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High levels of proinflammatory cytokines have been associated with a loss of tissue function in ocular autoimmune diseases, but the basis for this relationship remains poorly understood. Here we investigate a new role for tumor necrosis factor α in promoting N-glycan-processing deficiency at the surface of the eye through inhibition of N-acetylglucosaminyltransferase expression in the Golgi. Using mass spectrometry, complex-type biantennary oligosaccharides were identified as major N-glycan structures in differentiated human corneal epithelial cells. Remarkably, significant differences were detected between the efficacies of cytokines in regulating the expression of glycogenes involved in the biosynthesis of N-glycans. Tumor necrosis factor α but not IL-1β had a profound effect in suppressing the expression of enzymes involved in the Golgi branching pathway, including N-acetylglucosaminyltransferases 1 and 2, which are required for the formation of biantennary structures. This decrease in gene expression was correlated with a reduction in enzymatic activity and impaired N-glycan branching. Moreover, patients with ocular mucous membrane pemphigoid were characterized by marginal N-acetylglucosaminyltransferase expression and decreased N-glycan branching in the conjunctiva. Together, these data indicate that proinflammatory cytokines differentially influence the expression of N-glycan-processing enzymes in the Golgi and set the stage for future studies to explore the pathophysiology of ocular autoimmune diseases.

The chemistry of corroles is still an open field of investigation able to deliver new and unexpected results especially when they a peculiar reactivity, different from the parent porphyrins. The genesis of corrole is derived from the Johnson attempt to elaborate a synthetic route for the preparation vitamin B12 and the corrole name is due to the molecular skeleton of this macrocycle, similar to that of the corrin nucleus. The interest on this macrocycle has been boosted by the definition of synthetic routes for the preparation of 5,10,15-triarylcorroles, which make facile to prepare and consequently investigated the chemistry of this macrocycle. As a consequence, the chemistry of b-octaalkylcorroles has been shadowed by the expansion of the triaryl congeners. However, the chemistry of these two types of corrole show some interesting differences and in this contribution we want to show some examples of this different behavior.

Introduction Corroborating data suggest that the analysis of tear fluid might represent an additional tool in the ophthalmological practice. Areas covered The purpose of this review was to sum up the tear protein profiles in healthy and diseased ocular surface and to highlight biomarker usefulness in the early diagnosis as well as at follow-up. This analysis encompasses a deep examination of the protein profile expression under physiological and pathological conditions. Tear protein profile analysis will allow in the near future discriminating between different grades of inflammation, from acute trauma toward immune-, endocrine-, and nervous-related disorders of the ocular surface. Concluding remarks The review provides an overview of old and recent findings about inflammatory mediators identified at the ocular surface, under physiological and pathological conditions. To date, the analysis of tear fluid represents a new additional approach for diagnosis and management of ocular surface diseases. Understanding the pathophysiological mechanism could also offer significant advantages to develop strategies addressed to better clarify some complex ocular surface disorders. To sum up, the possibility to provide selective biomarkers as a future target of specific diseases should be considered for supporting diagnosis and management of ocular surface diseases.

Summary Volatolomics is gaining consideration as a viable approach to diagnose several diseases, and it also shows promising results to discriminate COVID-19 patients via breath analysis. This paper extends the study of the relationship between volatile compounds (VOCs) and COVID-19 to blood serum. Blood samples were collected from subjects recruited at the emergency department of a large public hospital. The VOCs were analyzed with a gas chromatography mass spectrometer (GC/MS). GC/MS data show that in more than 100 different VOCs, the pattern of abundances of 17 compounds identifies COVID-19 from non-COVID with an accuracy of 89% (sensitivity 94% and specificity 83%). GC/MS analysis was complemented by an array of gas sensors whose data achieved an accuracy of 89% (sensitivity 94% and specificity 80%)., Graphical abstract, Highlights • Volatile compounds released from human blood serum were analyzed • Blood serum of COVID-19 patients is identified by a pool of 17 volatile compounds • An array of gas sensors detects COVID-19 from serum volatile compounds analysis, Health sciences; Diagnostics; Biotechnology; Medical biotechnology

Vision-threatening retinal diseases affect millions of people worldwide, representing an important public health issue (high social cost) for both technologically advanced and new-industrialized countries. Overall RD group comprises the retinitis pigmentosa, the age-related macular degeneration (AMD), the diabetic retinopathy (DR), and idiopathic epiretinal membrane formation. Endocrine, metabolic, and even lifestyles risk factors have been reported for these age-linked conditions that represent a “public priority” also in this COVID-19 emergency. Chronic inflammation and neurodegeneration characterize the disease evolution, with a consistent vitreoretinal interface impairment. As the vitreous chamber is significantly involved, the latest diagnostic technologies of imaging (retina) and biomarker detection (vitreous) have provided a huge input at both medical and surgical levels. Complement activation and immune cell recruitment/infiltration as well as detrimental intra/extracellular deposits occur in association with a reactive gliosis. The cell/tissue aging route shows a specific signal path and biomolecular profile characterized by the increased expression of several glial-derived mediators, including angiogenic/angiostatic, neurogenic, and stress-related factors (oxidative stress metabolites, inflammation, and even amyloid formation). The possibility to access vitreous chamber by collecting vitreous reflux during intravitreal injection or obtaining vitreous biopsy during a vitrectomy represents a step forward for an individualized therapy. As drug response and protein signature appear unique in each single patient, therapies should be individualized. This review addresses the current knowledge about biomarkers and pharmacological targets in these vitreoretinal diseases. As vitreous fluids might reflect the early stages of retinal sufferance and/or late stages of neurodegeneration, the possibility to modulate intravitreal levels of growth factors, in combination to anti-VEGF therapy, would open to a personalized therapy of retinal diseases.

Positive Regulatory Domain (PRDM) gene family members commonly express two main molecular variants, the PR-plus isoform usually acting as tumor suppressor and the PR-minus one functioning as oncogene. Accordingly, PRDM2/RIZ encodes for RIZ1 (PR-plus) and RIZ2 (PR-minus). In human cancers, genetic or epigenetic modifications induce RIZ1 silencing with an expression level imbalance in favor of RIZ2 that could be relevant for tumorigenesis. Additionally, in estrogen target cells and tissues, estradiol increases RIZ2 expression level with concurrent increase of cell proliferation and survival. Several attempts to study RIZ2 function in HeLa or MCF-7 cells by its over-expression were unsuccessful. Thus, we over-expressed RIZ2 in HEK-293 cells, which are both RIZ1 and RIZ2 positive but unresponsive to estrogens. The forced RIZ2 expression increased cell viability and growth, prompted the G2-to-M phase transition and organoids formation. Accordingly, microarray analysis revealed that RIZ2 regulates several genes involved in mitosis. Consistently, RIZ silencing in both estrogen-responsive MCF-7 and -unresponsive MDA-MB-231 cells induced a reduction of cell proliferation and an increase of apoptosis rate. Our findings add novel insights on the putative RIZ2 tumor-promoting functions, although additional attempts are warranted to depict the underlying molecular mechanism.

This thesis explores how Public Art involves the community and how Public Art Administrators view this involvement and how they communicate with the public. In extension, the analysis aims to explore how public art and related community engagement can be evaluated, and also proposes a simple evaluation tool. The analysis is based upon an examination of the four chosen Northern California Public Art Programs through comparing their Public Art Master Plans. In addition to analyzing the Master Plans, a survey was also sent out to all Program Managers with additional questions about their channels of communications, their web traffic, evaluation, their interactions with the local politicians, and how the COVID-19 pandemic had affected these aspects for them. The analysis also consisted of examining all the digital tools the Public Art Programs were utilizing; their social media, the social media context for each city, and their websites. The analysis is also based upon the theories by Jurgen Habermas in his work The Structural Transformation of the Public Sphere. His perspective is applied on the analysis of the general public and on the attitude among the profession on the community’s involvement in public art, and in extension, the evaluation of public art. The main take-aways from the analysis is how the community is being described and viewed in the Master Plans, and by program staff. It becomes obvious that the general attitude is that the general public does not understand Public Art, and that they need to be educated and informed about it. Three perspectives of Public Art appears among the profession: The insider perspective, with the view of the community as passive receivers, the multidimensional perspective with a more differentiated approach both seeing the intrinsic value but also the measurable values, and the critical perspective questioning what public art is and what value it has at all. All of these call for a need of evaluation in a systematic and credible way. Social media and other types of new media can also contribute to communication, community engagement and evaluation. Finally, Public Art and the development of cities are heavily intertwined, but the true impact of Public Art needs to be evaluated, since the art does not stand alone - instead it is dependent on implementation, community engagement and a vibrant city.

Objective Mechanisms of action and optimal stimulation parameters of transcutaneous auricular vagus nerve stimulation (taVNS) are currently unknown. Pupil size has gained attention as a promising biomarker of vagal activation in different studies on animal models. The aim of this study is to investigate the effects of taVNS on pupil diameter in healthy subjects. Methods All subjects received taVNS at the left external acoustic meatus and control stimulation at the left earlobe during the same experimental session. Different intensities (0.5 mA; 1.0 mA; 2.0 mA; 3.0 mA) for both conditions were tested. Tonic pupil size was recorded in both eyes at baseline and during each stimulation using an infrared-automated pupillometer in three different illuminance conditions (scotopic, mesopic, photopic). Results In scotopic illuminance condition, a significant interaction between intensity and condition (real vs control) was found for the left eye. Post-Hoc analysis showed that during real taVNS at 2 mA, pupil size was significantly larger in comparison to baseline and 2 mA control stimulation. Conclusions Our study demonstrates that taVNS induces pupil dilation under specific illuminance conditions and at specific stimulation intensity. Significance The effects of taVNS are strictly dependent on technical aspects, such as stimulation parameters and experimental set-up.

Purpose: To unveil the long-term prognosis of Acanthamoeba keratitis based on clinical presentation and timing of diagnosis to better inform patients since the first visit regarding their length of...

Prostate cancer (PC) remains a widespread malignancy in men. Since the androgen/androgen receptor (AR) axis is associated with the pathogenesis of prostate cancer, suppression of AR-dependent signaling by androgen deprivation therapy (ADT) still represents the primary intervention for this disease. Despite the initial response, prostate cancer frequently develops resistance to ADT and progresses. As such, the disease becomes metastatic and few therapeutic options are available at this stage. Although the majority of studies are focused on the role of AR signaling, compelling evidence has shown that estrogens and their receptors control prostate cancer initiation and progression through a still debated mechanism. Epithelial versus mesenchymal transition (EMT) is involved in metastatic spread as well as drug-resistance of human cancers, and many studies on the role of this process in prostate cancer progression have been reported. We discuss here the findings on the role of estrogen/estrogen receptor (ER) axis in epithelial versus mesenchymal transition of prostate cancer cells. The pending questions concerning this issue are presented, together with the impact of the available data in clinical management of prostate cancer patients.

Prostate cancer (PC) is one of the most frequently diagnosed cancers and a leading cause of cancer-related deaths in Western society. Current PC therapies prevalently target the functions of androgen receptor (AR) and may only be effective within short time periods, beyond which the majority of PC patients progress to castration-resistant PC (CRPC) and metastatic disease. The role of estradiol/estradiol receptor (ER) axis in prostate transformation and PC progression is well established. Further, considerable efforts have been made to investigate the mechanism by which somatostatin (SST) and somatostatin receptors (SSTRs) influence PC growth and progression. A number of therapeutic strategies, such as the combination of SST analogues with other drugs, show, indeed, strong promise. However, the effect of the combined treatment of SST analogues and estradiol on proliferation, epithelial mesenchyme transition (EMT) and migration of normal- and cancer-derived prostate cells has not been investigated so far. We now report that estradiol plays anti-proliferative and pro-apoptotic effect in non-transformed EPN prostate cells, which express both ERα and ERβ. A weak apoptotic effect is observed in transformed CPEC cells that only express low levels of ERβ. Estradiol increases, mainly through ERα activation, the expression of SSTRs in EPN, but not CPEC cells. As such, the hormone enhances the anti-proliferative effect of the SST analogue, pasireotide in EPN, but not CPEC cells. Estradiol does not induce EMT and the motility of EPN cells, while it promotes EMT and migration of CPEC cells. Addition of pasireotide does not significantly modify these responses. Altogether, our results suggest that pasireotide may be used, alone or in combination with other drugs, to limit the growth of prostate proliferative diseases, provided that both ER isoforms (α and β) are present. Further investigations are needed to better define the cross talk between estrogens and SSTRs as well as its role in PC.

Adipose tissue is a key regulator of energy balance playing an active role in lipid storage as well as in synthesizing several hormones directly involved in the pathogenesis of obesity. Obesity represents a peculiar risk factor for a growing list of cancers and is frequently associated to poor clinical outcome. The mechanism linking obesity and cancer is not completely understood, but, amongst the major players, there are both chronic low-grade inflammation and deregulation of adipokines secretion. In obesity, the adipose tissue is pervaded by an abnormal number of immune cells that create an inflammatory environment supporting tumor cell proliferation and invasion. Adiponectin (APN), the most abundant adipokine, shows anti-inflammatory, anti-proliferative and pro-apoptotic properties. Circulating levels of APN are drastically decreased in obesity, suggesting that APN may represent the link factor between obesity and cancer risk. The present review describes the recent advances on the involvement of APN and its receptors in the etiology of different types of cancer.

Kv7.2-Kv7.5 channels mediate the M-current (IKM), a K+-selective current regulating neuronal excitability and representing an attractive target for pharmacological therapy against hyperexcitability diseases such as pain. Kv7 channels interact functionally with transient receptor potential vanilloid 1 (TRPV1) channels activated by endogenous and/or exogenous pain-inducing substances, such as bradykinin (BK) or capsaicin (CAP), respectively, however, whether Kv7 channels of specific molecular composition provide a dominant contribution in BK- or CAP-evoked responses is yet unknown. To this aim, Kv7 transcripts expression and function were assessed in F11 immortalized sensorial neurons, a cellular model widely used to assess nociceptive molecular mechanisms. In these cells, the effects of the pan-Kv7 activator retigabine were investigated, as well as the effects of ICA-27243 and (S)-1, two Kv7 activators acting preferentially on Kv7.2/Kv7.3 and Kv7.4/Kv7.5 channels, respectively, on BK- and CAP-induced changes in intracellular Ca2+ concentrations ([Ca2+]i). The results obtained revealed the expression of transcripts of all Kv7 genes, leading to an IKM-like current. Moreover, all tested Kv7 openers inhibited BK- and CAP-induced responses by a similar extent (~60%), at least for BK-induced Ca2+ responses, the potency of retigabine (IC50~1 &micro, M) was higher than that of ICA-27243 (IC50~5 &micro, M) and (S)-1 (IC50~7 &micro, M). Altogether, these results suggest that IKM activation effectively counteracts the cellular processes triggered by TRPV1-mediated pain-inducing stimuli, and highlight a possible critical contribution of Kv7.4 subunits.

The reaction of 5,10,15-tritolylcorrole with 3-dimethylaminoacrolein (3-DMA) and POCl3 gives a further example of the rebel reactivity of this contracted macrocycle. While no evidence was obtained for the formation of the expected &beta, acrolein corrole, the inner core substituted N21,N22-3-formylpropylcorrole and the 10-acrolein isocorrole were the reaction products. By increasing the temperature or the amount of the Vilsmeier reagent, the 10-isocorrole became the unique reaction product. The formation of the isocorrole by electrophilic attack of the Vilsmeier reagent to the 10-position of the corrole is unprecedented in the porphyrinoids field and it could pave the way for a novel route to the preparation of stable isocorroles.

Abstract Metabolomics has been applied to diagnose diseases, predict disease progression, and design therapeutic strategies in various areas of medicine. However, it remains to be applied to the ocular surface diseases, where biological samples are often of limited quantities. We successfully performed proof-of-concept metabolomics assessment of volume-limited cytology samples from a clinical form of chronic inflammatory cicatrizing conjunctivitis, i.e., ocular MMP and discovered metabolic changes of signaling lipid mediators upon disease onset and progression. The metabolomics assessment revealed active oxylipins, lysophospholipids, fatty acids, and endocannabinoids alterations, from which potential biomarkers linked to inflammatory processes were identified. Possible underlying mechanisms such as dysregulated enzyme activities (e.g., lipoxygenases, cytochrome P450, and phospholipases) were suggested which may be considered as potential therapeutic targets in future studies. Key messages Metabolic profile of the ocular surface can be measured using impression cytology samples. Metabolomics analysis of ocular pemphigoid is presented for the first time. The metabolomics assessment of OCP patients revealed active oxylipins, lysophospholipids, fatty acids, and endocannabinoids alterations. Several oxylipins are identified as diagnostic biomarkers for OCP.

OBJECTIVES: To analyze the effect of the employment of polyvinylpyrrolidone-iodine (PVP-I) 0.6% eye drop on the clinical course of patients affected by Adenoviral Keratoconjunctivitis (AKC). METHODS: Consecutive patients with clinical signs of AKC and positive results of AdenoPlus test were enrolled from four Italian Centres. Patients were randomized to receive: PVP-I 0.6% eye drops four times/daily for 20 days (Group A) or hyaluronate-based tear substitutes four times/daily for 20 days (Group B). Best-corrected visual acuity (BCVA), optical coherence tomography (OCT) Optovue iVue pachymetry map; corneal haze; conjunctival injection and chemosis; subepithelial corneal infiltrates (SEIs); corneal and conjunctival staining and corneal densitometry were recorded at diagnosis and at every follow-up visit. The primary outcome was the resolution time of AKC. RESULTS: Overall, 59 AKC patients (34 for Group A and 25 for Group B) completed the study. Patients of Group A showed a significantly shorter resolution time and lower incidence of SEIs compared to patients of Group B. In particular, SEIs were present at the last visit in 3/34 (8.82%) patients of the Group A vs 11/25 (44%) of the Group B (p = 0.005). Patients of Group A showed a significantly lower incidence of corneal haze compared to patients of Group B (0/34 vs 3/25; p = 0.038). No side effects were reported for both groups. CONCLUSIONS: Although further clinical evaluations are needed, according to our data the use of PVP-I 0.6% eye drop in the setting of AKC reduces the risk of SEIs as well as the resolution time of the disease.

Purpose To investigate clinical and inflammatory changes in the ocular surface of insulin-dependent type I diabetic patients. Methods Two hundred and nine eyes of 106 patients with diagnosis of type I diabetes were recruited in a prospective observational study. Ocular surface clinical assessment, corneal sensitivity and tear film stability tests were performed to evaluate ocular surface system function. Ocular Surface Disease Index (OSDI) questionnaire was administered to all enrolled subjects. Conjunctival impression cytology specimens were also collected to detect neuromediators and inflammatory molecules. Duration of disease, HbA1c levels and diabetic retinopathy stage were recorded. Results Corneal sensitivity assessed by Cochet-Bonnet esthesiometer was reduced in patients with more chronic disease, higher HbA1c levels and proliferative diabetic retinopathy. Tear break-up time (TBUT) was reduced in subjects with long-standing diabetes or with more severe retinopathy. OSDI questionnaire scores showed direct correlation with increased HbA1c values. Significant increase of NPY, STAT-5 and ICAM-1 was found in diabetic patients compared to healthy controls. A direct correlation between NPY concentration and ICAM-1 values in patients with type I diabetes was demonstrated. Conclusions Patients with long-standing type I diabetes showed chronic inflammation of the ocular surface, due to neurogenic dysregulation of para-inflammatory homeostatic mechanisms. These patients with ocular surface system failure complained of ocular discomfort but had modest reduction of corneal sensitivity and no signs of neurotrophic keratopathy. Disease duration, increased HbA1c levels and severe diabetic retinopathy appear the most critical factors.

Purpose Although stem cell activity represents a crucial feature in corneal and ocular surface homeostasis, other cells populating this region and the neighboring zones might participate and influence local microenvironment. Mast cells, the long-lived and tissue-sited immune cells, have been previously reported in corneoscleral specimens. Herein, mast cells were investigated in corneoscleral tissues and related to microenvironment protein expression. Methods Twenty-six (14 male/12 female; older than 60 years) human corneoscleral specimens were sectioned for light and fluorescent immunostaining (CD45, p63, Ck-3/7/12/19, tryptase/AA1, and chymase/CC1). Corneal, limbal, and conjunctival squares were produced for molecular and biochemical analysis. Statistical comparisons were carried out by ANOVA. Results Toluidine blue staining identified metachromatic intact or degranulated mast cells in the area below the palisades’ Vogt (Ck-3/12-positive epithelium and underneath p63 immunoreactivity). Tryptase immunoreactivity was observed close to palisades’ Vogt, whereas no specific signal was detected for chymase. Tryptase/AA1 transcripts were quantified in limbal and conjunctival RNA extracts, whereas no specific amplification was detected in corneal ones. Few mediators were overexpressed in limbal extracts with respect to corneal (Neural cell adhesion molecule (NCAM), Intercellular adhesion molecule 3 (ICAM3), Brain-derived Neurotrophic factor (BDNF), and neurotrophin 3 (NT3); P < 0.00083) and conjunctival (NCAM, ICAM3, and NT3; P < 0.05) protein extracts. A trend to an increase was observed for Nerve Growth Factor (NGF) in limbal extracts (P > 0.05). Conclusions The specific observation of tryptase phenotype and the interesting protein signature of microenvironment (adhesion molecules, growth factors, and neurotrophins), known to partake mast cell behavior, at least in other areas, would provide additional information to better understand this crucial zone in the framework of ocular surface healthiness.

A growing body of evidence implicates endoplasmic reticulum (ER) stress in the pathogenesis of chronic inflammatory and autoimmune disorders. Here, we demonstrate that the proinflammatory cytokine TNFα stimulates matrix metalloproteinase 9 (MMP9) at the ocular surface through a c-Fos-dependent mechanism of ER stress. We found positive reactivity of the molecular chaperone BiP/GRP78 in conjunctival epithelium of patients with ocular cicatricial pemphigoid and increased levels of BiP/GRP78, sXBP1 and GRP94 in human corneal epithelial cells treated with TNFα. Pharmacological blockade of ER stress in vitro using dexamethasone or the chemical chaperones TUDCA and 4PBA attenuated MMP9 expression and secretion in the presence of TNFα. Moreover, expression analysis of genes associated with inflammation and autoimmunity identified the c-Fos proto-oncogene as a mediator of ER stress responses in epithelial cells. Substantially less TNFα-induced MMP9 expression occurred when c-Fos signaling was suppressed with a function-blocking antibody. Taken together, these results indicate that activation of ER stress contributes to promote inflammation-mediated proteolytic activity and uncovers a target for restoring tissue homeostasis in ocular autoimmune disease.

Corneal grafts interact with their hosts via complex immunobiological processes that sometimes lead to graft failure. Prediction of graft failure is often a tedious task due to the genetic and nongenetic heterogeneity of patients. As in other areas of medicine, a reliable prediction method would impact therapeutic decision-making in corneal transplantation. Valuable insights into the clinically observed heterogeneity of host responses to corneal grafts have emerged from multidisciplinary approaches, including genomics analyses, mechanical studies, immunobiology, and theoretical modeling. Here, we review the emerging concepts, tools, and new biomarkers that may allow for the prediction of graft survival.

Topic: To focus on endogenous endophthalmitis management, particularly etiology-based medical and surgical therapy.Methods: Literature search of published studies from July 1990 to February 2019 on endogenous endophthalmitis available on PubMed was made without any language constraints.Results: A total of 78 articles were retrieved from 728 initially analyzed and 62 studies were included. Although the superiority of vitrectomy over tap and inject techniques is controversial, the most recent publications favor an early surgical approach for endogenous endophthalmitis. Vitrectomy is useful in severe cases complicated by marked vitreous opacity, retinal detachment, poor initial visual acuity, and more virulent pathogens. Oral or intravenous antibiotics are also necessary to treat systemic infection. Vitrectomy is superior to blood cultures in diagnosing the etiology of infection.Conclusions: Endogenous endophthalmitis is an important cause of visual acuity impairment. Prompt treatment with appropriate use of pharmacological or surgical therapy is mandatory to preserve visual function.Abbreviations: IOP: intra-ocular pressure; AIDS: acquired immune deficiency syndrome; EVS: endophthalmitis vitrectomy study; CEVE: complete and early vitrectomy for endophthalmitis.

Obesity is related to metabolic defects that may promote not only cancer initiation, but also its progression. The molecular basis for the association between obesity and cancer is not fully understood; however, many pathways are being investigated including hyperinsulinemia/insulin resistance (IR) and abnormalities of the insulin-like growth factor-1 (IGF-1) signaling, sex hormones biosynthesis and pathway, alterations in adipokines pathophysiology, and subclinical chronic low-grade inflammation. In this chapter, we analyze the current knowledge on the proposed biological mechanisms, especially focusing on the role of adiponectin (APN).

This focused review aims to explore pediatric non-viral keratitis and to compare associated risk factors, etiologies, antibiotic susceptibilities, empiric treatments and outcomes. The authors performed a literature research for articles, published on PubMed, Google Scholar, Scopus and Embase online library, relevant to pediatric keratitis etiology, risk factors, antibiotic susceptibilities, treatment and outcomes. From the bibliography of selected articles, additional relevant articles were also considered. Of 34 articles identified, 21 were suitable for the purpose of this review. Several risk factors are noted in the field of pediatric keratitis. Trauma is the most common in developing countries, while contact lenses wear is seen in developed economies. Previous ocular conditions and systemic diseases also contribute. Associated malnourishment and vitamin A deficit are fraught with a catastrophic prognosis. Among causative organisms, bacteria are more common than fungi and protozoa. Gram-positive organisms are predominant where contact lenses use is infrequent. Pseudomonas aeruginosa is often the leading pathogen in developed countries and is strongly associated with contact lens wear or malnourishment. Fungi are common in the tropics and associated with trauma. Levofloxacin seems the more effective empirical treatment when bacteria are suspected, but there is no agreement on a standard of care. There are differences in etiologic patterns between developing and developed countries and different regions globally. Risk factors follow the same trend; however, there is no standard regimen being followed for empirical treatment of pediatric infectious keratitis. Associated malnourishment and vitamin A deficiency result in poorer outcomes.