Exposure to environmental bacteria may have differing effects on tumour necrosis factor-alpha and interleukin-6-producing capacity in infancy.
BACKGROUND
Our previous study showed an association between increased concentration of endotoxin in house dust and elevated IFN-gamma responses in neonates. The impact of other microbial agents on immune responses in infancy is poorly known.


OBJECTIVE
To examine whether stimulated cytokine responses of mothers and their children are associated with concentrations of other microbial markers in addition to endotoxin in house dust samples.


METHODS
Mitogen-stimulated production of IFN-gamma, IL-4, IL-6 and TNF-alpha was measured in cord blood and in peripheral blood of mothers (n=29) and their children (n=29) 3 months after birth. Gas chromatography mass spectrometric analysis was applied to measure the concentrations of ergosterol (marker of fungal biomass), muramic acid (indicating the presence of Gram-positive bacteria) and 3-hydroxy fatty acids (C(10:0)-C(14:0), indicating the presence of Gram-negative bacteria) in house dust. Endotoxin was determined with Limulus assay.


RESULTS
Significant mother-to-child correlations were observed in stimulated production of TNF-alpha and IL-6 3 months after birth. 3-hydroxy fatty acid (C(10:0)-C(14:0)) levels in bed dust were inversely associated with the production of TNF-alpha and IL-6 in blood samples of mothers and their 3-month-old children. High concentrations of muramic acid in floor dust were related to increased production of TNF-alpha and IL-6 at the age of 3 months. In contrast to endotoxin, none of the other microbial markers were significantly associated with enhanced IFN-gamma-producing capacity from birth to 3 months.


CONCLUSIONS
Exposure to Gram-negative bacteria and their components may be associated with down-regulated immune responses in early infancy, indicated as an impaired production of pro-inflammatory cytokines following mitogen stimulation. Gram-positive bacteria and their constituents seem to have opposite effects. Of the measured markers, exposure to bioactive endotoxin appears to have the strongest impact on T-helper type 1 responses.
Lappalainen
M H J
MH
Department of Environmental Health, National Public Health Institute, Kuopio, Finland. Mikko.Lappalainen@ktl.fi
Roponen
M
M
Hyvärinen
A
A
Nevalainen
A
A
Laine
O
O
Pekkanen
J
J
Hirvonen
M-R
MR
D004391:Dust / Q000276:immunology*; D004731:Endotoxins / Q000276:immunology*; D004781:Environmental Exposure; D004875:Ergosterol / Q000276:immunology; D005227:Fatty Acids / Q000276:immunology; D005260:Female; D005312:Fetal Blood / Q000276:immunology; D005658:Fungi / Q000276:immunology; D006090:Gram-Negative Bacteria / Q000276:immunology; D006094:Gram-Positive Bacteria / Q000276:immunology; D006801:Humans; D007231:Infant, Newborn; D007371:Interferon-gamma / Q000276:immunology; D015847:Interleukin-4 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood*; D009112:Muramic Acids / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*
D004391:Dust; D004731:Endotoxins; D005227:Fatty Acids; D015850:Interleukin-6; D009112:Muramic Acids; D014409:Tumor Necrosis Factor-alpha; D015847:Interleukin-4; D007371:Interferon-gamma; D004875:Ergosterol