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Using a Bacterial Pathogen to Probe for Cellular and Organismic-level Host Responses

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Transcriptomic interplay between Acinetobacter baumannii , human macrophage and polymyxin.

Zhi Ying Kho, Mohammad Abul Kalam Azad, Yan Zhu

Biorxiv : the Preprint Server for Biology

|February 8, 2024

Summary

Understanding host-pathogen-drug interactions is key to optimizing antibiotic therapy. Polymyxin B and macrophages together disrupt bacterial stress responses, revealing new therapeutic targets for Acinetobacter baumannii infections.

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Area of Science:

Microbiology and Immunology
Host-Pathogen Interactions
Antimicrobial Resistance

Background:

Optimizing antibiotic therapy requires understanding host-pathogen-drug interactions.
Bacterial resistance to antibiotics, particularly against challenging pathogens like Acinetobacter baumannii, necessitates novel therapeutic strategies.
The role of host immune cells, such as macrophages, in modulating bacterial response to antibiotics remains largely unexplored.

Approach:

Dual RNA-sequencing was employed to analyze transcriptomic changes in Acinetobacter baumannii and human macrophages during co-culture infection.
An in vitro tripartite model was utilized to investigate the complex interplay within the Acinetobacter baumannii-macrophage-polymyxin B axis.
Specific bacterial genes (rcnB, ompW, traR/dksA) involved in stress tolerance were targeted to assess their impact on polymyxin B efficacy.

Key Points:

Polymyxin B treatment induced significant transcriptomic alterations in Acinetobacter baumannii, including oxidative stress, disrupted metal homeostasis, and altered osmoadaptation.
Macrophages responded to Acinetobacter baumannii infection by adapting heme catabolism, coagulation cascade, and hypoxia-inducible signaling.
Synergistic action between macrophages and polymyxin B was observed, disrupting multiple bacterial stress tolerance mechanisms.

Conclusions:

Targeting bacterial nickel/cobalt homeostasis (rcnB), osmotic stress defense (ompW), and stringent response (traR/dksA) enhances polymyxin B's antibacterial activity.
Genetic disruption of these bacterial pathways significantly impairs Acinetobacter baumannii's ability to tolerate polymyxin B.
These findings highlight potential therapeutic targets for developing novel treatments against Acinetobacter baumannii infections.