Figure 9.

Summary of PMN responses to ocular bacterial infections. This figure illustrates PMN responses that have been observed in the different areas of the eye during conjunctivitis, keratitis, uveitis, and endophthalmitis. During conjunctivitis, PMNs damage the conjunctival epithelial barrier by accumulating and releasing infected epithelia onto the surface of the conjunctiva. The presence of PMNs during this infection causes a decrease in transforming growth factor-beta (TGF-β) and interleukin-5 (IL-5), which is suggested to downregulate IgA humoral responses [26,56]. The PMN response during keratitis includes a release of neutrophil extracellular traps (NETs) to prevent the further dissemination of bacteria. PMNs have also been observed to bacteria in the cornea and produce IL-1β and IL-17 as part of their response [80,83,99,120,183,184]. In some uveitis models, PMNs are recruited quickly into the eye, and self-recruit by producing LTB4 and other proinflammatory molecules [133,142]. PMNs in the endophthalmitis also self-recruit by releasing recruiting chemokines such as TNF-α, but may also cause retinal damage by producing antimicrobial enzymes and reactive oxygen species (ROS) [10,206].