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Jessmi M L Ling

Publications and source records attributed to Jessmi M L Ling.

3 recordsLinked to original sources

Perspectives on interactions between lactoferrin and bacteria.

Lactoferrin has long been recognized for its antimicrobial properties, initially attributed primarily to iron sequestration. It has since become apparent that interaction between the host and bacteria is modulated by a complex series of interactions between lactoferrin and bacteria, lactoferrin and bacterial products, and lactoferrin and host cells. The primary focus of this review is the interaction between lactoferrin and bacteria, but interactions with the lactoferrin-derived cationic peptide lactoferricin will also be discussed. We will summarize what is currently known about the interaction between lactoferrin (or lactoferricin) and surface or secreted bacterial components, comment on the potential physiological relevance of the findings, and identify key questions that remain unanswered.

Animals↗

The mviN homolog in Burkholderia pseudomallei is essential for viability and virulence.

The virulence factors of Burkholderia pseudomallei, the causative agent of melioidosis, are not fully understood. We have identified a gene with homology to the Salmonella typhimurium mouse virulence gene, mviN, a member of the mouse virulence factor family. Expression studies with an insertional mutant containing a lux operon demonstrated that the expression of the gene is influenced by free-iron availability in the media and by growth phase. The mutant displayed an increased LD50 value in the hamster infection model and a loss of the ability to invade human lung epithelial cells. The mutant has a slower growth rate than that of the wild type. Both defects were restored to various degrees when complemented in trans with the mviN gene. The mutant contains an insertion at 1229 bp of the 1548 bp gene, resulting in a truncated protein that is presumably responsible for the defects. Deletion mutants of the entire B. pseudomallei mviN gene were obtained only in the presence of the complement vector. This result and the inability of the complemented deletion mutant to lose the plasmid in the absence of antibiotic selection suggest that the gene is essential to B. pseudomallei.

Animals↗

Genome-wide expression analysis of iron regulation in Burkholderia pseudomallei and Burkholderia mallei using DNA microarrays.

Burkholderia pseudomallei and B. mallei are the causative agents of melioidosis and glanders, respectively. As iron regulation of gene expression is common in bacteria, in the present studies, we have used microarray analysis to examine the effects of growth in different iron concentrations on the regulation of gene expression in B. pseudomallei and B. mallei. Gene expression profiles for these two bacterial species were similar under high and low iron growth conditions irrespective of growth phase. Growth in low iron led to reduced expression of genes encoding most respiratory metabolic systems and proteins of putative function, such as NADH-dehydrogenases, cytochrome oxidases, and ATP-synthases. In contrast, genes encoding siderophore-mediated iron transport, heme-hemin receptors, and a variety of metabolic enzymes for alternative metabolism were induced under low iron conditions. The overall gene expression profiles suggest that B. pseudomallei and B. mallei are able to adapt to the iron-restricted conditions in the host environment by up-regulating an iron-acquisition system and by using alternative metabolic pathways for energy production. The observations relative to the induction of specific metabolic enzymes during bacterial growth under low iron conditions warrants further experimentation.

Adaptation, Physiological↗