title: Growth temperature-dependent contributions of response regulators, σB, PrfA, and motility factors to Listeria monocytogenes invasion of Caco-2 cells.
abstract: Foodborne pathogens encounter rapidly changing environmental conditions during transmission, including exposure to temperatures below 37°C. The goal of this study was to develop a better understanding of the effects of growth temperatures and temperature shifts on regulation of invasion phenotypes and invasion-associated genes in Listeria monocytogenes. We specifically characterized the effects of L. monocytogenes growth at different temperatures (30°C vs. 37°C) on (i) the contributions to Caco-2 invasion of different regulators (including σ(B), PrfA, and 14 response regulators [RRs]) and invasion proteins (i.e., InlA and FlaA), and on (ii) gadA, plcA, inlA, and flaA transcript levels and their regulation. Overall, Caco-2 invasion efficiency was higher for L. monocytogenes grown at 30°C than for bacteria grown at 37°C (p = 0.0051 for the effect of temperature on invasion efficiency; analysis of variance); the increased invasion efficiency of the parent strain 10403S (serotype 1/2a) observed after growth at 30°C persisted for 2.5 h exposure to 37°C. For L. monocytogenes grown at 30°C, the motility RRs DegU and CheY and σ(B), but not PrfA, significantly contributed to Caco-2 invasion efficiency. For L. monocytogenes grown at 37°C, none of the 14 RRs tested significantly contributed to Caco-2 invasion, whereas σ(B) and PrfA contributed synergistically to invasion efficiency. At both growth temperatures there was significant synergism between the contributions to invasion of FlaA and InlA; this synergism was more pronounced after growth at 30°C than at 37°C. Our data show that growth temperature affects invasion efficiency and regulation of virulence-associated genes in L. monocytogenes. These data support increasing evidence that a number of environmental conditions can modulate virulence-associated phenotypes of foodborne bacterial pathogens, including L. monocytogenes.
authors: Department of Food Science, Cornell University, Ithaca, New York 14853, USA.
authors: Reid A
authors: RA
authors: Ivy
authors: Yvonne C
authors: YC
authors: Chan
authors: Barbara M
authors: BM
authors: Bowen
authors: Kathryn J
authors: KJ
authors: Boor
authors: Martin
authors: M
authors: Wiedmann
mesh_terms: D001426:Bacterial Proteins / Q000235:genetics / Q000502:physiology*; D018938:Caco-2 Cells; D005408:Flagellin / Q000235:genetics; D017353:Gene Deletion; D006801:Humans; D008089:Listeria monocytogenes / Q000235:genetics / Q000254:growth & development* / Q000472:pathogenicity*; D010454:Peptide Termination Factors / Q000235:genetics / Q000502:physiology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012808:Sigma Factor / Q000235:genetics / Q000502:physiology*; D013696:Temperature
chemical_list: D001426:Bacterial Proteins; D010454:Peptide Termination Factors; C545356:PrfA protein, Listeria monocytogenes; C079011:SigB protein, Bacteria; D012808:Sigma Factor; D005408:Flagellin; C067138:flaA protein, bacteria; C069761:internalin protein, Bacteria