The Diversity of Gut Microbiota at Weaning Is Altered in Prolactin Receptor-Null Mice

Abstract

Maternal milk supports offspring development by providing microbiota, macronutrients, micronutrients, immune factors, and hormones. The hormone prolactin (PRL) is an important milk component with protective effects against metabolic diseases. Because maternal milk regulates microbiota composition and adequate microbiota protect against the development of metabolic diseases, we aimed to investigate whether PRL/PRL receptor signaling regulates gut microbiota composition in newborn mice at weaning. 16SrRNA sequencing of feces and bioinformatics analysis was performed to evaluate gut microbiota in PRL receptor-null mice (Prlr-KO) at weaning (postnatal day 21). The normalized colon and cecal weights were higher and lower, respectively, in the Prlr-KO mice relative to the wild-type mice (Prlr-WT). Relative abundances (Simpson Evenness Index), phylogenetic diversity, and bacterial concentrations were lower in the Prlr-KO mice. Eleven bacteria species out of 470 differed between the Prlr-KO and Prlr-WT mice, with two genera (Anaerotruncus and Lachnospiraceae) related to metabolic disease development being the most common in the Prlr-KO mice. A higher metabolism of terpenoids and polyketides was predicted in the Prlr-KO mice compared to the Prlr-WT mice, and these metabolites had antimicrobial properties and were present in microbe-associated pathogenicity. We concluded that the absence of the PRL receptor altered gut microbiota, resulting in lower abundance and richness, which could contribute to metabolic disease development.

The Impact of Stress, Microbial Dysbiosis, and Inflammation on Necrotizing Enterocolitis

“…Patients with STAT1/STAT3 signaling defects exhibit an imbalance in the microbiome [ 83 ]. Further, the diversity of gut microbiota at weaning is altered in PRL receptor-null mice [ 84 ], suggesting some of these NEC-induced genes also modulate the microbiome, which could indirectly lead to an inflammatory environment.…”

“…Rabiul Auwul et al [ 87 ] RNASeq NEC tissues from preterm infants NEC n = 9 Ctrl n = 5 ↑ 398 ↓ 568 HBB, HBM, HBZ, ALAS2, HBA1, HBG1, HBA2, ASHP, HBQ1, HBD, IGJ, REG3A, POU2AF1, DEFA5, NEB, TNNT3, TNN11, TNNT1, MYL1 Metabolic processes, regulation of immune response, cell communication, and complement cascade. Zhuojun Xie et al [ 84 ] RNASeq NEC tissues, NEC-SC-diagnosed NEC with clinical resection, NOR derived from normal part of ileum in NEC-SC patients NEC n = 4 NEC-SC n = 3 Ctrl NOR n = 5 NEC vs. NEC-SC ↑ 37 ↓ 7 NEC vs. NOR ↑ 3465 ↓ 2499 NEC-SC vs.…”