The value of perinatal immune responses in predicting allergic disease at 6 years of age

Prescott, Susan L.; King, Barbara; Strong, T.L.; Holt, Patrick G.

doi:10.1034/j.1398-9995.2003.00263.x

Cited by 62 publications

(43 citation statements)

References 20 publications

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“…However, in individuals who have a lower capacity for IFN-g production, potentially on a genetic basis or under certain conditions, the activation of iNKT cells might induce the production of IL-4 and -13 and enhance the development of atopy and allergic responses. This concept gains support from findings in infants at genetic risk for developing atopy who have weaker neonatal IFN-g responses compared with low-risk infants (61), perhaps because of differential patterns of methylation of the IFN-g promoter (62). It is under such conditions that iNKT cell activation may play a significant role in directing T cell differentiation and Th2 polarization, increasing the risk for developing atopy and asthma.…”

Section: Discussionmentioning

confidence: 57%

Plasticity of Invariant NKT Cell Regulation of Allergic Airway Disease Is Dependent on IFN-γ Production

Matsuda

Takeda

Koya

et al. 2010

The Journal of Immunology

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Invariant NKT cells (iNKT cells) play a pivotal role in the development of allergen-induced airway hyperresponsiveness (AHR) and inflammation. However, it is unclear what role they play in the initiation (sensitization) phase as opposed to the effector (challenge) phase. The role of iNKT cells during sensitization was examined by determining the response of mice to intratracheal transfer of OVA-pulsed or OVA–α-galactosylceramide (OVA/αGalCer)-pulsed bone marrow-derived dendritic cells (BMDCs) prior to allergen challenge. Wild-type (WT) recipients of OVA-BMDCs developed AHR, increased airway eosinophilia, and increased levels of Th2 cytokines in bronchoalveolar lavage fluid, whereas recipients of OVA/αGalCer BMDCs failed to do so. In contrast, transfer of these same OVA/αGalCer BMDCs into IFN-γ–deficient (IFN-γ−/−) mice enhanced the development of these lung allergic responses, which was reversed by exogenous IFN-γ treatment following OVA-BMDC transfer. Further, Jα18-deficient recipients, which lack iNKT cells, developed the full spectrum of lung allergic responses following reconstitution with highly purified WT liver or spleen iNKT cells and transfer of OVA-BMDCs, whereas reconstituted recipients of OVA/αGalCer BMDCs failed to do so. Transfer of iNKT cells from IFN-γ−/− mice restored the development of these responses in Jα18-deficient recipients following OVA-BMDC transfer; the responses were enhanced following OVA/αGalCer BMDC transfer. iNKT cells from these IFN-γ−/− mice produced higher levels of IL-13 in vitro compared with WT iNKT cells. These data identify IFN-γ as playing a critical role in dictating the consequences of iNKT cell activation in the initiation phase of the development of AHR and airway inflammation.

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Section: Discussionmentioning

confidence: 57%

Plasticity of Invariant NKT Cell Regulation of Allergic Airway Disease Is Dependent on IFN-γ Production

Matsuda

Takeda

Koya

et al. 2010

The Journal of Immunology

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“…We also observed increasing production of IL-13 to allergenspecific stimulation with dust mite in association with increasing cumulative stress. Notably, the pattern of increased IL-13 response to house dust mite has been associated with allergic sensitization in older children (55). The production of IL-13 by CBMCs stimulated with cockroach extract was unchanged across the cumulative stress levels.…”

Section: Discussionmentioning

confidence: 89%

Prenatal Maternal Stress and Cord Blood Innate and Adaptive Cytokine Responses in an Inner-City Cohort

Wright¹,

Visness²,

Calatroni³

et al. 2010

Am J Respir Crit Care Med

207

157

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Rationale: Stress-elicited disruption of immunity begins in utero. Objectives: Associations among prenatal maternal stress and cord blood mononuclear cell (CBMC) cytokine responses were prospectively examined in the Urban Environment and Childhood Asthma Study (n 5 557 families). Methods: Prenatal maternal stress included financial hardship, difficult life circumstances, community violence, and neighborhood/block and housing conditions. Factor analysis produced latent variables representing three contexts: individual stressors and ecological-level strains (housing problems and neighborhood problems), which were combined to create a composite cumulative stress indicator. CBMCs were incubated with innate (lipopolysaccharide, polyinosinic-polycytidylic acid, cytosine-phosphate-guanine dinucleotides, peptidoglycan) and adaptive (tetanus, dust mite, cockroach) stimuli, respiratory syncytial virus, phytohemagglutinin, or medium alone. Cytokines were measured using multiplex ELISAs. Using linear regression, associations among increasing cumulative stress and cytokine responses were examined, adjusting for sociodemographic factors, parity, season of birth, maternal asthma and steroid use, and potential pathway variables (prenatal smoking, birth weight for gestational age). Measurements and Main Results: Mothers were primarily minorities (Black [71%], Latino [19%]) with an income less than $15,000 (69%). Mothers with the highest cumulative stress were older and more likely to have asthma and deliver lower birth weight infants. Higher prenatal stress was related to increased IL-8 production after microbial (CpG, PIC, peptidoglycan) stimuli and increased tumor necrosis factor-a to microbial stimuli (CpG, PIC). In the adaptive panel, higher stress was associated with increased IL-13 after dust mite stimulation and reduced phytohemagglutinin-induced IFN-g. Conclusions: Prenatal stress was associated with altered innate and adaptive immune responses in CBMCs. Stress-induced perinatal immunomodulation may impact the expression of allergic disease in these children.

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“…[136][137][138][139][140] Before age 12, boys have more severe asthma than girls, 142 with higher rates of admission to hospital. [158][159][160][161][162][163][164][165] In contrast, adult females have more severe asthma than males, with more hospital admissions, 161,166,167 slower improvement, 120 longer hospital stays 161 and higher rates of readmission. 168 Most authors have attributed these changes in prevalence and severity to events of puberty, 140,141 although mechanisms for differences between the sexes have not been established.…”

Section: Sex and Gendermentioning

confidence: 99%

“…For example, impairment in interferon γ production at 3 months was associated with a greater risk of wheeze. 115 Immaturity in neonatal immune responses may promote the persistence of the Th2 immune phenotype and development of atopy, 120 but an association with persistent asthma is as yet unproven. More recent work has focused on the role of the innate immune system in handling and presentation of antigens and suggests that polymorphisms in Toll-like receptors 121,122 may play a greater role than previously recognized in the development of the skewed immune responses associated with persistent asthma.…”

Section: Allergic Sensitizationmentioning

confidence: 99%

Asthma: epidemiology, etiology and risk factors

Subbarao¹,

Mandhane²,

Sears³

2009

Canadian Medical Association Journal

440

303

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The value of perinatal immune responses in predicting allergic disease at 6 years of age

Cited by 62 publications

References 20 publications

Plasticity of Invariant NKT Cell Regulation of Allergic Airway Disease Is Dependent on IFN-γ Production

Plasticity of Invariant NKT Cell Regulation of Allergic Airway Disease Is Dependent on IFN-γ Production

Prenatal Maternal Stress and Cord Blood Innate and Adaptive Cytokine Responses in an Inner-City Cohort

Asthma: epidemiology, etiology and risk factors

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