Copper homeostasis at the host vibrio interface: lessons from intracellular vibrio transcriptomics

Area of Science:

• Microbiology
• Immunology
• Marine Biology

Background:

• Vibrio species can survive within host cells, but the role of intracellular stages in pathogenicity is often overlooked.
• The virulence of Vibrio tasmaniensis LGP32 in oysters is linked to its ability to enter hemocytes, the oyster's immune cells.

Purpose of the Study:

• To investigate the mechanisms of intracellular survival of Vibrio tasmaniensis LGP32 within host cells.
• To determine the consequences of intracellular survival on host-pathogen interactions and oyster pathogenicity.

Main Methods:

• Utilized in vivo and in vitro assays to assess the requirement of hemocyte entry and survival for LGP32 cytotoxicity.
• Employed RNA sequencing to analyze gene transcription during intracellular stages, focusing on antioxidant and copper detoxification genes.
• Generated isogenic mutants to identify specific functions, such as oxidative stress resistance and copper efflux, essential for intracellular survival and virulence.

Main Results:

• Intracellular survival of LGP32 within hemocytes was essential for hemocyte cytolysis, both in vivo and in vitro.
• Intracellular LGP32 exhibited increased metabolic activity and upregulated antioxidant and copper detoxification genes.
• Resistance to oxidative stress and copper efflux were identified as critical for intracellular vibrio stages, hemocyte cytotoxicity, and in vivo virulence.

Conclusions:

• Copper resistance is a crucial mechanism for Vibrio tasmaniensis LGP32 to evade phagocytic killing, induce immune cell lysis, and colonize oysters.
• The ability to resist intraphagosomal killing, particularly through copper resistance, may be selected for in copper-rich marine environments.
• These findings highlight how environmental factors can drive the evolution of pathogenic vibrios capable of intracellular survival and immune evasion across animal species.