How Campylobacter jejuni Turns Gut Inflammation Into Fuel: ASM Infection and Immunity | September 2026

What Does This Review Add?

This review proposes a compelling metabolic explanation for how Campylobacter jejuni transitions from initial colonization resistance to rapid expansion during inflammatory gastroenteritis.

• C. jejuni may follow a two-phase colonization strategy: initial adaptation followed by inflammation-driven expansion.
• In the healthy colon, microbiota-derived butyrate supports colonocyte respiration and maintains physiological hypoxia, restricting pathogen growth.
• Infection triggers inflammation, crypt hyperplasia and replacement of mature colonocytes by glycolytic proliferating cells.
• Reduced epithelial oxygen consumption creates a more oxygenated, microaerobic niche ideally suited to C. jejuni.
• Host epithelial and inflammatory cells simultaneously generate L-lactate, which rises approximately 10-fold during experimental infection.
• C. jejuni exploits this lactate as a carbon source and electron donor for growth.
• Disruption of lactate uptake through LctP markedly reduces bacterial expansion during the inflammatory phase.
• Infection also alters the bile-acid environment, increasing primary and reducing secondary bile acids, potentially further promoting virulence.
• Virulence mechanisms including Cia proteins, HtrA and cytolethal distending toxin (CDT) may contribute to inflammation, barrier disruption and epithelial remodelling.

Why Does It Matter?

The traditional model views inflammation primarily as the host response attempting to eliminate infection. This review highlights a paradox: the inflammatory response itself may remodel the gut into a metabolic environment that helps the pathogen expand.

GastroAGI Takeaway

For C. jejuni, inflammation may become food. By increasing local oxygen and generating host-derived lactate, intestinal inflammation creates precisely the metabolic niche this microaerophilic pathogen needs to proliferate. Targeting pathogen nutrient acquisition, lactate utilisation, or inflammation-driven metabolic remodelling could eventually offer therapeutic strategies distinct from conventional antibiotics—but these concepts remain largely mechanistic and preclinical.