Airborne Particulates Affect Corneal Homeostasis and Immunity
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Purpose:
To determine the effects of airborne particulate matter (PM) <2.5 µm in vitro and on the normal and Pseudomonas aeruginosa (PA)-infected cornea.
Methods:
An MTT viability assay tested the effects of PM2.5 on mouse corneal epithelial cells (MCEC) and human corneal epithelial cells (HCET). MCEC were tested for reactive oxygen species using a 2',7'-dichlorodihydrofluorescein assay; RT-PCR determined mRNA levels of inflammatory and oxidative stress markers in MCEC (HMGB1, toll-like receptor 2, IL-1β, CXCL2, GPX1, GPX2, GR1, superoxide dismutase 2, and heme oxygenase 1) and HCET (high mobility group box 1, CXCL2, and IL-1β). C57BL/6 mice also were infected and after 6 hours, the PM2.5 was topically applied. Disease was graded by clinical score and evaluated by histology, plate count, myeloperoxidase assay, RT-PCR, ELISA, and Western blot.
Results:
After PM2.5 (25-200 µg/mL), 80% to 90% of MCEC and HCET were viable and PM exposure increased reactive oxygen species in MCEC and mRNA expression levels for inflammatory and oxidative stress markers in mouse and human cells. In vivo, the cornea of PA+PM2.5 exposed mice exhibited earlier perforation over PA alone (confirmed histologically). In cornea, plate counts were increased after PA+PM2.5, whereas myeloperoxidase activity was significantly increased after PA+PM2.5 over other groups. The mRNA levels for several proinflammatory and oxidative stress markers were increased in the cornea in the PA+PM2.5 over other groups; protein levels were elevated for high mobility group box 1, but not toll-like receptor 4 or glutathione reductase 1. Uninfected corneas treated with PM2.5 did not differ from normal.
Conclusions:
PM2.5 triggers reactive oxygen species, upregulates mRNA levels of oxidative stress, inflammatory markers, and high mobility group box 1 protein, contributing to perforation in PA-infected corneas.
Insights
Airborne particulate matter (PM) <2.5 µm exacerbates Pseudomonas aeruginosa (PA) eye infections, increasing corneal perforation and inflammation. PM2.5 exposure also triggers oxidative stress and elevates inflammatory markers in corneal cells.
Area of Science:
- Ophthalmology
- Environmental Health
- Toxicology
Background:
- Airborne particulate matter (PM2.5) is a growing environmental concern.
- Ocular infections, such as those caused by Pseudomonas aeruginosa (PA), can lead to severe vision impairment.
- The combined effects of PM2.5 and ocular pathogens on corneal health are not well understood.
Purpose of the Study:
- To investigate the in vitro and in vivo effects of PM2.5 on normal and PA-infected corneas.
- To determine the impact of PM2.5 on corneal epithelial cell viability, oxidative stress, and inflammatory responses.
- To evaluate the role of PM2.5 in exacerbating PA-induced keratitis and corneal perforation.
Main Methods:
- In vitro studies used MTT assays to assess cell viability of mouse corneal epithelial cells (MCEC) and human corneal epithelial cells (HCET) exposed to PM2.5.
- Oxidative stress and inflammatory marker gene expression (mRNA) were analyzed using RT-PCR in MCEC and HCET.
- In vivo studies involved topical application of PM2.5 to PA-infected mouse corneas, followed by clinical scoring, histology, bacterial plate counts, myeloperoxidase assays, RT-PCR, ELISA, and Western blotting.
Main Results:
- PM2.5 exposure (25-200 µg/mL) did not significantly reduce MCEC and HCET viability but increased reactive oxygen species in MCEC.
- PM2.5 exposure upregulated mRNA levels of inflammatory and oxidative stress markers in both mouse and human corneal cells.
- In vivo, PA-infected corneas exposed to PM2.5 showed earlier perforation, increased bacterial load, elevated myeloperoxidase activity, and higher expression of pro-inflammatory markers and High Mobility Group Box 1 (HMGB1) protein compared to PA infection alone.
Conclusions:
- PM2.5 acts as a significant risk factor, exacerbating Pseudomonas aeruginosa keratitis.
- The mechanism involves PM2.5-induced oxidative stress, inflammation, and upregulation of HMGB1.
- These effects contribute to accelerated corneal perforation in infected eyes.
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