Prenatal initiation of endotoxin airway exposure prevents subsequent allergen-induced sensitization and airway inflammation in mice

Gerhold, Kerstin; Avagyan, A.; Seib, Christine; Frei, Remo; Steinle, Johanna; Ahrens, Birgit; Dittrich, Anna-Maria; Blümchen, Katharina; Lauener, Roger; Hamelmann, Eckard

doi:10.1016/j.jaci.2006.05.022

Cited by 100 publications

(74 citation statements)

References 40 publications

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“…Furthermore, some families may have had their dog before the birth of the child. It has been observed in laboratory experiments on mice that prenatal plus post-natal exposure to endotoxin is associated with a robust shift toward predominantly Th1 immune response [33]. This result corresponds to the finding that exposure to farm environment during pregnancy and the child's first year of life leads to a lower prevalence of allergy [34].…”

supporting

confidence: 76%

Dog ownership and contact during childhood and later allergy development

Cm¹,

Morgenstern²,

Bischof³

et al. 2008

Eur Respir J

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The effect of dog ownership during childhood on the development of allergy has been investigated in few studies with conflicting results. The association between dog contact and indoor endotoxin exposure during infancy and the development of allergic sensitisation and atopic disease up to age 6 yrs was investigated.Two ongoing birth cohorts, the German Infant Nutrition Intervention Programme (GINI; n51,962) and the Influences of Lifestyle Related Factors on the Human Immune System and Development of Allergies in Children (LISA; n51,193), were analysed. In both studies, information on children's contact with dogs and their allergic symptoms and doctor-diagnosed allergic disease were collected during follow-up using questionnaires. Specific immunoglobulin E to common aeroallergens was measured at age 6 yrs. House dust samples were collected at age 3 months and the amount of endotoxin was determined.Dog ownership in early childhood was associated with a significantly lower rate of mixed pollen and inhalant sensitisation but not with dog sensitisation or allergic symptoms and diseases up to age 6 yrs. Regular contact with dogs, without ownership, during childhood was not associated with those health outcomes. No associations were found between house dust endotoxin exposure during infancy and sensitisation outcomes.In conclusion, dog ownership in early childhood protects against the development of inhalant sensitisation and this effect cannot be attributed to the simultaneous exposure to endotoxin.

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supporting

confidence: 76%

Dog ownership and contact during childhood and later allergy development

Cm¹,

Morgenstern²,

Bischof³

et al. 2008

Eur Respir J

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“…We provide evidence that cystatin protects from inflammation in a systemic fashion, as reflected by its effects on remarkably different compartments, such as the lung and the gut. Moreover, the protein inhibits Th2-related as well as macrophage-related inflammation, which stands in stark contrast to the effect of TLR2 and TLR4 agonists of bacterial origin that have recently been shown to downregulate Th2-driven allergic responses in mouse models (56,57). These components act through stimulation of Th1 responses, as evidenced by elevated production of IFN-␥ and other Th1 cytokines, which is clearly not the case for filarial cystatin.…”

Section: Discussionmentioning

confidence: 88%

A Helminth Immunomodulator Reduces Allergic and Inflammatory Responses by Induction of IL-10-Producing Macrophages

Schnoeller

Rausch

Pillai

et al. 2008

The Journal of Immunology

228

196

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The coincidence between infections with parasitic worms and the reduced prevalence of allergic disease in humans and in animal models has prompted the search for helminth molecules with antiallergic and antiinflammatory potential. We report herein that filarial cystatin, a secreted protease inhibitor of filarial nematodes, suppresses Th2-related inflammation and the ensuing asthmatic disease in a murine model of OVA-induced allergic airway responsiveness. Treatment with recombinant filarial cystatin inhibited eosinophil recruitment, reduced levels of OVA-specific and total IgE, down-regulated IL-4 production, and suppressed allergic airway hyperreactivity when applied during or after sensitization and before challenge with the allergen. Depletion of macrophages by clodronate-containing liposomes prevented the curative effects and restored the levels of infiltrating cells, IgE, and allergic airway reactivity. Blocking of IL-10 by application of anti-IL-10 receptor Abs restored the reduced number of infiltrating cells and the levels of OVA-specific IgE. In contrast, depletion of regulatory T cells by anti-CD25 Abs had only limited effects. Cystatin also modulated macrophage-mediated inflammation in a murine model of dextran sulfate sodium-induced colitis, leading to reduction of inflammatory infiltrations and epithelial damage. Our data demonstrate that treatment with a single helminth protein can exert the antiallergic effects of helminth infections.

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“…Of importance is the maternal environment, suggesting that maternal immunity may be transferred or at least influence the offspring. In experimental murine models, the mother is treated with lipopolysaccharide which attenuated allergic disease and associated inflammation in offspring [22][23][24]. One study explored the effect of LPS on female BALB/c mice before conception and during pregnancy.…”

Section: Animal Models Show the Benefit Of Microbial Exposure During mentioning

confidence: 99%

“…Prenatal and postnatal LPS exposure suppressed allergen-specific IgE production, eosinophilic airway inflammation and in vivo airway reactivity in response to methacholine. The suppression of allergen-mediated inflammatory responses was associated with an increased shift toward Th1 responses in culture (spleen cells) and may be mediated via Toll-like receptor (TLR) and T-bet expression by lung tissues [23]. Another group used a rat model and investigated the effect of prenatal LPS exposure on postnatal T cell differentiation and experimental allergic airway disease.…”

Section: Animal Models Show the Benefit Of Microbial Exposure During mentioning

confidence: 99%

Lactobacillus reuteri, Infant Allergy Prevention and Childhood Immune Maturation

Forsberg¹

2016

Probiotics and Prebiotics in Human Nutrition and Health

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The increasing allergy prevalence in affluent countries may be caused by reduced microbial stimulation, resulting in an abnormal postnatal immune maturation. This chapter concerns the theories behind the use of probiotics in randomized prevention trials, and how this supplementation affects the immunity of pregnant women, the immune development in their children, and possibly preventing allergic diseases. Most studies investigating the underlying mechanisms have focused on postnatal microbial exposure. An increasing body of evidence from studies suggests that the maternal microbial environment during pregnancy can program the immune development of the child. In human allergy intervention studies, probiotic supplementation to the mother during pregnancy, as well as to her baby postnatally, may be important for preventive effects. Also, prenatal environmental exposures may alter gene expression via epigenetic mechanisms, aiming to induce physiological adaptations to the anticipated postnatal environment. The maternal microbial environment during pregnancy may program the immune development of the child.

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Prenatal initiation of endotoxin airway exposure prevents subsequent allergen-induced sensitization and airway inflammation in mice

Cited by 100 publications

References 40 publications

Dog ownership and contact during childhood and later allergy development

Dog ownership and contact during childhood and later allergy development

A Helminth Immunomodulator Reduces Allergic and Inflammatory Responses by Induction of IL-10-Producing Macrophages

Lactobacillus reuteri, Infant Allergy Prevention and Childhood Immune Maturation

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