Brucella-driven host N-glycome remodeling controls infection.

Area of Science:

• Microbiology
• Glycobiology
• Infectious Diseases

Background:

• Host cell responses to bacterial infection are well-studied at transcriptomic, proteomic, and metabolic levels.
• Host glycome responses to bacterial pathogens are largely unexplored, limiting understanding of infection mechanisms.

Purpose of the Study:

• To investigate host glycome alterations during bacterial infection.
• To elucidate the role of Brucella effector proteins in manipulating host glycosylation.

Main Methods:

• Systematic analysis of the host glycome during Brucella spp. infection.
• Investigated the interaction of Brucella effector protein Rhg1 with the host oligosaccharide transferase complex.
• Evaluated Rhg1's role in Brucella replication and colonization in a mouse model.

Main Results:

• Brucella effector protein Rhg1 induces global reprogramming of the host cell N-glycome.
• Rhg1 interacts with the oligosaccharide transferase complex, controlling N-linked protein glycosylation.
• Rhg1 is crucial for Brucella replication and tissue colonization in vivo.

Conclusions:

• Brucella exploits effector protein Rhg1 to reprogram the host N-glycome.
• Host N-glycome manipulation by Rhg1 promotes bacterial intracellular parasitism and infection.
• This study provides a paradigm for bacterial control of host cell glycosylation during infection.