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22028815
Genome wide expression profiling reveals suppression of host defence responses during colonisation by Neisseria meningitides but not N. lactamica.

PLoS One, 2011;6(10):e26130.

Wong HE[1], Li MS, Kroll JS, Hibberd ML, Langford PR

Affiliations

PMID: 22028815DOI: 10.1371/journal.pone.0026130

Impact factor: 3.752

Abstract
Both Neisseria meningitidis and the closely related bacterium Neisseria lactamica colonise human nasopharyngeal mucosal surface, but only N. meningitidis invades the bloodstream to cause potentially life-threatening meningitis and septicaemia. We have hypothesised that the two neisserial species differentially modulate host respiratory epithelial cell gene expression reflecting their disease potential. Confluent monolayers of 16HBE14 human bronchial epithelial cells were exposed to live and/or dead N. meningitidis (including capsule and pili mutants) and N. lactamica, and their transcriptomes were compared using whole genome microarrays. Changes in expression of selected genes were subsequently validated using Q-RT-PCR and ELISAs. Live N. meningitidis and N. lactamica induced genes involved in host energy production processes suggesting that both bacterial species utilise host resources. N. meningitidis infection was associated with down-regulation of host defence genes. N. lactamica, relative to N. meningitidis, initiates up-regulation of proinflammatory genes. Bacterial secreted proteins alone induced some of the changes observed. The results suggest N. meningitidis and N. lactamica differentially regulate host respiratory epithelial cell gene expression through colonisation and/or protein secretion, and that this may contribute to subsequent clinical outcomes associated with these bacteria.
MeSH terms
Adaptation, Physiological; Bacterial Proteins; Bronchi; Cell Line; Complement C1s; Cytokines; Cytoplasm; Down-Regulation; Energy Metabolism; Epithelial Cells; Gene Expression Regulation; Genomics; Humans; Immunity; Inflammation Mediators; Microbial Viability; Neisseria lactamica; Neisseria meningitidis; Species Specificity; Time Factors; Transcriptome; Tumor Necrosis Factor-alpha
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