β-Glucosylceramides and Tocopherols Regulate Development and Function of Dendritic Cells

Lajiness, Jacquelyn D.; Amarsaikhan, Nansalmaa; Tat, Kiet; Tsoggerel, Angar; Cook‐Mills, Joan M.

doi:10.4049/jimmunol.2101188

Cited by 4 publications

(6 citation statements)

References 64 publications

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Section: Mouse Modelsmentioning

confidence: 99%

“…Animal models have also revealed a reproducible phenotype of allergen hyperresponsiveness in the offspring of allergic mothers which has led to important investigations of the contributions of the in utero environment to the development of the fetal/neonatal immune system. [21,22,[27][28][29][30] There are several allergens used in mouse models of allergic asthma, including house dust mite extract (HDM) and purified chicken egg ovalbumin (OVA). It is important to examine mechanisms of allergy with more than one type of allergen, Figure 1.…”

Section: Mouse Modelsmentioning

confidence: 99%

“…This altered in utero environment leads to changes in fetal DCs which predispose offspring to allergen hyperresponsiveness postnatally. [21,22,[27][28][29]51,58] In particular, the immune-modulatory lipid beta glucosylceramide (βGlcCer) is elevated in allergic moms and crosses the placenta to alter fetal dendritic cell differentiation [29,30] and has recently been shown to be both necessary and sufficient to establish allergic predisposition in offspring. [29] In humans, levels of βGlcCer, in conjunction with other immune modulatory lipids present in cord blood, have been shown to correlate with incidence of childhood wheeze.…”

Section: Pathophysiology Of Dendritic Cells In Asthmamentioning

confidence: 99%

“…[77] Furthermore, they do not increase in number in allergic mouse models [21,22,78] and have diminished capacity compared to other DC subsets to take up antigen. [30,79] The bulk of the literature indicates that cDC1s play a role in pulmonary tolerance. Also, animal models demonstrate worse allergic airway inflammation in response to HDM or OVA in the absence of CD103 + DCs.…”

Section: Mouse Cdc1smentioning

confidence: 99%

“…[123] pDCs are functionally distinct from cDCs in that they have a decreased capacity to uptake, process, and present antigens. [30,124,125] The primary cytokine pDCs produce is interferon-alpha (IFN-α) and they play a role in antiviral immunity (reviewed [126][127][128][129] ) and allergen tolerance through the induction of regulatory T cells. [123,[129][130][131][132] In the context of allergy and asthma, pDCs serve to inhibit airway hyperreactivity and allergic lung inflammation through IFN-α-mediated suppression of group 2 innate lymphoid cell (ILC2) survival and function [133] and to restrain sensitization to otherwise harmless antigens.…”

Section: Mouse Pdcsmentioning

confidence: 99%

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Catching Our Breath: Updates on the Role of Dendritic Cell Subsets in Asthma

Lajiness

Cook‐Mills

2023

Advanced Biology

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Dendritic cells (DCs), as potent antigen presenting cells, are known to play a central role in the pathophysiology of asthma. The understanding of DC biology has evolved over the years to include multiple subsets of DCs with distinct functions in the initiation and maintenance of asthma. Furthermore, asthma is increasingly recognized as a heterogeneous disease with potentially diverse underlying mechanisms. The goal of this review is to summarize the role of DCs and the various subsets therein in the pathophysiology of asthma and highlight some of the crucial animal models shaping the field today. Potential future avenues of investigation to address existing gaps in knowledge are discussed.

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Section: Mouse Modelsmentioning

confidence: 99%

Section: Mouse Modelsmentioning

confidence: 99%

Section: Pathophysiology Of Dendritic Cells In Asthmamentioning

confidence: 99%

Section: Mouse Cdc1smentioning

confidence: 99%

Section: Mouse Pdcsmentioning

confidence: 99%

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Catching Our Breath: Updates on the Role of Dendritic Cell Subsets in Asthma

Lajiness

Cook‐Mills

2023

Advanced Biology

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Increased allergic inflammation and decreased lung insulin sensitivity in offspring of obese allergic mothers

Damron,

Bloodworth,

Hoji

et al. 2024

Journal of Leukocyte Biology

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Epidemiological studies demonstrate that maternal obesity and maternal allergy are major risk factors for asthma in offspring. However, the impact of maternal allergy and obesity on offspring lung insulin signaling and allergen responsiveness is not known. To evaluate this, allergic and non-allergic female mice were fed a high fat diet or low-fat diet from 7 weeks before pregnancy until weaning. Neonatal pups were allergen-sensitized and allergen-challenged and then were assessed for obesity, insulin signaling, and allergic inflammation. Compared to pups of non-obese non-allergic mothers, allergen-challenged pups of obese non-allergic mothers, non-obese allergic mothers and obese allergic mothers had bronchoalveolar lavage eosinophilia, with the pups of obese allergic mothers having the highest bronchoalveolar lavage eosinophilia. These pups also had lower insulin-induced lung AKT-phosphorylation, indicating a decrease in lung parenchymal insulin sensitivity. In cross-fostering experiments, allergen-challenged pups exposed to both pre- and post-natal obese allergic mothers had the highest level of BAL eosinophilia. Maternal obesity or allergy increased offspring serum allergen-specific IgE and IL-5 that was highest when the mother was both obese and allergic. Also, allergen-challenged pups exposed to both pre- and post-natal obese allergic mothers had the highest level of IL5. In summary, offspring born to obese allergic mothers have decreased lung insulin sensitivity and have increased lung allergic inflammation. Interestingly, our data also demonstrates that there is both a pregnancy and post-pregnancy aspect of maternal allergy and obesity that enhance allergen responsiveness in offspring.

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Mechanisms for initiation of food allergy by skin pre‐disposed to atopic dermatitis

Gao,

Kosins,

Cook‐Mills

2024

Immunological Reviews

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SummaryFood allergy can be life‐threatening and often develops early in life. In infants and children, loss‐of‐function mutations in skin barrier genes associate with food allergy. In a mouse model with skin barrier mutations (Flakey Tail, FT+/− mice), topical epicutaneous sensitization to a food allergen peanut extract (PNE), an environmental allergen Alternaria alternata (Alt) and a detergent induce food allergy and then an oral PNE‐challenge induces anaphylaxis. Exposures to these allergens and detergents can occur for infants and children in a household setting. From the clinical and preclinical studies of neonates and children with skin barrier mutations, early oral exposure to allergenic foods before skin sensitization may induce tolerance to food allergens and thus protect against development of food allergy. In the FT+/− mice, oral food allergen prior to skin sensitization induce tolerance to food allergens. However, when the skin of FT+/− pups are exposed to a ubiquitous environmental allergen at the time of oral consumption of food allergens, this blocks the induction of tolerance to the food allergen and the mice can then be skin sensitized with the food allergen. The development of food allergy in neonatal FT+/− mice is mediated by altered skin responses to allergens with increases in skin expression of interleukin 33, oncostatin M and amphiregulin. The development of neonate food allergy is enhanced when born to an allergic mother, but it is inhibited by maternal supplementation with α‐tocopherol. Moreover, preclinical studies suggest that food allergen skin sensitization can occur before manifestation of clinical features of atopic dermatitis. Thus, these parameters may impact design of clinical studies for food allergy, when stratifying individuals by loss of skin barrier function or maternal atopy before offspring development of atopic dermatitis.

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β-Glucosylceramides and Tocopherols Regulate Development and Function of Dendritic Cells

Cited by 4 publications

References 64 publications

Catching Our Breath: Updates on the Role of Dendritic Cell Subsets in Asthma

Catching Our Breath: Updates on the Role of Dendritic Cell Subsets in Asthma

Increased allergic inflammation and decreased lung insulin sensitivity in offspring of obese allergic mothers

Mechanisms for initiation of food allergy by skin pre‐disposed to atopic dermatitis

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