Calcium Regulation of Bacterial Virulence.

Calcium (Ca(2+)) is a universal signaling ion, whose major informational role shaped the evolution of signaling pathways, enabling cellular communications and responsiveness to both the intracellular and extracellular environments. Elaborate Ca(2+) regulatory networks have been well characterized in eukaryotic cells, where Ca(2+) regulates a number of essential cellular processes, ranging from cell division, transport and motility, to apoptosis and pathogenesis. However, in bacteria, the knowledge on Ca(2+) signaling is still fragmentary. This is complicated by the large variability of environments that bacteria inhabit with diverse levels of Ca(2+). Yet another complication arises when bacterial pathogens invade a host and become exposed to different levels of Ca(2+) that (1) are tightly regulated by the host, (2) control host defenses including immune responses to bacterial infections, and (3) become impaired during diseases. The invading pathogens evolved to recognize and respond to the host Ca(2+), triggering the molecular mechanisms of adhesion, biofilm formation, host cellular damage, and host-defense resistance, processes enabling the development of persistent infections. In this review, we discuss: (1) Ca(2+) as a determinant of a host environment for invading bacterial pathogens, (2) the role of Ca(2+) in regulating main events of host colonization and bacterial virulence, and (3) the molecular mechanisms of Ca(2+) signaling in bacterial pathogens.