PubMed · 8529542
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C DeGuine, J L Pulec. 1995. Myringitis.. https://pubmed.ncbi.nlm.nih.gov/8529542/
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Ocular infection with herpes simplex virus leads to an inflammatory lesion in the cornea orchestrated by CD4+ Th1 lymphocytes. This immunopathologic disease, called herpetic stromal keratitis, is an important cause of impaired vision. In this study, we set out to determine whether established lesions of herpetic stromal keratitis could be controlled by topically administering naked plasmid DNA encoding cytokines to the corneal surface. A single topical administration of DNA encoding IL-10 was beneficial to the majority (75%) of treated animals, and 50% (vs 10% in controls) resolved their lesions completely over a 23-day observation period. Topical ocular application of DNA encoding foreign proteins was also shown to be an effective means of inducing systemic and mucosal immune responses. The direct application of DNA encoding cytokines may represent an additional therapeutic option for the management of immunoinflammatory disease.
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The present study examined the effects of 0.1% dimethyl sulfoxide (DMSO) on nicotinic acetylcholine receptors (nAChR) from mouse muscle and Torpedo californica electrocytes. Receptors were expressed in Xenopus laevis oocytes and studied with voltage-clamp. When applied simultaneously with acetylcholine, DMSO did not inhibit current amplitude of either receptor. Preincubation with DMSO for 1 min reduced current amplitude by approximately 50% from oocytes expressing electrocyte receptor. Preincubation did not affect the muscle receptor. With electric organ membranes, 0.1% DMSO did not block either [alpha-(125)I]bungarotoxin binding to the nAChR agonist site or [3H]phencyclidine binding to its high affinity site on resting or desensitized receptor. These data suggest that DMSO might be affecting the electrocyte receptor through a second messenger system.