title: Effect of Lactobacillus rhamnosus GR-1 supernatant and fetal sex on lipopolysaccharide-induced cytokine and prostaglandin-regulating enzymes in human placental trophoblast cells: implications for treatment of bacterial vaginosis and prevention of preterm labor.
abstract: OBJECTIVE
  The objective of the study was to determine the effect of fetal sex on the output of cytokines and prostaglandin-regulating enzymes in lipopolysaccharide (LPS) and probiotic lactobacilli-treated placental trophoblast cells.
  
  
  METHODS
  We examined the effect of LPS and Lactobacillus rhamnosus GR-1 supernatant in placental trophoblast cells on tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-10 using enzyme-linked immunosorbent assay and on prostaglandin-endoperoxide synthase 2 (PTGS2), 15-hydroxy prostaglandin dehydrogenase (PGDH), and toll-like receptor-4 (TLR-4) using Western blotting. Comparisons were performed using one-way analysis of variance and Student t test.
  
  
  RESULTS
  LPS increased the output of TNF-alpha, IL-10, and PTGS2 with a greater response in male placentae. L rhamnosus GR-1 supernatant inhibited the LPS-stimulated TNF-alpha and increased IL-10. It also up-regulated expression of PGDH in female placentae and partially reduced the LPS-stimulated PTGS2 in male placentae. There was no change in IL-1beta. Expression of TLR-4 was greater in placentae of male fetuses.
  
  
  CONCLUSIONS
  These findings suggest an underlying mechanism for the sex difference in the incidence of preterm birth and provide potential evidence for a therapeutic benefit of lactobacilli in reducing preterm labor.
authors.affiliation: Department of Physiology, University of Toronto, Toronto, ON, Canada.
authors.forename: Maryam
authors.initials: M
authors.lastname: Yeganegi
authors.forename: Carole S
authors.initials: CS
authors.lastname: Watson
authors.forename: Andrew
authors.initials: A
authors.lastname: Martins
authors.forename: Sung O
authors.initials: SO
authors.lastname: Kim
authors.forename: Gregor
authors.initials: G
authors.lastname: Reid
authors.forename: John R G
authors.initials: JR
authors.lastname: Challis
authors.forename: Alan D
authors.initials: AD
authors.lastname: Bocking
mesh_terms: D002478:Cells, Cultured; D051546:Cyclooxygenase 2 / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism*; D005260:Female; D006801:Humans; D006911:Hydroxyprostaglandin Dehydrogenases / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D052201:Lacticaseibacillus rhamnosus / Q000276:immunology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D007752:Obstetric Labor, Premature / Q000517:prevention & control*; D011247:Pregnancy; D019936:Probiotics; D012737:Sex Factors; D051197:Toll-Like Receptor 4 / Q000378:metabolism; D014327:Trophoblasts / Q000166:cytology / Q000201:enzymology / Q000382:microbiology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D016585:Vaginosis, Bacterial / Q000276:immunology / Q000378:metabolism / Q000628:therapy*
chemical_list: D016207:Cytokines; C508609:IL10 protein, human; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; C495345:TLR4 protein, human; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; C082161:lipopolysaccharide A; D016753:Interleukin-10; D006911:Hydroxyprostaglandin Dehydrogenases; C035859:15-hydroxyprostaglandin dehydrogenase; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human