Interaction of antimicrobial cyclic lipopeptides from Bacillus subtilis influences their effect on spore germination and membrane permeability in fungal plant pathogens.

Bacillus subtilis cyclic lipopeptides are known to have various antimicrobial effects including different types of interactions with the cell membranes of plant pathogenic fungi. The various spectra of activities of the three main lipopeptide families (fengycins, iturins, and surfactins) seem to be linked to their respective mechanisms of action on the fungal biomembrane. Few studies have shown the combined effect of more than one family of lipopeptides on fungal plant pathogens.

Ecological and mechanistic insights into the direct and indirect antimicrobial properties of Bacillus subtilis lipopeptides on plant pathogens.

Members of the genus Bacillus produce a wide variety of antimicrobial compounds. Cyclic lipopeptides (CLP) produced by Bacillus subtilis strains have been shown to protect host plants from a numbers of pathogens. The representative families of these CLP (surfactins, fengycins, and iturins) share a polypeptide ring linked to a lipid tail of varying length.

Production and antimicrobial activity of 3-hydroxypropionaldehyde from Bacillus subtilis strain CU12.

Bacillus subtilis strains are known to produce a vast array of antimicrobial compounds. However, some compounds remain to be identified. Disk assays performed in vitro with Bacillus subtilis CU12 showed a significant reduction in mycelial growth of Alternaria solani, Botrytis cinerea, Fusarium sambucinum, and Pythium sulcatum.

Animal model and in vitro studies of anti neurofilament antibodies mediated neurodegeneration in Alzheimer's disease.

Alzheimer's disease (AD) is associated with serum antibodies directed specifically against phosphorylated epitopes highly enriched in the heavy neurofilament protein NF-H of cholinergic neurons. Prolonged immunization of rats with these molecules but not with other NF-H isoforms results in cognitive impairments. This animal model, termed experimental autoimmune dementia (EAD), supports a role for such antibodies in neurodegeneration in AD.