Chronic caregiver stress and IgE expression, allergen-induced proliferation, and cytokine profiles in a birth cohort predisposed to atopy.
BACKGROUND
Psychologic stress modifies immune function and cytokine production.


OBJECTIVE
We examined relationships between caregiver stress on the following markers of early childhood immune response: (1) IgE expression (n=215); (2) mitogen-induced and allergen-specific (Dermatophagoides farinae [Der f 1] and cockroach [Bla g 2]) proliferative response (n=114); and (3) subsequent cytokine expression (INF-gamma, TNF-alpha, IL-10, and IL-13) in a prospective birth cohort predisposed to atopy.


METHODS
Caregiver stress was measured at 2-month intervals for the first 2 years of life and yearly thereafter by using the Perceived Stress Scale. A subsequent blood sample obtained from the children (median age, 2.1 years; range, 18-32 months) was analyzed for total serum IgE level and allergen-induced proliferation quantified as the stimulation index (SI; mean thymidine incorporation of the stimulated sample divided by that of the unstimulated sample). The relationship between stress and the proliferative response (SI >3 vs SI < or =3), and total IgE level (< or =100 IU/mL vs >100 IU/mL) was examined by using logistic regression. The relationship between cytokine levels and stress was analyzed by using linear regression.


RESULTS
In adjusted analyses higher caregiver stress in the first 6 months after birth was associated with a Der f 1 SI of greater than 3 (odds ratio [OR], 1.5; 95% CI, 1.0-2.3) and nominally associated with a Bla g 2 SI of greater than 3 (OR, 1.13; 95% CI, 0.7-1.8). Higher stress between ages 6 and 18 months was associated with a high total IgE level (OR, 2.03; 95% CI, 1.1-3.6). Higher stress was significantly associated with increased production of TNF-alpha, with a suggested trend between higher stress and reduced INF-gamma production.


CONCLUSIONS
Increased stress in early childhood was associated with an atopic immune profile in these children predisposed to atopy-asthma.
Wright
Rosalind J
RJ
Channing Laboratory, Brigham and Women's Hospital, 181 Longwood Avenue, Boston, MA 02115, USA. rosalind.wright@channing.harvard.edu
Finn
Patricia
P
Contreras
Johanna Paola
JP
Cohen
Sheldon
S
Wright
Robert O
RO
Staudenmayer
John
J
Wand
Matthew
M
Perkins
David
D
Weiss
Scott T
ST
Gold
Diane R
DR
D000485:Allergens / Q000276:immunology*; D039741:Antigens, Dermatophagoides / Q000276:immunology; D052179:Antigens, Plant; D060829:Arthropod Proteins; D017028:Caregivers; D002908:Chronic Disease; D003546:Cysteine Endopeptidases; D016207:Cytokines / Q000096:biosynthesis*; D005260:Female; D006801:Humans; D006967:Hypersensitivity / Q000209:etiology*; D007073:Immunoglobulin E / Q000097:blood*; D007223:Infant; D007371:Interferon-gamma / Q000096:biosynthesis; D016015:Logistic Models; D008213:Lymphocyte Activation; D008297:Male; D013315:Stress, Psychological / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D000485:Allergens; D039741:Antigens, Dermatophagoides; D052179:Antigens, Plant; D060829:Arthropod Proteins; D016207:Cytokines; D014409:Tumor Necrosis Factor-alpha; C105482:allergen Bla g 1; D007073:Immunoglobulin E; D007371:Interferon-gamma; D003546:Cysteine Endopeptidases; C451159:Dermatophagoides farinae antigen f 1