Interplay of host-immunity in fungal eye infections

The primary cause of blindness and visual impairment worldwide is fungal keratitis, an infection of the cornea. The predominant etiology of these fungal infections is influenced by several variables, including socioeconomic level, geographic origin, and climatic circumstances. Aspergillus spp. and Fusarium spp. are typically responsible for the infection in tropical and subtropical regions, whereas Candida spp. predominate in temperate zones. Anatomical barriers are a crucial first line of protection because most infectious agents are exogenous. By releasing antimicrobial chemicals like lysozyme, lactoferrin, lipocalin, and defensins that are found in tears or secreted over the cornea, corneal cells operate as the body's second line of defense. Additionally, immunity against fungal infections is provided by the cellular immune response that is triggered by the presence of fungi or their products at the corneal surface. T lymphocytes and neutrophils are drawn to the infection site as a result of activated signaling pathways in corneal cells. A comprehensive defense against fungal keratitis is provided by the antifungal mechanism acting as the host defense at the corneal surface. Furthermore, developing treatment plans for fungal keratitis may be influenced by knowledge of the molecular underpinnings of host protection against fungal infections. In the current work, we outlined the most recent developments in our understanding of the host-pathogen interaction and host-immune response in fungal keratitis of mouse and human corneal tissue.