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Prenatal stress is associated with altered patterns of cord blood cytokine production that may raise a child's asthma risk later in life, according to findings of one study.
“Prenatal stress appears to affect immune responses to both innate and adaptive stimuli at the time of birth—effects that may result in enhanced susceptibility to asthma or other atopic disorders,” said Dr. Rosalind J. Wright of Harvard Medical School in Boston and her associates (Am. J. Respir. Crit. Care Med. 2010 March 1 [doi:10.1164/rccm.200904-0637OC
The findings on seemingly stress-induced perinatal immune modulation may offer some new insight into the disproportionately high prevalence of asthma among ethnic minorities and disadvantaged urban communities.
In a prospective birth cohort study of urban, largely minority women, the investigators collected cord blood at birth and examined cord blood mononuclear cell (CBMC) cytokine responses to various innate and adaptive stimuli. Cytokine responses to both types of stimuli were significantly different in babies born to mothers with high levels of reported cumulative stress, compared with babies born to lower-stressed mothers.
In each case, the infants were at high risk for atopic diseases based on family history; either the mother or father had a history of asthma or allergy. Higher prenatal stress was related to increased production of interleukin-8 (IL-8) and tumor necrosis factor–alpha, for example, following microbial (CpG, PIC) stimuli.
For adaptive response, there was evidence that higher stress is tied to lower levels of interferon-gamma production in response to stimulation with PHA (a nonspecific mitogen), which has been linked to an increased risk for later atopic disease. Higher stress was also linked with an increased IL-13 response to dust mite antigen, which has been associated with allergic sensitization in older children.
The investigators studied 560 newborns and their mothers who live in Baltimore, Boston, New York, and St. Louis, and who were participating in the Urban Environment and Childhood Asthma Study. The mothers were primarily minorities (71% black and 19% Hispanic); 69% reported an annual income of less than $15,000.
Families answered detailed questions about various stressors in their lives, including financial hardship, community violence, and neighborhood and housing conditions.
The cohort will continue to be followed, enabling further assessment of the effects of prenatal and postnatal stress on infant immune development, and clinical outcomes, as the infants grow.
Disclosures: The study received funding from the National Institutes of Health. Dr. Wright also received funding from an NIH grant.
Prenatal stress is associated with altered patterns of cord blood cytokine production that may raise a child's asthma risk later in life, according to findings of one study.
“Prenatal stress appears to affect immune responses to both innate and adaptive stimuli at the time of birth—effects that may result in enhanced susceptibility to asthma or other atopic disorders,” said Dr. Rosalind J. Wright of Harvard Medical School in Boston and her associates (Am. J. Respir. Crit. Care Med. 2010 March 1 [doi:10.1164/rccm.200904-0637OC
The findings on seemingly stress-induced perinatal immune modulation may offer some new insight into the disproportionately high prevalence of asthma among ethnic minorities and disadvantaged urban communities.
In a prospective birth cohort study of urban, largely minority women, the investigators collected cord blood at birth and examined cord blood mononuclear cell (CBMC) cytokine responses to various innate and adaptive stimuli. Cytokine responses to both types of stimuli were significantly different in babies born to mothers with high levels of reported cumulative stress, compared with babies born to lower-stressed mothers.
In each case, the infants were at high risk for atopic diseases based on family history; either the mother or father had a history of asthma or allergy. Higher prenatal stress was related to increased production of interleukin-8 (IL-8) and tumor necrosis factor–alpha, for example, following microbial (CpG, PIC) stimuli.
For adaptive response, there was evidence that higher stress is tied to lower levels of interferon-gamma production in response to stimulation with PHA (a nonspecific mitogen), which has been linked to an increased risk for later atopic disease. Higher stress was also linked with an increased IL-13 response to dust mite antigen, which has been associated with allergic sensitization in older children.
The investigators studied 560 newborns and their mothers who live in Baltimore, Boston, New York, and St. Louis, and who were participating in the Urban Environment and Childhood Asthma Study. The mothers were primarily minorities (71% black and 19% Hispanic); 69% reported an annual income of less than $15,000.
Families answered detailed questions about various stressors in their lives, including financial hardship, community violence, and neighborhood and housing conditions.
The cohort will continue to be followed, enabling further assessment of the effects of prenatal and postnatal stress on infant immune development, and clinical outcomes, as the infants grow.
Disclosures: The study received funding from the National Institutes of Health. Dr. Wright also received funding from an NIH grant.
Prenatal stress is associated with altered patterns of cord blood cytokine production that may raise a child's asthma risk later in life, according to findings of one study.
“Prenatal stress appears to affect immune responses to both innate and adaptive stimuli at the time of birth—effects that may result in enhanced susceptibility to asthma or other atopic disorders,” said Dr. Rosalind J. Wright of Harvard Medical School in Boston and her associates (Am. J. Respir. Crit. Care Med. 2010 March 1 [doi:10.1164/rccm.200904-0637OC
The findings on seemingly stress-induced perinatal immune modulation may offer some new insight into the disproportionately high prevalence of asthma among ethnic minorities and disadvantaged urban communities.
In a prospective birth cohort study of urban, largely minority women, the investigators collected cord blood at birth and examined cord blood mononuclear cell (CBMC) cytokine responses to various innate and adaptive stimuli. Cytokine responses to both types of stimuli were significantly different in babies born to mothers with high levels of reported cumulative stress, compared with babies born to lower-stressed mothers.
In each case, the infants were at high risk for atopic diseases based on family history; either the mother or father had a history of asthma or allergy. Higher prenatal stress was related to increased production of interleukin-8 (IL-8) and tumor necrosis factor–alpha, for example, following microbial (CpG, PIC) stimuli.
For adaptive response, there was evidence that higher stress is tied to lower levels of interferon-gamma production in response to stimulation with PHA (a nonspecific mitogen), which has been linked to an increased risk for later atopic disease. Higher stress was also linked with an increased IL-13 response to dust mite antigen, which has been associated with allergic sensitization in older children.
The investigators studied 560 newborns and their mothers who live in Baltimore, Boston, New York, and St. Louis, and who were participating in the Urban Environment and Childhood Asthma Study. The mothers were primarily minorities (71% black and 19% Hispanic); 69% reported an annual income of less than $15,000.
Families answered detailed questions about various stressors in their lives, including financial hardship, community violence, and neighborhood and housing conditions.
The cohort will continue to be followed, enabling further assessment of the effects of prenatal and postnatal stress on infant immune development, and clinical outcomes, as the infants grow.
Disclosures: The study received funding from the National Institutes of Health. Dr. Wright also received funding from an NIH grant.