Allergen-Independent Maternal Transmission of Asthma Susceptibility

Hamada, Kaoru; Suzaki, Yasue; Goldman, Alejandra; Ning, Yao; Goldsmith, C.-A. W.; Palecanda, Aiyappa; Coull, Brent A.; Hubeau, Cédric; Kobzik, Lester

doi:10.4049/jimmunol.170.4.1683

Cited by 121 publications

(186 citation statements)

References 35 publications

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“…Consistent with the original model (18), histopathological examination showed that pups born of asthmatic mothers, when submitted to suboptimal asthma induction, develop substantial inflammatory infiltration in their airways, comprised of eosinophils and mononuclear cells surrounding the bronchi and vessels (Fig. 4A).…”

Section: Pc 61 Pretreatment Increases or Reduces Asthma Susceptibilitmentioning

confidence: 64%

“…This protocol allows the distinction between inbred mice that are differentially susceptible to asthma, in an allergen nonspecific manner (18). This model has facilitated studies on the impact of maternal asthma on exposure to CpGs (20), breastfeeding (21), and allergen-specific T cell function during pregnancy (19).…”

Section: Discussionmentioning

confidence: 99%

“…The model of maternal asthma using OVA-sensitized and aerosol-exposed BALB/c female mice was detailed previously (18). The modification of this protocol is represented in Fig.…”

Section: Allergen Sensitization and Aerosol Exposurementioning

confidence: 99%

“…We previously described a murine model of maternal asthma where intentionally suboptimal sensitization and exposure to allergens allow the identification of neonates with increased susceptibility to asthma (18). This model of natural predisposition to asthma has proven useful to investigate immunobiological mechanisms involved in the maternal transfer of asthma risk without other confounding genetic and environmental factors (19 -21).…”

Section: Targeting Of Cd25 and Glucocorticoid-induced Tnf Receptor Famentioning

confidence: 99%

“…injection of 5 g of OVA in 1 mg of aluminum hydroxide (day 5) followed by 3% OVA aerosols (days [12][13][14]. Final physiologic and pathologic analyses were performed on days 15 and 16, as described previously (18).…”

Section: Allergen Sensitization and Aerosol Exposurementioning

confidence: 99%

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Targeting of CD25 and Glucocorticoid-Induced TNF Receptor Family-Related Gene-Expressing T Cells Differentially Modulates Asthma Risk in Offspring of Asthmatic and Normal Mother Mice

Hubeau¹,

Apostolou

Kobzik

2007

The Journal of Immunology

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Immunological mechanisms leading to increased asthma susceptibility in early life remain obscure. In this study, we examined the effects of neonatal Ab treatments targeting T cell populations on the development of an asthma syndrome. We used a model of increased asthma susceptibility where offspring of asthmatic BALB/c mother mice are more prone (than normal pups) to develop the disease. Neonatal pretreatment of naive pups with mAb directed against the IL-2Rα chain (CD25), the costimulatory molecule glucocorticoid-induced TNFR family related gene, and the inhibitory molecule CTLA-4 elicited contrasting effects in offspring depending on the mother’s asthma status. Specifically, neonatal CD25high T cell depletion stimulated asthma susceptibility in normal offspring whereas it ameliorated the condition of pups born of asthmatic mothers. Conversely, glucocorticoid-induced TNFR family related gene ligation as a primary signal reduced the spleen cellularity and largely abrogated asthma susceptibility in asthma-prone offspring, without inducing disease in normal pups. Striking changes in Th1/Th2 cytokine levels, especially IL-4, followed mAb pretreatment and were consistent with the impact on asthma susceptibility. These results point to major differences in neonatal T cell population and responsiveness related to maternal asthma history. Interventions that temporarily remove and/or inactivate specific T cell subsets may therefore prove useful to attenuate early life asthma susceptibility and prevent the development of Th2-driven allergic airway disease.

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Section: Pc 61 Pretreatment Increases or Reduces Asthma Susceptibilitmentioning

confidence: 64%

Section: Discussionmentioning

confidence: 99%

“…The model of maternal asthma using OVA-sensitized and aerosol-exposed BALB/c female mice was detailed previously (18). The modification of this protocol is represented in Fig.…”

Section: Allergen Sensitization and Aerosol Exposurementioning

confidence: 99%

Section: Targeting Of Cd25 and Glucocorticoid-induced Tnf Receptor Famentioning

confidence: 99%

Section: Allergen Sensitization and Aerosol Exposurementioning

confidence: 99%

See 3 more Smart Citations

Targeting of CD25 and Glucocorticoid-Induced TNF Receptor Family-Related Gene-Expressing T Cells Differentially Modulates Asthma Risk in Offspring of Asthmatic and Normal Mother Mice

Hubeau¹,

Apostolou

Kobzik

2007

The Journal of Immunology

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Epigenetic Mechanisms in Asthma

Miller¹,

Herbstman²

2009

Epigenetics and Human Health

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The effects of prenatal “psychological” stressor exposure on lung inflammation and hyperresponsiveness in adult rat offspring

Carmo

Righetti

Tibério

et al. 2016

Developmental Psychobiology

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The aim of this study was to establish whether exposure of pregnant rats to uncontrollable (psychological) stressors might change the likelihood of their offspring to exhibit functional and histopathological abnormalities suggestive of asthma in adulthood. Pregnant rats (n = 16) underwent one of three treatments: electric shocks of a maximum duration of 10 s that could be escaped (controllable group; C) those that could not be escaped (uncontrollable group; U) or no shocks (control group; N). The offspring (n = 54) were kept in animal house under standard conditions until 3 months of age, when lung hyperresponsiveness, histopathology, immunohistochemical measurements of the cytokines interleukin (IL) 2, IL-4, IL-5, and IL-13 and actin as well as oxidative stress based on iNOS-positive cell counts and isoprostane PGF2α contents were assessed. The results showed that prenatal exposure to physical stressors (shocks) caused lung hyperresponsiveness and increased cytokine expression; exposure to uncontrollable shock (group U) had a differential effect on the expression of IL-2, IL-5, and IL-13 in inflammatory cells compared to exposure to controllable shock (group C), which characterizes the "psychological" aspect of stress. The results show that not only stress but also its uncontrollability during gestation might increase the likelihood that the offspring will exhibit functional and histopathological abnormalities suggestive of asthma. These findings strengthen the importance of psychological control with regard to environmental stimuli for the occurrence of several illnesses, suggesting the desirability of integration among various fields of science.

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Allergen-Independent Maternal Transmission of Asthma Susceptibility

Cited by 121 publications

References 35 publications

Targeting of CD25 and Glucocorticoid-Induced TNF Receptor Family-Related Gene-Expressing T Cells Differentially Modulates Asthma Risk in Offspring of Asthmatic and Normal Mother Mice

Targeting of CD25 and Glucocorticoid-Induced TNF Receptor Family-Related Gene-Expressing T Cells Differentially Modulates Asthma Risk in Offspring of Asthmatic and Normal Mother Mice

Epigenetic Mechanisms in Asthma

The effects of prenatal “psychological” stressor exposure on lung inflammation and hyperresponsiveness in adult rat offspring

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