Coxiella burnetii protein CBU2016 supports CCV expansion.
David R ThomasSarah E GarnishChen Ai KhooBhavna PadmanabhanNichollas E ScottHayley J NewtonPublished in: Pathogens and disease (2024)
Coxiella burnetii is a globally distributed obligate intracellular pathogen. Although often asymptomatic, infections can cause acute Q fever with influenza-like symptoms and/or severe chronic Q fever. C. burnetii develops a unique replicative niche within host cells called the Coxiella-containing vacuole (CCV), facilitated by the Dot/Icm type IV secretion system translocating a cohort of bacterial effector proteins into the host. The role of some effectors has been elucidated; however, the actions of the majority remain enigmatic and the list of true effectors is disputable. This study examined CBU2016, a unique C. burnetii protein previously designated as an effector with a role in infection. We were unable to validate CBU2016 as a translocated effector protein. Employing targeted knock-out and complemented strains, we found that the loss of CBU2016 did not cause a replication defect within Hela, THP-1, J774, or iBMDM cells or in axenic media, nor did it affect the pathogenicity of C. burnetii in the Galleria mellonella infection model. Absence of CBU2016 did, however, result in a consistent decrease in the size of CCVs in HeLa cells. These results suggest that although CBU2016 may not be a Dot/Icm effector, it is still able to influence the host environment during infection.
Keyphrases
- cell cycle arrest
- induced apoptosis
- type iii
- regulatory t cells
- dendritic cells
- cell death
- oxidative stress
- endoplasmic reticulum stress
- escherichia coli
- pi k akt
- liver failure
- drug induced
- signaling pathway
- early onset
- binding protein
- depressive symptoms
- small molecule
- intensive care unit
- cell proliferation
- pseudomonas aeruginosa
- staphylococcus aureus
- reactive oxygen species
- energy transfer
- respiratory failure