Cytokine production by peripheral blood mononuclear cells of women with a history of preterm birth.
Preterm birth is associated with elevated production of pro-inflammatory cytokines such as TNFalpha at the maternal-fetal interface. Previous studies have suggested that women with a history of preterm birth produce aberrantly strong inflammatory responses to bacterial lipopolysaccharide (LPS). However many intrauterine infections in women are associated with pathogens including Ureaplasma urealyticum, Mycoplasma hominis and Streptococcus agalactiae (group B streptococcus) that contain pro-inflammatory factors other than LPS. We evaluated whether peripheral blood leukocytes from women with a history of preterm birth produce elevated amounts of TNFalpha upon stimulation with pathogens associated with preterm birth and if pre-treatment with aspirin, an anti-inflammatory medication, decreases the ex vivo production of this cytokine. Heat-killed bacteria elicited increased TNFalpha production from leukocytes in a dose-dependent manner, but no differences in TNFalpha production between leukocytes from women with preterm birth and control women with term birth were detected. In women who consumed aspirin each day for one week, TNFalpha production was increased in leukocytes from control women stimulated with Escherichia coli and U. urealyticum, but was reduced or unchanged in leukocytes from women with preterm birth. Similar trends were observed for a subset of samples stimulated with U. urealyticum and assayed for IL-6, IL-10, IL-1beta and TNFalpha by bead array. We conclude that leukocytes from women with a history of preterm birth do not have elevated pro-inflammatory responses to pathogens, and that reproductive history is associated with different effects of aspirin on pro-inflammatory cytokine production.
Peltier
Morgan R
MR
Women's and Children's Research Institute, Winthrop University Hospital, Mineola, NY 11501, USA. mpeltier@winthrop.org
Faux
David S
DS
Hamblin
Steven D
SD
Silver
Robert M
RM
Esplin
M Sean
MS
D001241:Aspirin / Q000627:therapeutic use; D016207:Cytokines / Q000187:drug effects / Q000276:immunology*; D004926:Escherichia coli / Q000187:drug effects / Q000276:immunology; D005260:Female; D006801:Humans; D016753:Interleukin-10 / Q000276:immunology; D053583:Interleukin-1beta / Q000187:drug effects / Q000276:immunology; D015850:Interleukin-6 / Q000276:immunology; D009000:Monocytes / Q000187:drug effects / Q000276:immunology*; D019535:Mycoplasma hominis / Q000187:drug effects / Q000276:immunology; D011247:Pregnancy; D011251:Pregnancy Complications, Infectious / Q000276:immunology* / Q000382:microbiology; D047928:Premature Birth / Q000188:drug therapy / Q000276:immunology*; D013292:Streptococcus agalactiae / Q000187:drug effects / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000187:drug effects / Q000276:immunology; D016990:Ureaplasma urealyticum / Q000187:drug effects / Q000276:immunology; D044465:White People
D016207:Cytokines; D053583:Interleukin-1beta; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D001241:Aspirin