campos C, Buck F, Ruckdeschel K, Aepfelbacher M.
Yersinia virulence factor YopM induces sustained RSK activation by interfering with dephosphorylation.
PLoS One. 2010 Oct 5;5(10).

Hentschke M, Wolters M, Sobottka I, Rohde H, Aepfelbacher M.
ramR mutations in clinical isolates of Klebsiella pneumoniae with reduced susceptibility to tigecycline.
BMC Mol Biol. 2009 Dec 14;10:107.

Hentschke M, Christner M, Sobottka I, Aepfelbacher M, Rohde H.
Combined ramR mutation and presence of a Tn1721-associated tet(A) variant in a clinical isolate of Salmonella enterica Serovar Hadar resistant to Tigecycline.
Antimicrob Agents Chemother. 2009 Dec 22. [Epub ahead of print]

Schneegans T, Borgmeyer U, Hentschke M, Gronostajski RM, Schachner M, Tilling T.
Nuclear factor I-A represses expression of the cell adhesion molecule L1.
BMC Mol Biol. 2009 Dec 14;10:107.

Hentschke M, Hentschke S, Borgmeyer U, Hübner CA, Kurth I.
The murine AE4 promoter predominantly drives type B intercalated cell specific transcription.
Histochem Cell Biol. 2009 Oct;132(4):405-12. Epub 2009 Jun 21.

Pfeffer CK, Stein V, Keating DJ, Maier H, Rinke I, Rudhard Y, Hentschke M, Rune GM, Jentsch TJ, Hübner CA.
NKCC1-dependent GABAergic excitation drives synaptic network maturation during early hippocampal development.
J Neurosci. 2009 Mar 18;29(11):3419-30.

Roppenser B, Röder A, Hentschke M, Ruckdeschel K, Aepfelbacher M.
Yersinia enterocolitica differentially modulates RhoG activity in host cells.
J Cell Sci. 2009 Mar 1;122(Pt 5):696-705. Epub 2009 Feb 10.

Hentschke M, Süsens U, Borgmeyer U.
Transcriptional ERRgamma2-mediated activation is regulated by sentrin-specific proteases.
Biochem J. 2009 Apr 1;419(1):167-76.

Hentschke S, Malzfeldt E, Salwender HJ, Braumann D, Stang A, Hentschke M.
Hu-antibody positive limbic encephalitis in a patient with Hodgkin lymphoma.
Leuk Lymphoma. 2008 Dec;49(12):2374-6.

Hentschke M, Saager B, Horstkotte MA, Scherpe S, Wolters M, Kabisch H, Grosse R, Heisig P, Aepfelbacher M, Rohde H.
Emergence of linezolid resistance in a methicillin resistant Staphylococcus aureus strain.
Infection. 2008 Feb;36(1):85-7. Epub 2007 Dec 28.

Jacobs S, Ruusuvuori E, Sipilä ST, Haapanen A, Damkier HH, Kurth I, Hentschke M, Schweizer M, Rudhard Y, Laatikainen LM, Tyynelä J, Praetorius J, Voipio J, Hübner CA.
Mice with targeted Slc4a10 gene disruption have small brain ventricles and show reduced neuronal excitability.
Proc Natl Acad Sci U S A. 2008 Jan 8;105(1):311-6. Epub 2007 Dec 28.

Hentschke M, Trülzsch K, Heesemann J, Aepfelbacher M, Ruckdeschel K.
Serogroup-related escape of Yersinia enterocolitica YopE from degradation by the ubiquitin-proteasome pathway.
Infect Immun. 2007 Sep;75(9):4423-31. Epub 2007 Jul 2.

Hentschke S, Hentschke M, Hummel K, Salwender HJ, Braumann D, Stang A.
Bilateral thalamic infarction after reinfusion of DMSO-preserved autologous stem-cells.
Leuk Lymphoma. 2006 Nov;47(11):2418-20.

Jansen T, Graue N, Dissemond J, Hillen U, Hentschke M, Grabbe S.
Telangiectasias on the neck as a presenting cutaneous sign of Fabry disease.
J Dermatol. 2006 Sep;33(9):652-4.

Hentschke M, Kurth I, Borgmeyer U, Hübner CA.
Germ cell nuclear factor is a repressor of CRIPTO-1 and CRIPTO-3.
J Biol Chem. 2006 Nov 3;281(44):33497-504. Epub 2006 Sep 5.