Microbiological screening of corneas stored in organ culture medium at Lions Eye Bank of Western Australia from 2011 to 2022.

Purpose: The purpose of this study was to analyse the contamination rate of corneal samples stored in OCM at Lions Eye Bank of Western Australia over a 12-year period.

Methods: All OCM samples used to preserve corneas from 2011 to 2022 (inclusive) underwent microbiological testing. Samples were collected into aerobic and anaerobic culture bottles on day 3-5 of corneal preservation and 24 h after transfer to thinning medium.

Keeping an 'eye' on ocular GVHD.

Ocular graft versus host disease (GVHD) is a common manifestation in patients undergoing allogeneic haematopoietic stem cell transplantation (allo-HSCT). Ocular GVHD affects approximately 10% of patients with acute GVHD and more than 50% of patients with chronic GVHD. Symptoms of dry eye disease are one of the clinical hallmarks of ocular GVHD, and inflammatory changes to the ocular surface, cornea, conjunctiva, eyelids and lacrimal glands have been observed.

Effects of age on retinal macrophage responses to acute elevation of intraocular pressure.

There is accumulating evidence that aging shifts the central nervous system milieu towards a proinflammatory state, with increased reactivity of microglia in the aging eye and brain having been implicated in the development of age-related neurodegenerative conditions. Indeed, alterations to microglial morphology and function have been recognized as a part of normal aging. Here, we sought to assess the effects of age on the retinal microglial and macrophage response to acute intraocular pressure (IOP) elevation.

Systemic exposure to CpG-ODN elicits low-grade inflammation in the retina.

Previous studies have reported that topical exposure to the toll-like receptor (TLR) 9 ligand CpG-ODN causes widespread ocular inflammation, including retinal microglial activation and posterior segment inflammation. Here we sought to determine the effects of systemic exposure to CpG-ODN in the retina and whether this inflammatory response was altered with Cxcr1 deficiency or hyperglycemia. Male non-diabetic Cxcr1 and Cxcr1 littermates (normoglycemic controls) and Cxcr1Ins2and Cxcr1Ins2 diabetic mice were injected intraperitoneally with 40 μg CpG-ODN.

Ocular antigen does not cause disease unless presented in the context of inflammation.

Ocular antigens are sequestered behind the blood-retina barrier and the ocular environment protects ocular tissues from autoimmune attack. The signals required to activate autoreactive T cells and allow them to cause disease in the eye remain in part unclear. In particular, the consequences of peripheral presentation of ocular antigens are not fully understood.