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Postnatal Administration of Lactobacillus rhamnosus HN001 Ameliorates Perinatal Broad‐Spectrum Antibiotic‐Induced Reduction in Myelopoiesis and T Cell Activation in Mouse Pups
Author(s) -
Fuglsang Eva,
Krych Lukasz,
Lundsager Mia Thorup,
Nielsen Dennis Sandris,
Frøkiær Hanne
Publication year - 2018
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201800510
Subject(s) - lactobacillus rhamnosus , spleen , myelopoiesis , antibiotics , progenitor cell , granulopoiesis , gut flora , biology , bone marrow , immunology , cytotoxic t cell , microbiology and biotechnology , medicine , lactobacillus , stem cell , bacteria , in vitro , biochemistry , genetics
Scope This study addresses whether administration of Lactobacillus rhamnosus HN001 could mitigate the effects of a compromised gut microbiota on the composition of mature leukocytes and granulocyte‐macrophage progenitor cells (GMPs) in newborn mice. Methods and results Pregnant dams receive oral broad‐spectrum antibiotics, which dramatically decrease the gut microbial composition analyzed by 16S rRNA sequencing. Perinatal antibiotic treatment decreases the proportions of bone marrow (BM) GMPs (postnatal day (PND2): 0.5% vs 0.8%, PND4: 0.2% to 0.6%) and mature granulocytes (33% vs 24% at PND2), and spleen granulocytes (7% vs 17% at PND2) and B cells (PND2:18% vs 28%, PND4:11% vs 22%). At PND35, T helper (Th) cells (20% vs 14%) and cytotoxic T (Tc) cells (10% vs 8%) decrease in the spleen. Oral administration of L. rhamnosus HN001 to neonatal pups (PND1‐7) restores the antibiotic‐induced changes of GMPs and granulocytes in BM and spleen, and further increases splenic granulocytes in control pups. At PND35, splenic proportions of B and Th but not Tc cells are restored. Conclusion Postnatal administration of a single bacterial strain efficiently restores granulopoiesis and most T cell activation in neonatal mice that suffer from a perinatal antibiotic‐induced compromised gut microbiota at birth.