Infectious keratitis refers to a group of corneal disorders in which corneal tissues suffer inflammation and damage caused by pathogenic infections. Among these disorders, fungal keratitis (FK) and acanthamoeba keratitis (AK) are particularly severe and can cause permanent blindness if not diagnosed early and accurately. In Vivo Confocal Microscopy (IVCM) allows for imaging of different corneal layers and provides an important tool for an early and accurate diagnosis. In this paper, we introduce the IVCM-Keratitis dataset, which comprises of a total of 4001 sample images of AK and FK, as well as non-specific keratitis (NSK) and healthy corneas classes. We use this dataset to develop multiple deep-learning models based on Convolutional Neural Networks (CNNs) to provide automated assistance in enhancing the diagnostic accuracy of confocal microscopy in infectious keratitis. Densenet161 had the best performance among these models, with an accuracy, precision, recall, and F1 score of 93.55%, 92.52%, 94.77%, and 96.93%, respectively. Our study highlights the potential of deep learning models to provide automated diagnostic assistance for infectious keratitis via confocal microscopy images, particularly in the early detection of AK and FK. The proposed model can provide valuable support to both experienced and inexperienced eye-care practitioners in confocal microscopy image analysis, by suggesting the most likely diagnosis. We further demonstrate that these models can highlight the areas of infection in the IVCM images and explain the reasons behind their diagnosis by utilizing saliency maps, a technique used in eXplainable Artificial Intelligence (XAI) to interpret these models.

Age-related macular degeneration (AMD), a progressive chronic disease of the central retina, is associated with aging and is a leading cause of blindness worldwide. Here, we demonstrate that leukotriene B ₄ (LTB ₄ ) receptor 1 (BLT1) promotes laser-induced choroidal neovascularization (CNV) in a mouse model for wet-type AMD. CNV was significantly less in BLT1-deficient (BLT1-KO) mice compared with BLT1-WT controls. Expression of several proangiogenic and profibrotic factors was lower in BLT1-KO eyes than in BLT1-WT eyes. LTB ₄ production in the eyes was substantially increased in the early phase after laser injury. BLT1 was highly expressed in M2 macrophages in vitro and in vivo, and ocular BLT1 ⁺ M2 macrophages were increased in the aged eyes after laser injury. Furthermore, M2 macrophages were rapidly attracted by LTB ₄ and subsequently produced VEGF-A– through BLT1-mediated signaling. Consequently, intravitreal injection of M2 macrophages augmented CNV formation, which was attenuated by BLT1 deficiency. Thus, laser-induced injury to the retina triggered LTB ₄ production and attracted M2 macrophages via BLT1, leading to development of CNV. A selective BLT1 antagonist (CP105696) and 3 LTB ₄ inhibitors (zileuton, MK-886, and bestatin) reduced CNV in a dose-dependent manner. CP105696 also inhibited the accumulation of BLT1 ⁺ M2 macrophages in the laser-injured eyes of aged mice. Together, these results indicate that the LTB ₄ -BLT1 axis is a potentially novel therapeutic target for CNV of wet-type AMD.

Purpose: To specify histopathologic and immunohistochemical features of chronic and delayed mustard gas keratopathy. Methods: Corneal buttons from patients with chronic and delayed mustard gas keratopathy were examined for routine histopathology special histologic stainings, and immunohistochemistry for CD31 and CD68. Results: Twenty-five corneal buttons from 25 patients with chronic and delayed mustard gas keratopathy were evaluated. Irregular epithelial thickness (100%), degenerative changes (24) (96%), thickened epithelial basement membrane (23) (92%), keratocytes loss (18) (72%), and destroyed Bowman layer (18) (72%) were predominant histopathologic features. Amyloid degeneration was the most commonly observed degenerative change in the specimens (83%). Immunoreactivity for CD68 and CD31 was detected in 88% and 56%, respectively. Conclusions: In this observational case series, although all corneal layers from epithelium to the endothelium were involved from mild to severe degrees, the anterior corneal layers were more affected on histopathology than the posterior parts in chronic and delayed mustard gas keratopathy.