Drawing Parallels Among Past Public Health Crises and COVID-19.

In the early stages of the coronavirus disease 2019 (COVID-19) pandemic, there were shortages of personal protective equipment (PPE) and health-care personnel across severely affected regions. Along with a lack of testing, these shortages delayed surveillance, and possible containment of the virus. The pandemic also took unprecedented tolls on the mental health of many health-care workers who treated and witnessed the deaths of critically ill patients. To address these effects and prepare for a potential second wave, a literature review was performed on the response of health-care systems during the influenza pandemics of 1918, 1957, 2009, and the epidemics of Ebola, severe acute respiratory syndrome (SARS), and Middle East respiratory syndrome (MERS). We can use lessons identified to develop a competent and effective response to the current and future pandemics. The public must continue to engage in proper health mitigation strategies, including use of face coverings, physical distancing, and hand washing. The impact the pandemic has had on the mental health of frontline health-care workers cannot be disregarded as it is essential in ensuring effective patient care and mitigating psychological comorbidities. The lessons identified from past public health crises can help contain and limit morbidity and mortality with the ongoing COVID-19 pandemic.

The microbiome affects liver sphingolipids and plasma fatty acids in a murine model of the Western diet based on soybean oil.

Studies in mice using germfree animals as controls for microbial colonization have shown that the gut microbiome mediates diet-induced obesity. Such studies use diets rich in saturated fat, however, Western diets in the United States America are enriched in soybean oil, composed of unsaturated fatty acids, either linoleic or oleic acid. Here, we addressed whether the microbiome is a variable in fat metabolism in mice on a soybean oil diet. We used conventionally-raised, low-germ, and germfree mice fed for 10 weeks diets either high or low in high-linoleic-acid soybean oil as the sole source of fat. Conventional and germfree mice gained relative fat weight and all mice consumed more calories on the high fat vs. low fat soybean oil diet. Plasma fatty acid levels were generally dependent on diet, with microbial colonization status affecting iso-C18:0, C20:3n-6, C14:0, and C15:0 levels. Colonization status, but not diet, impacted levels of liver sphingolipids including ceramides, sphingomyelins, and sphinganine. Our results confirm that absorbed fatty acids are mainly a reflection of the diet and that microbial colonization influences liver sphingolipid pools regardless of diet.

Resilience of small intestinal beneficial bacteria to the toxicity of soybean oil fatty acids.

Over the past century, soybean oil (SBO) consumption in the United States increased dramatically. The main SBO fatty acid, linoleic acid (18:2), inhibits in vitro the growth of lactobacilli, beneficial members of the small intestinal microbiota. Human-associated lactobacilli have declined in prevalence in Western microbiomes, but how dietary changes may have impacted their ecology is unclear. Here, we compared the in vitro and in vivo effects of 18:2 on Lactobacillus reuteri and L. johnsonii. Directed evolution in vitro in both species led to strong 18:2 resistance with mutations in genes for lipid biosynthesis, acid stress, and the cell membrane or wall. Small-intestinal Lactobacillus populations in mice were unaffected by chronic and acute 18:2 exposure, yet harbored both 18:2- sensitive and resistant strains. This work shows that extant small intestinal lactobacilli are protected from toxic dietary components via the gut environment as well as their own capacity to evolve resistance.