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M Münstermann

Publications and source records attributed to M Münstermann.

5 recordsLinked to original sources
PubMed1999

Complement activation by bacterial surface glycolipids: a study with planar bilayer membranes.

Planar asymmetric glycolipid/phospholipid bilayer membranes were used as a reconstitution model of the lipid matrix of the outer membrane of Gram-negative bacteria to study complement (C) activation by various bacterial surface glycolipids with the aim of defining the C activation pathway. As glycolipids the lipopolysaccharides of Salmonella enterica serovar Minnesota R mutant strains R595 (Re LPS) and R4 (Rd2 LPS), pentaacyl lipid A from the LPS of the Escherichia coli Re mutant F515, and glycosphingolipid GSL-1 of Sphingomonas paucimobilis IAM 12576 were used. Methylester and carboxyl-reduced derivatives of GSL-1 were used to elucidate the role of the carboxyl group as common functional group of LPS and GSL-1 for C activation. The formation of lytic pores was monitored via the measurement of changes in membrane current. For all glycolipids we observed a considerable increase in membrane current soon after addition of whole human serum due to the formation of lytic pores in the membranes. Pore formation was dependent on the presence of C9, indicating that the observed current changes were due to C activation. We found that in our reconstitution system of the outer membrane lipid A, Re LPS, and Rd2 LPS activated the classical pathway, the activation being independent of specific anti-LPS antibodies. In contrast, GSL-1 and the methylester derivative of GSL-1 activated the alternative pathway even at the low serum concentrations used in this study (about 0.2% v/v). Interestingly, the carboxyl reduced GSL-1 activated the classical pathway.

Antibodies↗
PubMed1998

Molecular mechanisms of polymyxin B-membrane interactions: direct correlation between surface charge density and self-promoted transport.

We have studied the interaction of the polycationic peptide antibiotic polymyxin B (PMB) with asymmetric planar bilayer membranes via electrical measurements. The bilayers were of different compositions, including those of the lipid matrices of the outer membranes of various species of Gram-negative bacteria. One leaflet, representing the bacterial inner leaflet, consisted of a phospholipid mixture (PL; phosphatidylethanolamine, -glycerol, and diphosphatidylglycerol in a molar ratio of 81:17:2). The other (outer) leaflet consisted either of lipopolysaccharide (LPS) from deep rough mutants of PMB-sensitive (Escherichia coli F515) or -resistant strains (Proteus mirabilis R45), glycosphingolipid (GSL-1) from Sphingomonas paucimobilis IAM 12576, or phospholipids (phosphatidylglycerol, diphytanoyl-phosphatidylcholine). In all membrane systems, the addition of PMB to the outer leaflet led to the induction of current fluctuations due to transient membrane lesions. The minimal PMB concentration required for the induction of the lesions and their size correlated with the charge of the lipid molecules. In the membrane system resembling the lipid matrix of a PMB-sensitive strain (F515 LPS/PL), the diameters of the lesions were large enough (d = 2.4 nm +/- 8%) to allow PMB molecules to permeate (self-promoted transport), but in all other systems they were too small. A comparison of these phenomena with membrane effects induced by detergents (dodecyltriphenylphosphonium bromide, dodecyltrimethylammonium bromide, sodiumdodecylsulfate) revealed a detergent-like mechanism of the PMB-membrane interaction.

Anti-Bacterial Agents↗
PubMed1975

[Clotting abnormalities in the Lyell's syndrome (acute toxic epidermal necrolysis) (author's transl)].

Acute toxic epidermal necrolysis (Lyell's syndrome) ended fatally in a 48-year-old patient with chronic recurrent bronchial pneumonia. A marked haemorrhagic diathesis had developed, with signs of severe clotting and platelet abnormalities, indicating that the clotting disorder was, in the first instance, the result of "toxic" liver and bone-marrow damage (in connection with the recurrent pneumonia and its previous drug treatment), and not disseminated intravascular coagulation. The clotting abnormalities in this patient were probably less the result of "necrolysis" of the epidermis than an accompanying effect of the generatized intoxication of multiple aetiologies of the entire organism, which probably also precipitated the fulminating course of the Lyell's syndrome. An important part, of course, was the preceding protracted administration of chloramphenicol for the recurrent bronchial pneumonia.

Blood Platelet Disorders↗