Dry eye illness is explained as a “multifactorial disease of the tears and ocular surface that results in symptoms of discomfort, visual disturbance, and tear film instability with potential damage to the ocular surface. It is accompanied by increased osmolarity of the tear film and subacute inflammation of the ocular surface” (Messmer, 2015).

The spread of Dry Eye Disease (DED) is elevated and extends from (5 to 33)% of the adult people worldwide (Bartlett et al., 2015). DED is believed to become a symptomatic illness (Bartlett et al., 2015), and many patients suffer eye irritation, dryness, ocular fatigue, stinging, and fluctuating optical disturbances (Johnson, 2009). These symptoms can drive to considerable functional weakness in daily and public activities, productivity, and quality of life among influenced patients (Miljanovic et al., 2007).

With the prevalence of electronic products, contact lenses, environmental pollution, makeup and other effects, the number of sick people with dry eye disease (DED) will persist to increase at an average of more than 10% per year, as well tend to become younger (Yu et al., 2021).

The ocular surface immune reply is a complex and rigorous regulatory procedure designed to defend and protect the ocular surface, but if the organizing is disturbed, it will drive to DED (Pflugfelder and Paiva, 2017).

Studies implemented in dry eye patients and animal models have discovered that dryness is a strong stress (in the similar magnitude to microbial manufactures) to the ocular surface that begins a secondary immune reply that can drive to a vicious cycle (Dursun et al., 2002).

Dry eye illness is significantly linked with depression and anxiety disorders (Li et al., 2012). The pathogenesis of dry eye disease (DED) has not yet been completely explained, but the eye surface immune inflammatory reply as the concentration of the mechanism has been growingly concerned.

Inflammation is the most substantial and popular risk agent for DED, and researches have presented that patients with Dry eye Disease (DED) can detect great amounts of lymphocyte leakage in lacrimal gland tissue and the ocular surface, at the similar time, the secretion of lactoferrin declined, the cell inflammatory agents, conducting to further extension of the inflammation scope. Ophthalmic surface inflammation is actually both a first reason and a following consequence of Dry eye Disease (Baudouin, 2001).

Immune reply can be classified into adaptive immunity and innate immunity. The inherent reply is actually the natural immunity of the individual body, recognized as the initial natural protection line, which fundamentally contains neutrophils, macrophages, dendritic cells, natural killer cells, and monocytes etc. Adaptive immunity is gained immunity, which commonly shapes an extremely targeted immune procedure after the invasion of particular pathogenic microorganisms. However, the two immune processes are together engaged in the immune organizing of dry eye disease (DED) (Schaumburg et al., 2011).

The ocular surface is a very distinctive uncovered mucosa. It is enveloped with a specialized stratified epithelium that renders like a fence to inflammatory, microbial, and environmental insults. Next to the intestine, anyway, the conjunctival epithelium owns the second highest thickness of mucus-generating goblet cells. It as well harbors a set of resident immune cells, like dendritic cells, natural killer, macrophages, γδ and CD8+ and CD4 T cells that work fundamentally in antimicrobial protection but may engage in the pathogenesis of dry eye (Stern et al., 2002).

The cornea epithelium must resist daily ecological challenges while preserving comfort and clarity. The ocular surface epithelia and lacrimal glands manufacture an array of antimicrobial agents containing, lactoferrin, α and β defensins, lysozyme, and IgA that are existent in the tear film and work to preserve a paucibacterial microenvironment (Zavaro et al., 1980).

Hyperosmolar stress owns an immediate pro-inflammatory influence on the ocular surface epithelium. However, it has been presented to stimulate secretion of pro-inflammatory cytokines (for example IL-6, IL-1β, and TNF-α), chemokines and matrix metalloproteinases like MMP-9 and MMP-3, activate mitogen-activated protein kinases (MAPKs), and stimulate apoptosis (Luo et al., 2004).

Treatments to support endogenous natural immunomodulatory and anti-inflammatory mechanisms also seem to own promise. The Western diet is oftentimes insufficient in anti-inflammatory polyunsaturated fatty acids (PUFAs) (James et al., 2000).

In the clinical therapy of DED, immunomodulatory medications represented by lifitegrast as well anti-inflammatory medications represented by cyclosporine A, can perform a good ameliorative influence (Wan et al., 2015). Thence, it is of strategic importance to further research the immune inflammatory mechanism of Dry Eye Disease (DED).

Oral supplementation with omega-3 (n-3) PUFAs and gamma-linolenic acid (GLA, n-6) has been discovered to develop tear stability and ocular irritation symptoms, decrease inflammatory mediators, and block conjunctival dendritic cell maturation in sick people with dry eye (Macsai, 2008).

Other nutritional supplements like curcumin have strong anti-inflammatory impacts and have been discovered to suppress IL-1β manufacture via dendritic cell maturation and osmotically stressed cornea epithelial cells (Rogers et al., 2010).

In summary, dry eye disease is a popular and usually happening ophthalmology with diverse and complex reasons, and its happening is on the upward orientation. It is explained as eye surface illness caused by a set of agents, elevated osmotic pressure, ocular surface inflammation and injury, tear film instability, and neurosensory abnormalities perform a pathogenic function, depicted by the lack of tear film equilibrium accompanied by eye symptoms. And these contain burning sensation, dryness, foreign body sensation, photophobia, red eyes, itching sensation, fluctuating vision, blurred vision, and visual tiredness.

References

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Dursun, D., Wang, M., Monroy, D. et al. (2002). A mouse model of keratoconjunctivitis sicca. Invest Ophthalmol Vis Sci., 43(3):632–8.

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