Abstract
Some tissues of the eye are susceptible to damage due to their exposure to the outside environment and inability to regenerate. Immune privilege, although beneficial to the eye in terms of homeostasis and protection, can be harmful when breached or when an aberrant response occurs in the face of challenge. In this review, we highlight the role of the PMN (polymorphonuclear leukocyte) in different bacterial ocular infections that invade the immune privileged eye at the anterior and posterior segments: keratitis, conjunctivitis, uveitis, and endophthalmitis. Interestingly, the PMN response from the host seems to be necessary for pathogen clearance in ocular disease, but the inflammatory response can also be detrimental to vision retention. This “Pyrrhic Victory” scenario is explored in each type of ocular infection, with details on PMN recruitment and response at the site of ocular infection. In addition, we emphasize the differences in PMN responses between each ocular disease and its most common corresponding bacterial pathogen. The in vitro and animal models used to identify PMN responses, such as recruitment, phagocytosis, degranulation, and NETosis, are also outlined in each ocular infection. This detailed study of the ocular acute immune response to infection could provide novel therapeutic strategies for blinding diseases, provide more general information on ocular PMN responses, and reveal areas of bacterial ocular infection research that lack PMN response studies.
Highlights
In the 1940s, the unresponsive nature of the ocular immune environment was recognized by Sir Peter Medawar, who observed that foreign tissue grafts were not rejected when placed in the anterior chamber (AC) of the eye [1]
Studies on mechanisms to reduce humoral responses and increase adaptive responses in this disease may be helpful. These bacterial conjunctivitis studies reveal a trend that will be seen throughout this review: polymorphonuclear leukocytes (PMNs) recruitment into the eye is mainly dependent on the expression of bacterial virulence factors, and the PMN response is damaging to the host cells of the eye
The significance of MagA in endophthalmitis and PMN recruitment was confirmed by Hunt et al [241], who reported that mouse eyes infected with WT K. pneumoniae had greater PMN influx, which resulted in significantly more retinal function loss than eyes infected with an isogenic mucoviscosity-associated gene A (magA)-deficient strain
Summary
In the 1940s, the unresponsive nature of the ocular immune environment was recognized by Sir Peter Medawar, who observed that foreign tissue grafts were not rejected when placed in the anterior chamber (AC) of the eye [1]. Another contributing factor to immune privilege is the inhibitory ocular microenvironment of the eye This unique environment consists of cell-bound and soluble immunosuppressive factors, which inhibits the recruitment and activity of immune cells. Several mechanisms of immunosuppression and immunoregulation are utilized by the eye to establish and preserve immune privilege Other factors such as complement system proteins, antimicrobial peptides, and resident immune cells contribute to destroying pathogens without damaging ocular tissue. In the face of severe infection, ocular immunosuppression cannot always effectively keep all immune cells from infiltrating and responding This may be due to dysfunction of the protective blood–retina barrier caused by the pathogen, resulting in an infiltration of non-resident immune cells. Whether PMN are affected in this environment is an open question
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