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Publications (2)6.09 Total impact

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    ABSTRACT: Sepsis is controlled by endogenous glucocorticoids (GCs). Previous studies provided evidence that crosstalk of the monomeric GC receptor (GR) with proinflammatory transcription factors is the crucial mechanism underlying the suppressive GC effect. Here we demonstrate that mice with a dimerization-deficient GR (GR(dim)) are highly susceptible to sepsis in 2 different models, namely cecal ligation and puncture and lipopolysaccharide (LPS)-induced septic shock. TNF-α is normally regulated in these mice, but down-regulation of IL-6 and IL-1β is diminished. LPS-treated macrophages derived from GR(dim) mice are largely resistant to GC actions in vitro in terms of morphology, surface marker expression, and gene expression. Treatment with recombinant IL-1 receptor antagonist improved survival of GR(dim) mice and mice lacking the GR in macrophages (GR(LysMCre)) mice. This suggests that regulation of IL-1β in macrophages by GCs is pivotal to control sepsis.
    The FASEB Journal 02/2012; 26(2):722-9. · 5.70 Impact Factor
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    ABSTRACT: The immune system and the central nervous system are able to affect each other. Proinflammatory cytokines induce the expression of CRH or AVP in the hypothalamus and ACTH in the pituitary gland. Thus, enhanced adrenal release of cortisol suppresses the activation of NF-κB and activates antiinflammatory cytokines. The cholinergic antiinflammatory pathway, the efferent arm of the inflammatory reflex, is another mechanism of the CNS to control inflammation. It consists of the efferent vagus nerve, the neurotransmitter actylcholine and the α7 subunit of the nicotinic acteylcholine receptor. Probably, the transmission of information takes place to postsynaptic sympathetic fibres in the celiac plexus which terminate in the spleen and act on splenic immune cells. Cholinesterase inhibitors have antiinflammatory effects in experimental sepsis when administered early.
    ains · Anästhesiologie · Intensivmedizin 09/2010; 45(9):574-8; quiz 579. · 0.39 Impact Factor