Abstract
Air pollution is a serious environmental issue worldwide in developing countries’ megacities, affecting the population’s health, including the ocular surface, by predisposing or exacerbating other ocular diseases. Herpes simplex keratitis (HSK) is caused by the herpes simplex virus type 1 (HSV-1). The primary or recurring infection in the ocular site causes progressive corneal scarring that may result in visual impairment. The present study was designed to study the immunopathological changes of acute HSK under urban polluted air, using the acute HSK model combined with an experimental urban polluted air exposure from Buenos Aires City. We evaluated the corneal clinical outcomes, viral DNA and pro-inflammatory cytokines by RT-PCR and ELISA assays, respectively. Then, we determined the innate and adaptive immune responses in both cornea and local lymph nodes after HSV-1 corneal by immunofluorescence staining and flow cytometry. Our results showed that mice exposed to polluted air develop a severe form of HSK with increased corneal opacity, neovascularization, HSV-1 DNA and production of TNF-α, IL-1β, IFN-γ, and CCL2. A high number of corneal resident immune cells, including activated dendritic cells, was observed in mice exposed to polluted air; with a further significant influx of bone marrow-derived cells including GR1+ cells (neutrophils and inflammatory monocytes), CD11c+ cells (dendritic cells), and CD3+ (T cells) during acute corneal HSK. Moreover, mice exposed to polluted air showed a predominant Th1 type T cell response over Tregs in local lymph nodes during acute HSK with decreased corneal Tregs. These findings provide strong evidence that urban polluted air might trigger a local imbalance of innate and adaptive immune responses that exacerbate HSK severity. Taking this study into account, urban air pollution should be considered a key factor in developing ocular inflammatory diseases.
Highlights
The ocular surface mucosa comprises the cornea, conjunctiva and tear film, and acts as the first barrier against external threats, including polluted components present in the air
To study the effect of chronic exposure to air pollution during acute herpes simplex keratitis (HSK), we used an in vivo mouse model, housing them in a chamber exposed to either polluted air from Buenos Aires or filtered clear air in combination with a well-described mouse model for acute herpes simplex virus type 1 (HSV-1) keratitis
Our results showed that HSK mice exposed to polluted air had a significant increase in clinical scores, opacity, and neovascularization compared to the group exposed to clear filtered air (Figures 1A–C)
Summary
The ocular surface mucosa comprises the cornea, conjunctiva and tear film, and acts as the first barrier against external threats, including polluted components present in the air. Our group and others have demonstrated in vitro that corneal and conjunctival epithelial cells increase the secretion of pro-inflammatory cytokines with redox imbalance under incubation with diesel exhaust particles (DEP) (the main component of urban PM); in vivo exposure to air pollution from Buenos Aires altered the ocular surface cellularity, redox imbalance and the inflammatory cytokines on the cornea [9,10,11]. Three studies have shown that air pollution increases the susceptibility of respiratory mucosa to the H1N1 influenza [12, 13] virus and respiratory syncytial virus (RSV) [14] Based on these previous findings, we will explore the potential effects of chronic air pollution exposure on cornea immunity in the common infectious disease, herpes simplex keratitis (HSK)
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