Volatile affairs in microbial interactions

Microorganisms are important factors in shaping our environment. One key characteristic that has been neglected for a long time is the ability of microorganisms to release chemically diverse volatile compounds. At present, it is clear that the blend of volatiles released by microorganisms can be very complex and often includes many unknown compounds for which the chemical structures remain to be elucidated. The biggest challenge now is to unravel the biological and ecological functions of these microbial volatiles. There is increasing evidence that microbial volatiles can act as infochemicals in interactions among microbes and between microbes and their eukaryotic hosts. Here, we review and discuss recent advances in understanding the natural roles of volatiles in microbe–microbe interactions. Specific emphasis will be given to the antimicrobial activities of microbial volatiles and their effects on bacterial quorum sensing, motility, gene expression and antibiotic resistance.     

Galactofuranose attenuates cellular adhesion of Aspergillus fumigatus

Galactofuranose (Gal f ) is a major molecule found in cell wall polysaccharides, secreted glycoproteins, membrane lipophosphoglycans and sphingolipids of Aspergillus fumigatus . The initial step in the Galf synthetic pathway is the re-arrangement of UDP-galactopyranose to UDP-Galf through the action of UDP-galactopyranose mutase. A mutant lacking the Af UGM1 gene encoding the UDP-galactopyranose mutase has been constructed. In the mutant, though there is a moderate reduction in the mycelial growth associated with an increased branching, it remains as pathogenic and as resistant to cell wall inhibitors and phagocytes as the wild-type parental strain. The major phenotype seen is a modification of the cell wall surface that results in an increase in adhesion of the mutants to different inert surfaces (glass and plastic) and epithelial respiratory cells. The adhesive phenotype is due to the unmasking of the mannan consecutive to the removal of galactofuran by the ugm1 mutation. Removal of the mannan layer from the mutant surface by a mannosidase treatment abolishes mycelial adhesion to surfaces.     

Desensitization to ANG II in guinea pig ileum depends on membrane repolarization: role of maxi-K+ channel

Desensitization of ANG II tonic contractile response of theguinea pig ileum is related to membrane repolarization determined byCa²⁺-activatedK⁺(maxi-K⁺) channelopening. ANG II-stimulated depolarized myocytes presented sustainedactivation of maxi-K⁺ channels,characterized by reduction from 415 to 12 ms of the closed timeconstant. ANG II desensitization was prevented by 100 nM iberiotoxin,being reversible within 30 min. Depolarization by KCl, higher than 4 mM, impaired desensitization, suggesting that the membrane potentialmust attain a threshold to counteract the repolarization induced bymaxi-K⁺ channel opening. Once thisvalue is attained, there is no time dependency because thedesensitization process was shut off by addition of KCl along the timecourse of the tonic response. In contrast, the sustained ACh toniccomponent was not altered by these maneuvers. We conclude thatdesensitization of the ANG II tonic component is foremost due to theopening of maxi-K⁺ channels,leading to membrane repolarization, thus closing the voltage-dependentCa²⁺ channels responsible for theCa²⁺ influx that sustains thetonic component in this muscle.

     

Genetic diversity of <Emphasis Type="Italic">Leishmania amazonensis</Emphasis>strains isolated in northeastern Brazil as revealed by DNA sequencing,PCR-based analyses and molecular karyotyping

Background  

Leishmania (Leishmania) amazonensis infection in man results in a clinical spectrum of disease manifestations ranging from cutaneous to mucosal or visceral involvement. In the present study, we have investigated the genetic variability of 18 L. amazonensis strains isolated in northeastern Brazil from patients with different clinical manifestations of leishmaniasis. Parasite DNA was analyzed by sequencing of the ITS flanking the 5.8 S subunit of the ribosomal RNA genes, by RAPD and SSR-PCR and by PFGE followed by hybridization with gene-specific probes.