Gestation and breastfeeding in schistosomotic mice differentially alters the expression of histone deacetylases (HDACs) in adult offspring

Holanda, Gabriela Calixto Ribeiro de; Souto, Fabrício Oliveira; Silva, Maria da Conceição; Lorena, Virgínia Maria Barros de; Costa, Vlaudia Maria Assis; Albuquerque, Mônica Camelo Pessôa de Azevedo; Souza, Valdênia Maria Oliveira de; Filho, José Luiz de Lima

doi:10.1590/0074-02760190366

Cited by 4 publications

(2 citation statements)

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“…Consistently, in mice being born or breastfed by a mother infected with Schistosoma mansoni, the expression of HDACs was induced. In addition, gestation or breastfeeding seem to favor various IL-10dependent pathways, but not cells with a Treg phenotype [296]. Furthermore, in another mouse study, chronic schistosomiasis during the pregnancy led to the Th2 differentiation impairment in the offspring through reduced levels of histone acetylation at the promoter of the gene encoding IL-4, as observed in naïve T cells [249].…”

Section: Parasitesmentioning

confidence: 99%

Perinatal and Early-Life Nutrition, Epigenetics, and Allergy

et al. 2021

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Epidemiological studies have shown a dramatic increase in the incidence and the prevalence of allergic diseases over the last several decades. Environmental triggers including risk factors (e.g., pollution), the loss of rural living conditions (e.g., farming conditions), and nutritional status (e.g., maternal, breastfeeding) are considered major contributors to this increase. The influences of these environmental factors are thought to be mediated by epigenetic mechanisms which are heritable, reversible, and biologically relevant biochemical modifications of the chromatin carrying the genetic information without changing the nucleotide sequence of the genome. An important feature characterizing epigenetically-mediated processes is the existence of a time frame where the induced effects are the strongest and therefore most crucial. This period between conception, pregnancy, and the first years of life (e.g., first 1000 days) is considered the optimal time for environmental factors, such as nutrition, to exert their beneficial epigenetic effects. In the current review, we discussed the impact of the exposure to bacteria, viruses, parasites, fungal components, microbiome metabolites, and specific nutritional components (e.g., polyunsaturated fatty acids (PUFA), vitamins, plant- and animal-derived microRNAs, breast milk) on the epigenetic patterns related to allergic manifestations. We gave insight into the epigenetic signature of bioactive milk components and the effects of specific nutrition on neonatal T cell development. Several lines of evidence suggest that atypical metabolic reprogramming induced by extrinsic factors such as allergens, viruses, pollutants, diet, or microbiome might drive cellular metabolic dysfunctions and defective immune responses in allergic disease. Therefore, we described the current knowledge on the relationship between immunometabolism and allergy mediated by epigenetic mechanisms. The knowledge as presented will give insight into epigenetic changes and the potential of maternal and post-natal nutrition on the development of allergic disease.

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Section: Parasitesmentioning

confidence: 99%

Perinatal and Early-Life Nutrition, Epigenetics, and Allergy

et al. 2021

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“…Taken together, these findings suggest that the dichotomous features (stimulatory and tolerogenic) of maternal milk 13 were highlighted by S. mansoni infection in the absence of the IL-12 cytokine family. Breast milk from infected mothers has been previously shown to increase the expression of histone deacetylases (HDACs) involved in anti-inflammatory protein gene transcriptions 14 , while it contains proteins linked to the upgrading of glucose metabolism and the half-life of antigen-presenting cells, suggesting it promotes adaptive immunity as well as antibody production 15 . These results suggest that previous contact with breast milk may help in development of neutralizing antibody-dependent immunity in the immunodeficiency state linked to the Th1/Th17 profile (IL-12 family) response, as well as increase the suppressive environment by impairing IL-6 synthesis.…”

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confidence: 99%

Suckling by Schistosoma mansoni-infected mothers restored IgG2a and TGF-β production, but not IL-6 and delayed-type hypersensitivity in IL-12/IL-23-deficient mice

Silva

Holanda

et al. 2021

Rev. Soc. Bras. Med. Trop.

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INTRODUCTION Suckling by schistosomotic mice improves anti-ovalbumin (OA) antibody production, while delayed-type hypersensitivity (DTH) remains unaffected. This property of milk from schistosomotic mice was investigated in IL-12/IL-23-deficient mice (IL-12p40KO). METHODS We compared anti-OA DTH, IgG2a and cytokines in wild-type and IL-12p40KO mice suckled by infected (SIM) or non-infected (CONTROL) mothers. RESULTS SIM mice showed similar intensity and eosinophils in the DTH, which was abolished in IL-12p40KO and IL-12p40KO-SIM mice. In IL-12p40KO-SIM, IgG2a and TGF-β levels were higher, but IL-6 levels were lower. CONCLUSIONS Milk from schistosomotic mothers may evoke IgG2a without eliciting DTH in IL-12/IL-23 deficiencies, by changing TGF-β/IL-6 levels.

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