Abstract:
Adaptive stress tolerance responses are the driving force behind the survival ability of
Listeria monocytogenes in different environmental niches, within foods, and ultimately, the ability to
cause human infections. Although the bacterial stress adaptive responses are primarily a necessity
for survival in foods and the environment, some aspects of the stress responses are linked to bacterial
pathogenesis. Food stress-induced adaptive tolerance responses to acid and osmotic stresses can
protect the pathogen against similar stresses in the gastrointestinal tract (GIT) and, thus, directly aid its
virulence potential. Moreover, once in the GIT, the reprogramming of gene expression from the stress
survival-related genes to virulence-related genes allows L. monocytogenes to switch from an avirulent
to a virulent state. This transition is controlled by two overlapping and interlinked transcriptional
networks for general stress response (regulated by Sigma factor B, (SigB)) and virulence (regulated by
the positive regulatory factor A (PrfA)). This review explores the current knowledge on the molecular
basis of the connection between stress tolerance responses and the pathogenesis of L. monocytogenes.
The review gives a detailed background on the currently known mechanisms of pathogenesis and
stress adaptation. Furthermore, the paper looks at the current literature and theories on the overlaps
and connections between the regulatory networks for SigB and PrfA.
