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TNF\u2010\u03b1 is a major mediator that is rapidly upregulated, diffusing also to the retina and causes apoptosis of the ganglion cells and degeneration of their optic nerve axons (mediating steps to glaucomatous damage). Anti\u2010TNF\u2010\u03b1 antibodies are in animals very effective in protecting the retinal cells and the optic nerve\u2014and might therefore be useful prophylactically against secondary glaucoma in future such patients. Here we evaluate (1)\n                      <jats:italic>toxicity<\/jats:italic>\n                      and (2)\n                      <jats:italic>efficacy<\/jats:italic>\n                      of two TNF\u2010\u03b1 inhibitors (adalimumab and infliximab), in rabbits by\n                      <jats:italic>subconjunctival<\/jats:italic>\n                      administration.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      For drug\n                      <jats:italic>toxicity<\/jats:italic>\n                      , animals with\n                      <jats:italic>normal, unburned<\/jats:italic>\n                      corneas were injected with adalimumab (0.4, 4, or 40\u2009mg), or infliximab (1, 10, or 100\u2009mg). For drug\n                      <jats:italic>efficacy<\/jats:italic>\n                      , other animals were subjected to alkali burn before such injection, or steroids (for control). The rabbits were evaluated clinically with slit lamp and photography, electroretinography, optical coherence tomography, and intraocular pressure manometry. A sub\u2010set of eyes were stained ex vivo after 3\u2009days for retinal cell apoptosis (TUNEL). In other experiments the optic nerves were evaluated by paraphenylenediamine staining after 50 or 90\u2009days. Loss of retinal cells and optic nerve degeneration were quantified.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Subconjunctival administration of 0.4\u2009mg or 4.0\u2009mg adalimumab were well tolerated, whereas 40.0\u2009mg was toxic to the retina. 1, 10, or 100\u2009mg infliximab were also well tolerated. Analysis of the optic nerve axons after 50\u2009days confirmed the safety of 4.0\u2009mg adalimumab and of 100\u2009mg infliximab. For\n                      <jats:italic>efficacy, 4.0\u2009mg adalimumab subconjunctivally in 0.08\u2009mL<\/jats:italic>\n                      provided practically full protection against retinal cell apoptosis 3\u2009days following alkali burn, and infliximab 100\u2009mg only slightly less. At 90\u2009days following burn injury, control optic nerves showed about 50% axon loss as compared to 8% in the adalimumab treatment group.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Subconjunctival injection of 4.0\u2009mg adalimumab<\/jats:italic>\n                      in rabbits shows no eye toxicity and provides excellent neuroprotection, both short (3\u2009days) and long\u2010term (90\u2009days). Our total. accumulated data from several of our studies, combined with the present paper, suggest that corneal injuries, including surgery, might benefit from routine administration of anti\u2010TNF\u2010\u03b1 biologics to reduce inflammation and future secondary glaucoma.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/aos.15786","type":"journal-article","created":{"date-parts":[[2023,10,7]],"date-time":"2023-10-07T01:46:34Z","timestamp":1696643194000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["The prophylactic value of\n                    <scp>TNF<\/scp>\n                    \u2010\u03b1 inhibitors against retinal cell apoptosis and optic nerve axon loss after corneal surgery or trauma"],"prefix":"10.1111","volume":"102","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4544-4452","authenticated-orcid":false,"given":"Eleftherios 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