Study shows phages can promote mammalian cellular growth and survival

Reviewed by Megan Craig, M.Sc.Oct 26 2023

Bacteriophages, also called phages, are viruses that infect and kill bacteria, their natural hosts. But from a macromolecular viewpoint, phages can be viewed as nutritionally enriched packets of nucleotides wrapped in an amino acid shell. A study published October 26^th in the open access journal PLOS Biology by Jeremy J. Barr at Monash University, Victoria, Australia, and colleagues suggests that mammalian cells internalize phages as a resource to promote cellular growth and survival.

Phage interactions with bacteria are well known, and interactions between bacteria and their mammalian host can lead to a range of symbioses. However, the impact of bacteriophages on mammalian cellular and immunological processes is not well understood. In order to investigate how mammalian cells' immune responses interact with and are modulated by interactions with phages, researchers applied the well-studied phage T4 to mammalian cells in vitro and analyzed the cellular responses using luciferase reporter and antibody microarray assays. The phage-free supernatant served as a comparative control.

The researchers found that T4 phages did not activate DNA-mediated inflammatory pathways, but triggered a sequence of signaling pathway events that promote cellular growth and survival. Future studies are needed, however, to determine why cells use phage particles as resources, and whether they have specifically evolved via adaptation to benefit from this internalization.

According to the authors, "This preliminary study provides novel insights into the impact phages have on mammalian systems, with broader potential implications across the fields of immunology, phage therapy, microbiome, and human health."

This work provides new insights into the additional benefits that bacteriophages may have on their mammalian hosts. This is of particular importance given the increased use of phage therapy to treat antibiotic-resistant infections."

Jeremy J. Barr at Monash University