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Updated: May 27, 2026
Long Term Chronic Pseudomonas aeruginosa Airway Infection in Mice
Published on: March 17, 2014
Modulation of Pseudomonas aeruginosa lipopolysaccharide-induced lung inflammation by chronic iron overload in rat
Bá Vuong Lê1, Hafida Khorsi-Cauet, Véronique Bach
1Peritox Laboratory EA4285-UMI 01, Faculty of Medicine, Picardy Jules Verne University, Amiens, France.
Abstract:
Iron constitutes a critical nutrient source for bacterial growth, so iron overload is a risk factor for bacterial infections. This study aimed at investigating the role of iron overload in modulating bacterial endotoxin-induced lung inflammation. Weaning male Wistar rats were intraperitoneally injected with saline or iron sucrose [15 mg kg(-1) body weight (bw), 3 times per week, 4 weeks]. They were then intratracheally injected with Pseudomonas aeruginosa lipopolysaccharide (LPS) (5 μg kg(-1) bw) or saline. Inflammatory indices were evaluated 4 or 18 h post-LPS/saline injection. At 4 h, LPS-treated groups revealed significant increases in the majority of inflammatory parameters (LPS-binding protein (LBP), immune cell recruitment, inflammatory cytokine synthesis, myeloperoxidase activity, and alteration of alveolar-capillary permeability), as compared with control groups. At 18 h, these parameters reduced strongly with the exception for LBP content and interleukin (IL)-10. In parallel, iron acted as a modulator of immune cell recruitment; LBP, tumor necrosis factor-α, cytokine-induced neutrophil chemoattractant 3, and IL-10 synthesis; and alveolar-capillary permeability. Therefore, P. aeruginosa LPS may only act as an acute lung inflammatory molecule, and iron overload may modulate lung inflammation by enhancing different inflammatory parameters. Thus, therapy for iron overload may be a novel and efficacious approach for the prevention and treatment of bacterial lung inflammations.
Insights
Iron overload exacerbates bacterial endotoxin-induced lung inflammation by enhancing inflammatory responses. Targeting iron overload may offer a novel strategy for preventing and treating bacterial lung infections.
Area of Science:
- Immunology
- Microbiology
- Pathology
Background:
- Iron is essential for bacterial growth, making iron overload a risk factor for infections.
- Bacterial endotoxins, like lipopolysaccharide (LPS), trigger inflammatory responses in the lungs.
Purpose of the Study:
- To investigate how iron overload influences lung inflammation induced by Pseudomonas aeruginosa LPS.
- To understand the role of iron in modulating immune responses during bacterial endotoxin exposure.
Main Methods:
- Male Wistar rats were subjected to iron sucrose injection to induce iron overload.
- Lung inflammation was induced by intratracheal instillation of Pseudomonas aeruginosa LPS.
- Inflammatory markers, including immune cell recruitment and cytokine levels, were assessed at 4 and 18 hours post-LPS exposure.
Main Results:
- LPS administration significantly increased inflammatory parameters at 4 hours, including LPS-binding protein (LBP), immune cell influx, cytokine production, and alveolar-capillary permeability.
- Most inflammatory markers decreased by 18 hours, except for LBP and interleukin-10 (IL-10).
- Iron overload modulated immune cell recruitment, LBP, tumor necrosis factor-α, cytokine-induced neutrophil chemoattractant 3, and IL-10 synthesis, and altered alveolar-capillary permeability.
Conclusions:
- Pseudomonas aeruginosa LPS induces acute lung inflammation, while iron overload acts as a modulator, enhancing various inflammatory parameters.
- Therapeutic strategies targeting iron overload could be effective for preventing and treating bacterial lung inflammation.
