265 - Intestinal Microbial Alterations and Retinopathy of Prematurity

Poster Number: 265
Publication Number: 265.131

Esther S. Kim, UCLA Mattel Childrens Hospital, Santa Monica, CA, United States; Elena J. Coley, University of California, Los Angeles David Geffen School of Medicine, Los Angeles, CA, United States; Elaine Hsiao, UCLA, Los Angeles, CA, United States; Alison Chu, UCLA Mattel Childrens Hospital, Los Angeles, CA, United States; Kara L. Calkins, University of California, Los Angeles David Geffen School of Medicine, LA, CA, United States

Background: Retinopathy of prematurity (ROP) is the leading cause of childhood blindness and affects 25% of extremely premature infants. The etiology of ROP is multi-factorial. Inflammatory gut microbes play a role in the pathogenesis of adult ocular diseases. To date, there is very little research exploring the gut-brain axis in infants with ROP. 

Objective: This study’s objective was to investigate the association of the gut microbiome and systemic inflammation in infants with ROP.

Design/Methods: This single-site, prospective cohort study included infants ≤30 weeks gestational age or birthweight ≤2 kg who completed ROP screenings. Weekly stool and blood samples were obtained. The cohort was divided into 2 groups: 1) Infants without ROP (NO ROP) and 2) infants with any ROP (ROP). The gut microbiome was assessed by 16s rRNA sequencing (Illumina MiSeq). Analyses were done with QIIME 2 and GraphPad Prism 8, and adjusted p-values were calculated. Plasma interleukins (IL)-6 and -8 were measured by a 2-multi-plexed immunometric assay.

Results: Table 1 displays subject characteristics (n=21). When compared to the NO ROP group, the ROP group had a greater relative abundance of Escherichia-Shigella (18-fold change, p< 0.001) and a lower abundance of Enterobacteriaceae (0.4-fold change, p=0.001) (Fig 1). Distinct clustering was noted between the groups (Shannon a-diversity, p=0.03 and Jaccard beta diversity, p=0.001) (Fig 1). When compared to the NO ROP group, IL-6 concentrations were greater in the ROP group at week 1 (p=0.001) and week 2 (p=0.01). Likewise, IL-8 was greater in the ROP group vs. the NO ROP group at week 2 (p=0.02) (Fig 2).  Conclusion(s): In this study, infants with ROP had a unique pro-inflammatory intestinal microbial signature characterized by an increase in Escherichia-Shigella and elevated circulating cytokines. Cytokines may mediate cross-talk between the gut and retina. This study suggests that a microbial and inflammatory shift may be a potential biomarker and therapeutic target for ROP.
EstherKim_CVfinal.pdf

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