Bacterial infection of the posterior segment of the eye (endophthalmitis) leads to a robust host response that often results in irreversible damage to the layers of the retina, significant vision loss, and in some patients, enucleation of the globe. While a great deal of effort has gone into understanding the role of bacterial virulence factors in disease initiation and propagation, it is becoming increasingly clear that the host response to infection plays a major role in causing the damage associated with endophthalmitis. Researchers have identified the host receptors which detect infecting organisms and initiate the cascade of events that result in inflammation. This inflammation may damage nonregenerative tissues of the eye while attempting to clear the infection. Both Gram-positive and Gram-negative bacteria can cause endophthalmitis. These organisms initiate an immune response by activating toll-like receptor (TLR) pathways. Once an inflammatory response is initiated, the expression of immunomodulators, such as proinflammatory chemokines and cytokines, affect the recruitment of PMNs and other inflammatory cells into the eye. We and others have reported that knockout mice that do not express specific inflammatory pathways and molecules have an attenuated response to infection and retain significant retinal function. These findings suggest that host immune mediators are important components of the response to infections in the posterior segment of the eye, and the timing and level of their production may be related to the severity of the damage and the ultimate visual outcome. If that is the case, a better understanding of the complex and often redundant role of these pathways and inflammatory mediators may identify host molecules as potential anti-inflammatory therapeutic targets. This review highlights potential anti-inflammatory targets during acute inflammation in endophthalmitis, compares and contrasts those with findings in other models of ocular inflammation, and translates current immunomodulatory strategies for other types of infection and inflammation to this blinding disease. Given the poor visual outcomes seen in patients treated with antibiotics alone or in combination with corticosteroids, immunomodulation in addition to antibiotic therapy might be more effective in preserving vision than current regimens.

眼后段的细菌感染（眼内炎）会导致强烈的宿主反应，这通常会导致不可逆转的视网膜层损害，严重的视力丧失，以及在某些患者中会摘除眼球。尽管人们已经做出了很大的努力来了解细菌毒力因子在疾病引发和传播中的作用，但越来越明显的是，宿主对感染的反应在引起与眼内炎有关的损害中起着重要作用。研究人员已经鉴定出宿主受体，它们可以检测感染性生物并引发一系列导致炎症的事件。在试图清除感染时，这种炎症可能会损害眼睛的非再生组织。革兰氏阳性菌和革兰氏阴性菌均可引起眼内炎。这些生物体通过激活收费样受体（TLR）途径来启动免疫反应。一旦引发炎症反应，免疫调节剂（例如促炎性趋化因子和细胞因子）的表达就会影响PMN和其他炎症细胞向眼睛的募集。我们和其他人已报道，不表达特定炎症途径和分子的基因敲除小鼠对感染的反应减弱，并保留重要的视网膜功能。这些发现表明，宿主免疫介质是眼后段感染反应的重要组成部分，其产生的时机和水平可能与损伤的严重程度和最终的视觉效果有关。如果是这样，更好地了解这些途径的复杂性和通常是多余的作用和炎性介质可将宿主分子鉴定为潜在的抗炎治疗靶标。这篇综述突出了眼内炎急性炎症期间潜在的抗炎目标，将其与其他眼部炎症模型的发现进行了比较和对比，并将当前针对其他类型感染和炎症的免疫调节策略转化为这种致盲性疾病。鉴于在单独使用抗生素或与皮质类固醇结合治疗的患者中看到的视觉效果较差，因此与目前的治疗方法相比，除抗生素治疗外的免疫调节可能更有效。这篇综述突出了眼内炎急性炎症期间潜在的抗炎目标，将其与其他眼部炎症模型的发现进行了比较和对比，并将当前针对其他类型感染和炎症的免疫调节策略转化为这种致盲性疾病。鉴于在单独使用抗生素或与皮质类固醇结合治疗的患者中看到的视觉效果较差，因此与目前的治疗方法相比，除抗生素治疗外的免疫调节可能更有效。这篇综述突出了眼内炎急性炎症期间潜在的抗炎目标，将其与其他眼部炎症模型的发现进行了比较和对比，并将当前针对其他类型感染和炎症的免疫调节策略转化为这种致盲性疾病。鉴于在单独使用抗生素或与皮质类固醇结合治疗的患者中看到的视觉效果较差，因此与目前的治疗方法相比，除抗生素治疗外的免疫调节可能更有效。