Rapid Icm/Dot T4SS Inactivation Prevents Resuscitation of Heat-Induced VBNC Legionella pneumophila by Amoebae.

Legionella pneumophila, the causative agent of Legionnaires' disease, employs the Icm/Dot Type IV secretion system (T4SS) to replicate in amoebae and macrophages. The opportunistic pathogen responds to stress by forming 'viable but non-culturable' (VBNC) cells, which cannot be detected by standard cultivation-based techniques. In this study, we document that L.

Small molecule communication of : the ins and outs of autoinducer and nitric oxide signaling.

SUMMARY is a Gram-negative environmental bacterium, which survives in planktonic form, colonizes biofilms, and infects protozoa. Upon inhalation of -contaminated aerosols, the opportunistic pathogen replicates within and destroys alveolar macrophages, thereby causing a severe pneumonia termed Legionnaires' disease. Gram-negative bacteria employ low molecular weight organic compounds as well as the inorganic gas nitric oxide (NO) for cell-cell communication.

Nitric oxide signaling through three receptors regulates virulence, biofilm formation, and phenotypic heterogeneity of .

Unlabelled: The causative agent of Legionnaires' disease, , is an environmental bacterium, that replicates in macrophages, parasitizes amoeba, and forms biofilms. employs the quorum sensing (Lqs) system and the transcription factor LvbR to control various bacterial traits, including virulence and biofilm architecture. LvbR negatively regulates the nitric oxide (NO) receptor Hnox1, linking quorum sensing to NO signaling.

The Legionella autoinducer LAI-1 is delivered by outer membrane vesicles to promote interbacterial and interkingdom signaling.

Legionella pneumophila is an environmental bacterium, which replicates in amoeba but also in macrophages, and causes a life-threatening pneumonia called Legionnaires' disease. The opportunistic pathogen employs the α-hydroxy-ketone compound Legionella autoinducer-1 (LAI-1) for intraspecies and interkingdom signaling. LAI-1 is produced by the autoinducer synthase Legionella quorum sensing A (LqsA), but it is not known, how LAI-1 is released by the pathogen.

ER-dependent membrane repair of mycobacteria-induced vacuole damage.

Tuberculosis still remains a global burden and is one of the top infectious diseases from a single pathogen. , the causative agent, has perfected many ways to replicate and persist within its host. While mycobacteria induce vacuole damage to evade the toxic environment and eventually escape into the cytosol, the host recruits repair machineries to restore the MCV membrane.