A study demonstrated that the retina in mice carrying the Rd8 mutation of CRB1 is characterized by the presence of bacterial invasion.

Whereas normal CRB1 expression is enriched in the apical junctional complexes of retinal pigment epithelium and colon enterocytes, CRB1 mutations attenuate its expression in both sites.

The resulting alterations of the outer blood-retinal barrier and intestinal epithelial barrier in Rd8 mice led to the translocation of intestinal bacteria from the lower gastrointestinal (GI) tract to the retina, leading to secondary retinal degeneration.

Systemic bacterial depletion or reintroduction of normal Crb1 expression into the colon rescued Rd8 mutation-associated retinal degeneration without reversing retinal barrier breach.

The study suggests that antimicrobial agents have the potential to treat CRB1-associated retinal degeneration. 

Hence, it paves the way for further research in humans towards a promising treatment of genetic retinal degeneration.