Chris Galanos
Max Planck Society
176 Papers
4.3K Citations
Chris Galanos is an academic researcher from Max Planck Society. The author has contributed to research in topics: Lipid A & Lipopolysaccharide. The author has an hindex of 63, co-authored 175 publications. Previous affiliations of Chris Galanos include University of Texas Southwestern Medical Center.
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Papers
•Journal Article
Phase I Trial of Intravenously Administered Endotoxin (Salmonella abortus equi) in Cancer Patients
TL;DR: Hematological changes included transient decreases in WBCs affecting granulocytes, monocytes, and lymphocytes in a marked different pattern and endogenous cytokine release occurred in an LPS dose-dependent manner as measured by tumor necrosis factor-alpha, interleukin-6, and macrophage colony-stimulating factor serum levels.
Characterisation of protein co-extracted together with LPS in Escherichia coli, Salmonella minnesota and Yersinia enterocolitica.
TL;DR: It is demonstrated that the porin proteins of Escherichia coli, Yersinia enterocolitica, and Salmonella minnesota were extracted from bacteria as a high molecular weight protein-lipopolysaccharide complex and once exposed to phenolic conditions, the protein was no longer soluble in the phenol-chloroform-petroleum ether extraction mixture, indicating a highly specific lipopoly Saccharide-protein association.
Analysis of Salmonella lipopolysaccharides by sodium deoxycholate-polyacrylamide gel electrophoresis.
Tetsuo Komuro,Chris Galanos +1 more
TL;DR: The high quality of resolution by DOC-PAGE was constant for amounts of LPS up to 20 micrograms and does not require boiling of the samples in DOC, which may be an advantage over SDS-PAGES.
Differential Contribution of Toll-Like Receptors 4 and 2 to the Cytokine Response to Salmonella enterica Serovar Typhimurium and Staphylococcus aureus in Mice
Annalisa Lembo,Christoph Kalis,Carsten J. Kirschning,Vincenzo Mitolo,Emilio Jirillo,Hermann Wagner,Chris Galanos,Marina A. Freudenberg +7 more
TL;DR: Neither TLR4 nor, surprisingly, TLR2 was required in the MyD88-dependent response to Staphylococcus aureus, and the contribution of TLR 2 was only minor.
Toll-like receptor and IL-12 signaling control susceptibility to contact hypersensitivity
Stefan F. Martin,Jan C. Dudda,Eva Bachtanian,Annalisa Lembo,Stefanie Liller,Christoph Dürr,Markus M. Heimesaat,Stefan Bereswill,György Fejer,Ralitsa Vassileva,Thilo Jakob,Nikolaus Freudenberg,Christian C. Termeer,Caroline Johner,Chris Galanos,Marina A. Freudenberg +15 more
TL;DR: It is shown that the concomitant absence of TLR2 and TLR4 prevented the induction of CHS to TNCB in IL-12–competent mice, and CHS was inducible in germ-free wild-type and IL- 12Rβ2–deficient mice, but not in germ–free TLR 4/IL-12R β2 double deficient mice, suggesting that the necessary TLR activation may proceed via endogenous ligands.