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Lithium chloride promotes host resistance against Pseudomonas aeruginosa keratitis
Kang Chen1, Yongjian Wu, Min Zhu
1Department of Immunology, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Purpose:
To explore the role of lithium chloride (LiCl) in Pseudomonas aeruginosa (PA) keratitis.
Methods:
B6 mice were subconjunctivally injected with LiCl in contrast to appropriate control sodium chloride (NaCl), and then routinely infected with PA. Clinical score, slit-lamp photography, hematoxylin and eosin (H&E) staining, and bacterial plate counts were used to determine the role of LiCl in PA keratitis. Messenger ribonucleic acid and protein levels of inflammatory cytokines in PA-challenged mouse corneas and in vitro cultured macrophages and neutrophils were measured with real-time PCR and enzyme-linked immunosorbent assay (ELISA), respectively. Apoptosis of the infiltrating inflammatory cells in the PA-infected murine corneas was assessed using terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end labeling staining and propidium iodide staining associated with flow cytometry. In cultured murine macrophages and neutrophils, cell apoptosis was determined with annexin V/propidium iodide double staining associated with flow cytometry and western blot analysis for cleaved caspase-3 and cleaved poly(ADP-ribose) polymerase.
Results:
Treatment with LiCl reduced the severity of corneal disease by reducing corneal inflammatory response and bacterial burden. Moreover, LiCl increased anti-inflammatory cytokine interleukin-10 levels, decreased proinflammatory cytokine tumor necrosis factor-α levels, and enhanced apoptosis of infiltrating macrophages and neutrophils in the PA-infected mouse corneas. In vitro studies further confirmed that LiCl elevated anti-inflammatory cytokine expression but reduced proinflammatory cytokine production, as well as promoted cell apoptosis in murine macrophages and neutrophils.
Conclusions:
This study demonstrates a protective role of LiCl in PA keratitis. LiCl promotes host resistance against PA infection by suppressing inflammatory responses, enhancing inflammatory cell apoptosis, and promoting bacterial clearance.
Insights
Lithium chloride (LiCl) reduces Pseudomonas aeruginosa (PA) keratitis severity by lowering inflammation and bacterial load. LiCl also promotes inflammatory cell death, aiding host defense against PA infection.
Area of Science:
- Ophthalmology
- Infectious Diseases
- Immunology
Background:
- Pseudomonas aeruginosa (PA) keratitis is a severe ocular infection.
- Understanding host-pathogen interactions is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the therapeutic potential of lithium chloride (LiCl) in managing PA keratitis.
- To elucidate the mechanisms by which LiCl affects the ocular immune response and bacterial clearance.
Main Methods:
- Subconjunctival injection of LiCl in a murine model of PA keratitis.
- Assessment of clinical disease, bacterial load, and corneal histology.
- Quantification of inflammatory cytokine expression (mRNA and protein) using RT-PCR and ELISA.
- Evaluation of inflammatory cell apoptosis via TUNL, PI, Annexin V/PI staining, and Western blot analysis for apoptosis markers.
Main Results:
- LiCl treatment significantly reduced corneal disease severity, inflammation, and bacterial burden.
- LiCl increased anti-inflammatory cytokine IL-10 and decreased pro-inflammatory cytokine TNF-α.
- LiCl promoted apoptosis of infiltrating macrophages and neutrophils in infected corneas and in vitro.
Conclusions:
- LiCl exhibits a protective role in PA keratitis.
- LiCl enhances host resistance by modulating inflammatory responses, inducing inflammatory cell apoptosis, and facilitating bacterial clearance.
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