2010
Lactobacillus rhamnosus GR-1 Stimulates Colony-Stimulating Factor 3 (Granulocyte) (CSF3) Output in Placental Trophoblast Cells in a Fetal Sex-Dependent Manner1
Yeganegi M, Leung C, Martins A, Kim S, Reid G, Challis J, Bocking A. Lactobacillus rhamnosus GR-1 Stimulates Colony-Stimulating Factor 3 (Granulocyte) (CSF3) Output in Placental Trophoblast Cells in a Fetal Sex-Dependent Manner1. Biology Of Reproduction 2010, 84: 18-25. PMID: 20811016, PMCID: PMC4480822, DOI: 10.1095/biolreprod.110.085167.Peer-Reviewed Original ResearchConceptsPlacental trophoblast cellsTrophoblast cellsPreterm birthFetal sex-dependent mannerAnti-inflammatory effectsJanus kinaseSex-dependent mannerColony-stimulating factor 3Mitogen-activated protein kinase 14Western blot analysisPreterm laborPhosphorylation of STAT3Interleukin-10Bacterial vaginosisTherapeutic benefitFemale fetusesProtein kinase 14Placenta culturesAbsence of pretreatmentMAPK14 inhibitorSignal transducerTranscription 3Cell preparationsUnderlying mechanismBlot analysis
2009
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
Yeganegi M, Watson C, Martins A, Kim S, Reid G, Challis J, Bocking A. 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. American Journal Of Obstetrics And Gynecology 2009, 200: 532.e1-532.e8. PMID: 19285652, DOI: 10.1016/j.ajog.2008.12.032.Peer-Reviewed Original ResearchMeSH KeywordsCells, CulturedCyclooxygenase 2CytokinesFemaleHumansHydroxyprostaglandin DehydrogenasesInterleukin-10Interleukin-1betaLacticaseibacillus rhamnosusLipopolysaccharidesMaleObstetric Labor, PrematurePregnancyProbioticsSex FactorsToll-Like Receptor 4TrophoblastsTumor Necrosis Factor-alphaVaginosis, BacterialConceptsToll-like receptor 4Prostaglandin-endoperoxide synthase 2Placental trophoblast cellsIL-10Prostaglandin dehydrogenaseTrophoblast cellsPreterm laborTNF-alphaMale placentasFetal sexOutput of cytokinesHuman placental trophoblast cellsTumor necrosis factorEffects of lipopolysaccharideLipopolysaccharide-induced cytokineEnzyme-linked immunosorbentStudent's t-testPreterm birthBacterial vaginosisIL-1betaReceptor 4Necrosis factorTherapeutic benefitFemale placentasMale fetuses
2008
Reduced Expression of Basal and Probiotic-inducible G-CSF in Intestinal Mononuclear Cells Is Associated with Inflammatory Bowel Disease
Martins A, Colquhoun P, Reid G, Kim S. Reduced Expression of Basal and Probiotic-inducible G-CSF in Intestinal Mononuclear Cells Is Associated with Inflammatory Bowel Disease. Inflammatory Bowel Diseases 2008, 15: 515-525. PMID: 19058228, DOI: 10.1002/ibd.20808.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsEscherichia coliGranulocyte Colony-Stimulating FactorHumansInflammatory Bowel DiseasesInterleukin-12Interleukin-23Intestinal MucosaLacticaseibacillus rhamnosusLeukocytes, MononuclearMiceMice, Inbred C57BLMucous MembraneProbioticsReceptors, Granulocyte Colony-Stimulating FactorTumor Necrosis Factor-alphaConceptsGranulocyte-colony stimulating factorInflammatory bowel diseaseHuman peripheral blood mononuclear cellsPeripheral blood mononuclear cellsG-CSF productionIntestinal mononuclear cellsBlood mononuclear cellsMononuclear cellsRhamnosus GR-1L. rhamnosus GR-1IL-23Bowel diseaseIntestinal lamina propria mononuclear cellsGr-1Intestinal lamina propria cellsLamina propria mononuclear cellsNon-IBD patientsReceptor knockout miceReceptor-deficient miceProinflammatory cytokine productionLamina propria cellsBone marrow-derived macrophagesIntestinal tissue samplesMarrow-derived macrophagesG-CSF release
2006
G‐CSF‐mediated inhibition of JNK is a key mechanism for Lactobacillus rhamnosus‐induced suppression of TNF production in macrophages
Kim S, Sheikh H, Ha S, Martins A, Reid G. G‐CSF‐mediated inhibition of JNK is a key mechanism for Lactobacillus rhamnosus‐induced suppression of TNF production in macrophages. Cellular Microbiology 2006, 8: 1958-1971. PMID: 16889627, DOI: 10.1111/j.1462-5822.2006.00763.x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone Marrow CellsCell LineCytokinesEnterococcus faecalisEscherichia coliGranulocyte Colony-Stimulating FactorHumansInterleukin-10JNK Mitogen-Activated Protein KinasesLacticaseibacillus rhamnosusMacrophage ActivationMacrophagesMacrophages, PeritonealMiceMice, Inbred C57BLP38 Mitogen-Activated Protein KinasesPhosphorylationProbioticsSignal TransductionSTAT3 Transcription FactorTumor Necrosis Factor-alphaConceptsGranulocyte-colony stimulating factorTNF productionL. rhamnosus GGGr-1Rhamnosus GGReceptor knockout miceAnti-inflammatory effectsMonocytic cell line THP-1Human monocytic cell line THP-1Cell line THP-1Lipopolysaccharide-activated macrophagesActivation of STAT3C-Jun N-terminal kinaseImmunomodulatory effectsTumor necrosisImmunomodulatory propertiesKnockout miceParacrine routeStimulating factorMacrophagesTHP-1Subsequent inhibitionMouse macrophagesCulture supernatantsNovo protein synthesis