Maternal high-fat hypercaloric diet during pregnancy results in persistent metabolic and respiratory abnormalities in offspring

Griffiths, Pamela; Walton, Cheryl; Samsell, Lennie; Perez, Miriam K.; Piedimonte, Giovanni

doi:10.1038/pr.2015.226

Cited by 40 publications

(49 citation statements)

References 32 publications

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“…We now show increased AHR in offspring of both early and combined in utero and later life HFD exposure. By varying diets at weaning, our results differ from a previously published rat model of HFD exposure at pregnancy onset showing increased airway reactivity in weanling offspring and adult rats that continued on HFD (Griffiths et al 2016). Those authors reported but did not show any differences between HFD cross at weaning in the offspring.…”

Section: Discussioncontrasting

confidence: 99%

Maternal high‐fat diet in mice leads to innate airway hyperresponsiveness in the adult offspring

MacDonald

Moran

Scherman

et al. 2017

Physiological Reports

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Maternal obesity prior to and during pregnancy has been associated with an increased incidence of childhood asthma. As diets rich in saturated fat are linked to obesity and inflammation, we created a murine model to investigate the effect of maternal high‐fat diet (HFD) on adult offspring airway hyperreactivity (AHR), a cardinal feature of asthma. Balb/cByJ dams were fed a HFD (60% fat Calories) or normal‐fat diet (NFD) (10% fat Calories) from 8 weeks prior to first breeding through their pregnancies. Pups were weaned to either a HFD or NFD (at 4 weeks of age). AHR was measured in the 10‐week‐old offspring following inhaled methacholine challenge by end‐inflation technique. Bronchial alveolar lavage fluid (BALF) was analyzed for cell count, total protein, and IL‐6. Offspring of HFD dams weaned to NFD had increased AHR compared to offspring of NFD dams weaned to NFD. Offspring of HFD dams that remained on HFDs had increased AHR compared to offspring of NFD dams weaned to HFDs. Offspring of HFD dams had higher BALF cell counts, higher neutrophil percentage, greater total protein, and IL‐6 in the BALF. These results demonstrate that a maternal diet high in saturated fat through pregnancy and lactation plays a key role in programming adult offspring AHR.

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Section: Discussioncontrasting

confidence: 99%

Maternal high‐fat diet in mice leads to innate airway hyperresponsiveness in the adult offspring

MacDonald

Moran

Scherman

et al. 2017

Physiological Reports

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show abstract

“…Among other mechanisms, consumption of a high‐fat diet during pregnancy may contribute to the development of asthma in offspring. Indeed, structural changes, higher level of cytokines and increased airway resistance have been observed in rats born from mothers fed a high‐fat diet during gestation . Similar structural changes have been observed in lung epithelial cells in adult mice fed with a high‐fat diet .…”

Section: Obesity and Asthmasupporting

confidence: 53%

Innate lymphoid cells at the interface between obesity and asthma

et al. 2017

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SummaryObesity and asthma prevalence has dramatically and concomitantly increased over the last 25 years, and many epidemiological studies have highlighted obesity as an important risk factor for asthma. Although many studies have been performed, the underlying mechanisms remain poorly understood. Innate mechanisms have been involved in both diseases, in particular through the recently described innate lymphoid cells (ILCs). ILCs are subdivided into three groups that are defined by their cytokine production and by their master transcription factor expression, in sharp correlation with their T helper counterparts. However, unlike T helper cells, ILCs do not express antigen-specific receptors, but respond to damage-induced signals. ILCs have been found in target tissues of both diseases, and data have implicated these cells in the pathogenesis of both diseases. In particular group 2 ILCs (ILC2) are activated in both the adipose and lung tissues under the effect of interleukin-33 and interleukin-25 expression. However, counter-intuitively to the well-known association between obesity and asthma, ILC2 are beneficial for obesity but deleterious for asthma. This review will examine the roles of ILCs in each disease and recent data highlighting ILCs as a putative link between obesity and asthma.

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“…87 More importantly, pups born to dams fed a HFD diet during gestation exhibit impaired antigen-specific immune responses as evidenced by: (a) higher mortality rates in an E. coli sepsis model; (b) increased bacterial burden; (c) larger abscesses following Methicillin-resistant Staphylococcus aureus infection 87 ; and exacerbated respiratory disease following infection with respiratory syncytial virus. 88,89 Furthermore, in utero HFD exposure resulted in reduced production of IL-6 and TNF by splenocytes following ex vivo LPS stimulation. In contrast, IL-17, IL-6, and TNF production by colonic lamina propria lymphocytes was significantly higher in pups born to HFD-fed dams following stimulation.…”

Section: Maternal Obesity and Alterations In Offspring Lymphoid Tissumentioning

confidence: 99%

“…One key study concluded that gestational HFD exposure results in fewer splenic lymphocytes and thinner thymic cortex . More importantly, pups born to dams fed a HFD diet during gestation exhibit impaired antigen‐specific immune responses as evidenced by: (a) higher mortality rates in an E. coli sepsis model; (b) increased bacterial burden; (c) larger abscesses following Methicillin‐resistant Staphylococcus aureus infection; and exacerbated respiratory disease following infection with respiratory syncytial virus . Furthermore, in utero HFD exposure resulted in reduced production of IL‐6 and TNFα by splenocytes following ex vivo LPS stimulation.…”

Section: Introductionmentioning

confidence: 99%

Impact of pregravid obesity on maternal and fetal immunity: Fertile grounds for reprogramming

Sureshchandra

Marshall

Messaoudi

2019

Journal of Leukocyte Biology

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Maternal pregravid obesity results in several adverse health outcomes during pregnancy, including increased risk of gestational diabetes, preeclampsia, placental abruption, and complications at delivery. Additionally, pregravid obesity and in utero exposure to high fat diet have been shown to have detrimental effects on fetal programming, predisposing the offspring to adverse cardiometabolic, endocrine, and neurodevelopmental outcomes. More recently, a deeper appreciation for the modulation of offspring immunity and infectious disease‐related outcomes by maternal pregravid obesity has emerged. This review will describe currently available animal models for studying the impact of maternal pregravid obesity on fetal immunity and review the data from clinical and animal model studies. We also examine the burden of pregravid obesity on the maternal–fetal interface and the link between placental and systemic inflammation. Finally, we discuss future studies needed to identify key mechanistic underpinnings that link maternal inflammatory changes and fetal cellular reprogramming events.

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Maternal high-fat hypercaloric diet during pregnancy results in persistent metabolic and respiratory abnormalities in offspring

Cited by 40 publications

References 32 publications

Maternal high‐fat diet in mice leads to innate airway hyperresponsiveness in the adult offspring

Maternal high‐fat diet in mice leads to innate airway hyperresponsiveness in the adult offspring

Innate lymphoid cells at the interface between obesity and asthma

Impact of pregravid obesity on maternal and fetal immunity: Fertile grounds for reprogramming

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