Publications by authors named "Jennifer L Wayland"

Obesity is a risk factor for increased lung damage and disease severity during influenza virus infection. White adipose tissue (WAT) inflammation is a key driver of disease pathogenesis in obesity. Whether and how obesity modifies lung and WAT immune cell character and function in obesity to amplify influenza disease severity remains unknown.

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Article Synopsis
  • Vertical transmission of obesity plays a significant role in the ongoing obesity epidemic and related metabolic diseases, yet current models fail to accurately reflect human obesity.
  • This study introduces a new mouse model that simulates "human-like" obesity by using a specific diet and housing conditions, revealing that maternal obesity negatively impacts neonatal survival, increases offspring fat accumulation, and heightens their risk for obesity-related diseases.
  • The findings suggest that severe maternal obesity alters the offspring's microbiome and creates a harmful inflammatory environment during pregnancy, which is supported by similar patterns observed in a human birth cohort study.
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Inflammation-driven preterm birth (PTB) is modeled in mice using lipopolysaccharide (LPS) challenge. Here, we present a protocol for cytokine and uterine immune cell characterization in a mouse model of LPS-induced PTB. We describe steps for LPS challenge, in vivo cytokine capture assay, and isolation of uterine immune cells for flow cytometry.

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Article Synopsis
  • Influenza virus-induced pneumonia poses significant public health risks, with obesity, metabolic diseases, and female sex identified as independent factors worsening the disease.
  • The lack of experimental models for studying severe obesity in female mice has limited research, but this study successfully induced severe obesity in female mice using a high-fat diet and thermoneutral housing.
  • The findings reveal that while traditionally lean mice show similar responses to influenza, introducing severe obesity and metabolic disease in female mice results in disease severity comparable to that of obese males, highlighting the critical role of these factors in influenza severity.
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Clinical evidence points to a function for B cell-activating factor (BAFF) in pregnancy. However, direct roles for BAFF-axis members in pregnancy have not been examined. Here, via utility of genetically modified mice, we report that BAFF promotes inflammatory responsiveness and increases susceptibility to inflammation-induced preterm birth (PTB).

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Circadian rhythms are generated by cell autonomous circadian clocks that perform a ubiquitous cellular time-keeping function and cell type-specific functions important for normal physiology. Studies show inducing the deletion of the core circadian clock transcription factor in adult mouse cardiomyocytes disrupts cardiac circadian clock function, cardiac ion channel expression, slows heart rate, and prolongs the QT-interval at slow heart rates. This study determined how inducing the deletion of in adult cardiomyocytes impacted the electrophysiological phenotype of a knock-in mouse model for the arrhythmogenic long QT syndrome ( ).

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Daily changes in the incidence of sudden cardiac death (SCD) reveal an interaction between environmental rhythms and internal circadian rhythms. Circadian rhythms are physiological rhythms that alter physiology to anticipate daily changes in the environment. They reflect coordinated activity of cellular circadian clocks that exist throughout the body.

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