Topical pharmacologic interventions versus placebo for epidemic keratoconjunctivitis.
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ABSTRACT:
SUBMITTER: Liu SH
PROVIDER: S-EPMC8892837 | biostudies-literature | 2022 Mar
REPOSITORIES: biostudies-literature
Publications
Topical pharmacologic interventions versus placebo for epidemic keratoconjunctivitis.
Liu Su-Hsun SH Hawkins Barbara S BS Ng Sueko M SM Ren Mark M Leslie Louis L Han Genie G Kuo Irene C IC
The Cochrane database of systematic reviews 20220303
<h4>Background</h4>Viruses cause about 80% of all cases of acute conjunctivitis. Human adenoviruses are believed to account for 65% to 90% of cases of viral conjunctivitis, or 20% to 75% of all causes of infectious keratoconjunctivitis worldwide. Epidemic keratoconjunctivitis (EKC) is a highly contagious subset of adenoviral conjunctivitis that has been associated with large outbreaks at military installations and at medical facilities. It is accompanied by severe conjunctival inflammation, wate ...[more]
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Project description:Human adenoviruses (HAdV), species D in particular (HAdV-D), are frequently associated with epidemic keratoconjunctivitis (EKC). Although the infection originates at the ocular surface epithelium, the mechanisms by which HAdV-Ds bypass the membrane-associated mucin (MAM)-rich glycocalyx of the ocular surface epithelium to trigger infection and inflammation remain unknown. Here, we report that an EKC-causing adenovirus (HAdV-D37), but not a non-EKC-causing one (HAdV-D19p), induces ectodomain release of MUC16-a MAM with barrier functions at the ocular surface-from cultured human corneal and conjunctival epithelial cells. HAdV-D37, but not HAdV-D19p, is also found to decrease the glycocalyx barrier function of corneal epithelial cells, as determined by rose bengal dye penetrance assays. Furthermore, results from quantitative PCR (qPCR) amplification of viral genomic DNA using primers specific to a conserved region of the E1B gene show that, in comparison to infection by HAdV-D19p, infection by HAdV-D37 is significantly increased in corneal epithelial cells. Collectively, these results point to a MUC16 ectodomain release-dependent mechanism utilized by the EKC-causing HAdV-D37 to initiate infection at the ocular surface. These findings are important in terms of understanding the pathogenesis of adenoviral keratoconjunctivitis. Similar MAM ectodomain release mechanisms may be prevalent across other mucosal epithelia in the body (e.g., the airway epithelium) that are prone to adenoviral infection. IMPORTANCE Human adenoviruses (HAdVs) are double-stranded DNA viruses that cause infections across all mucosal tissues in the body. At the ocular surface, HAdVs cause keratoconjunctivitis (E. Ford, K. E. Nelson, and D. Warren, Epidemiol Rev 9:244-261, 1987, and C. M. Robinson, D. Seto, M. S. Jones, D. W. Dyer, and J. Chodosh, Infect Genet Evol 11:1208-1217, 2011, doi:10.1016/j.meegid.2011.04.031)-a highly contagious infection that accounts for nearly 60% of conjunctivitis cases in the United States (R. P. Sambursky, N. Fram, and E. J. Cohen, Optometry 78:236-239, 2007, doi:10.1016/j.optm.2006.11.012, and A. M. Pihos, J Optom 6:69-74, 2013, doi:10.1016/j.optom.2012.08.003). The infection begins with HAdV entry within ocular surface epithelial cells; however, the mechanisms used by HAdVs to transit the otherwise protective mucosal barrier of ocular surface epithelial cells prior to entry remain unknown. Here, we report that the highly virulent keratoconjunctivitis-causing HAdV-D37 induces release of the extracellular domain (ectodomain) of MUC16, a major component of the mucosal barrier of ocular surface epithelial cells, prior to infecting underlying cells. Currently, there is no specific treatment for controlling this infection. Understanding the early steps involved in the pathogenesis of keratoconjunctivitis and using this information to intercept adenoviral entry within cells may guide the development of novel strategies for controlling the infection.
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Project description:ObjectiveTo evaluate whether exercise therapy, with or without other physical therapy interventions, is superior to placebo intervention for osteoarthritis (OA).DesignSystematic review and meta-analysis. Data sources: MEDLINE and EMBASE via OVID, CINAHL and SPORTDiscus via EBSCO were searched from inception to February 2021. Study selection: Randomised controlled trials (RCTs) of adults with OA investigating an intervention involving exercise therapy with a placebo comparator. Data extraction and analysis: Data were extracted and checked for accuracy and completeness by pairs of reviewers. Primary outcomes were self-reported pain, function and quality of life (QoL). Comparative treatment effects were analysed by random effects model for short- and longer-term follow up. Methodological quality was evaluated using the Cochrane risk of bias tool, and the Grading of Recommendations Assessment system was used to evaluate the certainty of evidence.Results13 RCTs involving 1079 patients were identified and included. Meta-analysis demonstrated improved pain (10 studies (GRADE low certainty), SMD -1.1 (95%CI -1.7 to -0.4)) and function (8 studies (GRADE low certainty), SMD -0.8 (95%CI -1.5 to -0.2)) in the short-term with exercise versus placebo, but no significant difference in the longer-term (pain 3 studies; function 3 studies).ConclusionCurrent evidence demonstrates that exercise therapy is superior to placebo in the short-term for pain and function in OA. The certainty of this evidence is low to very low and further research is very likely to have an important impact on our confidence in the estimate of effects.
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Project description: Not available
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