# From gatekeepers to mitochondrial mischief: how bacterial outer membrane proteins crash the host cell party

## TL;DR

This review explains how bacteria use outer membrane proteins to manipulate host mitochondria, aiding infection and suggesting new antimicrobial strategies.

## Contribution

The paper provides a focused analysis of β-barrel outer membrane proteins that specifically target mitochondria during infection.

## Key findings

- Bacterial outer membrane proteins exploit mitochondrial similarities to manipulate host cell functions.
- β-barrel OMPs deliver to mitochondria and modulate immune responses or induce cell death.
- These proteins represent potential targets for innovative antimicrobial therapies.

## Abstract

Gram-negative bacteria are equipped with a unique cell envelope structure that includes an outer membrane populated by diverse outer membrane proteins (OMPs). These OMPs are not only essential for bacterial survival, mediating critical functions such as nutrient transport, antibiotic resistance, and structural integrity, but they also play pivotal roles as virulence factors during host-pathogen interactions. Recent research highlights the ability of OMPs to manipulate host cellular processes, often targeting mitochondria to induce cell death or modulate immune responses. This review explores the multifunctional roles of bacterial OMPs, emphasizing their structural features, biogenesis, and pathogenic mechanisms. Furthermore, it delves into how bacterial OMPs exploit host cell machinery, particularly mitochondria, to promote infection, as well as their potential as targets for innovative antimicrobial strategies. Specifically, this review focuses on β-barrel OMPs that reach host mitochondria, detailing their delivery routes and mechanisms of organelle manipulation, while excluding non-β-barrel toxins and secretion-system effectors, to provide a defined perspective on mitochondria-targeting OMP virulence mechanisms.

This review reveals how bacterial outer membrane proteins exploit similarities with mitochondria to hijack host cell functions, highlighting novel insights into bacterial virulence and potential strategies for antimicrobial intervention.