Gut to Eye Axis: Probiotic Mitigates Dysbiosis and Improves Ocular Functions in Mice

It is known that a dysbiotic gut together with bacterial infection can disrupt ocular functions. As demonstrated by our laboratory, and others that obese phenotype in mice is metabolically prone to ocular hypertension phenotype, including retino‐vascular occlusion. These physiological perturbations arising presumably from alterations in the microbial population(s) of the host lead to loss of ocular homeostasis. We thus hypothesized that restoration of the gut‐microbiome via long‐term probiotic administration may help improve ocular functioning that has been derailed by the dysregulated “1‐carbon metabolism” as a result of high fat diet (HFD) consumption. To test this hypothesis, we used 4 different experimental groups of mice, designated as: Group‐I : WT mice (C57BL/6J); Group‐II : WT + HFD, Group‐III: WT + HFD + PB ( Lactobacillus rhamnosus ), and Group‐IV : WT + PB ( Lactobacillus rhamnosus ). The PB ( Lactobacillus rhamnosus ) intervention was done orally employing 2.5x10 5 CFU/day for a continuous period of 16 weeks. Visual function analysis, and detailed retinal angiography of the WT + HFD mice revealed somewhat abnormal vascular patterns, and impaired ocular functions. These conditions were subsequently improved by PB (Lactobacillus rhamnosus ) supplementation. Further experimentations using electro‐retinography (ERG), ocular coherence tomography (OCT), and the fluorescein angiography (FA) analyses on WT+ HFD + PB ( Lactobacillus rhamnosus ) treated mice and other experimental groups supported the observed beneficial effects. Taken together, our findings indicate that PB ( Lactobacillus rhamnosus ) treatment could restore ocular metabolism, in part, via mitigating the adverse retino‐vascular remodeling phenotype as induced by the dysbiotic environment, most likely, via modulation of the “gut‐to‐eye axis” through reconstitution of the gut‐microbiota. Support or Funding Information HL139047 and AR071789