Health is wealth as the saying goes and new research now shows that it is possible to have a healthy, less stressed society through familiar and inexpensive foods. One such food might be the Japanese natto which is made from softened soybeans that have been boiled or steamed and fermented with a bacteria called Bacillus subtilis var. natto. Bacillus subtilis var. natto is found in soil, plants, animals, and the human stomach and intestines. Most of the natto consumed in Japan is made from the Miyagino strain.
A research group led by Professor Eriko Kage-Nakadai at the Graduate School of Human Life and Ecology, Osaka Metropolitan University, examined the effects of Bacillus subtilis var. natto consumption on the lifespan of the host using Caenorhabditis elegans worms. The researchers found that Caenorhabditis elegans fed Bacillus subtilis var. natto had a significantly longer lifespan than those fed the standard diet, and further elucidated that the p38 MAPK pathway and insulin/IGF-1-like signaling pathway, which are known to be involved in innate immunity and lifespan, were involved in the lifespan-enhancing effects of Bacillus subtilis var. natto. They also examined stress tolerance, which has been shown to have a correlation with longevity, and found that resistance to UV light and oxidative stress is enhanced.
For the first time, we were able to demonstrate the possibility of lifespan-extending effects of Caenorhabditis elegans through the ingestion of Bacillus subtilis var. natto. We hope that future experiments on mammals and epidemiological studies will help to realize a healthy and longer-living society if we can apply this research to humans.”
Professor Eriko Kage-Nakadai, Graduate School of Human Life and Ecology, Osaka Metropolitan University
The research results were published online in the Journal of Applied Microbiology on April 20, 2023.
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Teramoto, N., et al. (2023) Impacts of Bacillus subtilis var. natto on the lifespan and stress resistance of Caenorhabditis elegans.Journal of Applied Microbiology. doi.org/10.1093/jambio/lxad082.
In a recent review published in Nature Reviews Microbiology, researchers explored existing literature on long coronavirus disease (COVID). They highlighted key immunological findings, similarities with other diseases, symptoms, associated pathophysiological mechanisms, and diagnostic and therapeutic options, including coronavirus disease 2019 (COVID-19) vaccinations.
Long COVID refers to a multisystemic disease among SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2)-positive individuals, with increasing prevalence rates by the day. Studies have reported on long COVID risk factors, symptoms, pathophysiology, diagnosis, and treatment options, with increasing similarities between long COVID and other diseases such as POTS (postural orthostatic tachycardia syndrome) and ME/CFS (myalgic encephalomyelitis/ chronic fatigue syndrome).
About the review
In the present review, researchers explored the existing data on long COVID immunology, symptoms, pathophysiology, diagnosis, and therapeutic options.
Key long COVID findings and similarities with other diseases
Studies have reported persistently reduced exhausted T lymphocytes, dendritic cells, cluster of differentiation 4+ (CD4+) lymphocyte and CD8+ lymphocyte counts, and greater PD1 (programmed cell death protein-1) expression. In addition, increase in innate cell immunological activities, non-classical monocytes, expression of interferons (IFNs)-β, λ1, and interleukins (IL)-1β, 4,6, tumor necrosis factor (TNF). Cytotoxic T lymphocyte expansion has been linked to gastrointestinal long COVID symptoms, and persistent increase in CCL11 (C-X-C motif chemokine 11) expression has been linked to cognitive dysfunction among long COVID patients.
Elevated autoantibody titers have been reported among long COVID patients, such as autoantibodies against ACE2 (angiotensin-converting enzyme 2), angiotensin II receptor type I (AT1) receptors, β2-adrenoceptors, angiotensin 1–7 Mas receptors, and muscarinic M2 receptors. Reactivation of Epstein-Barr virus (EBV) and human herpes virus-6 (HHV-6) has been reported in long COVID patients and ME/CFS. EBV reactivation has been linked to neurocognitive impairments and fatigue in long COVID.
SARS-CoV-2 persistence reportedly drives long COVID symptoms. SARS-CoV-2 proteins and/or ribonucleic acid (RNA) have been detected in cardiovascular, reproductive, cranial, ophthalmic, muscular, lymphoid, hepatic, and pulmonary tissues, and serum, breast, urine, and stool obtained from long COVID patients. Similar immunological patterns are noted between long COVID and ME/CFS, with elevated cytokine levels in the initial two to three years of disease, followed by reduction with time, without symptomatic improvements in ME/CFS. Lower cortisol levels, mitochondrial dysfunction, post-exertional malaise, dysautonomia, mast cell activation, platelet hyperactivation, hypermobility, endometriosis, menstrual alterations, and intestinal dysbiosis occur in both conditions.
Long COVID symptoms and underlying pathophysiological mechanisms
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Long COVID-associated organ damage reportedly results from COVID-19-induced inflammation and associated immune responses. Cardiovascular long COVID symptoms such as chest pain and palpitations have been associated with endothelial dysfunction, micro-clotting, and lowered vascular density. Long COVID has been associated with an increased risk of renal damage and type 2 diabetes. Ophthalmic symptoms of long COVID, including altered pupillary responses to light, result from the loss of small nerve fibers in the cornea, increased dendritic cell density, and impaired retinal microvasculature. Respiratory symptoms such as persistent cough and breathlessness result from altered pulmonary perfusion, epithelial injury, and air entrapment in the airways.
Cognitive and neurological long COVID symptoms include loss of memory, cognitive decline, sleep difficulties, paresthesia, balancing difficulties, noise and light sensitivity, tinnitus, and taste and/or smell loss. Underlying pathophysiological mechanisms include kynurenine pathway activation, endothelial injury, coagulopathy, lower cortisol levels, loss of myelin, microglial reactivation, oxidative stress, hypoxia, and tetrahydrobiopterin deficiency. Gastrointestinal symptoms such as pain in the abdomen, nausea, appetite loss, constipation, and heartburn have been associated with elevated Bacteroides vulgatus and Ruminococcus gnavus counts and lower Faecalibacterium prausnitzii counts. Neurological symptoms often have a delayed onset, worsen with time and persist longer than respiratory and gastrointestinal symptoms, and long COVID presents similarly in children and adults.
Diagnostic and therapeutic options for long COVID, including COVID-19 vaccines
The diagnosis and treatment of long COVID are largely symptom-based, including tilt tests for POTS, magnetic resonance imaging (MRI) to detect cardiovascular and pulmonary impairments, and electrocardiograms to detect QRS complex fragmentation. Salivary tests and serological tests, including red blood cell deformation, lipid profile, complete blood count, D-dimer, and C-reactive protein (CRP) evaluations, can be performed to assess immunological biomarker levels. PCR (polymerase chain reaction) analysis is used for SARS-CoV-2 RNA detection and quantification, and antibody testing is performed to assess humoral immune responses against SARS-CoV-2.
Pharmacological treatments include intravenous Ig for immune dysfunction, low-dosage naltrexone for neuronal inflammation, beta-blockers for POTS, anticoagulants for microclot formation, and stellate ganglion blockade for dysautonomia. Other options include antihistamines, paxlovid, sulodexide, and pycnogenol. Non-pharmacological options include cognitive pacing for cognitive impairments, diet limitations for gastrointestinal symptoms, and increasing salt consumption for POTS. COVID-19 vaccines have conferred minimal protection against long COVID, the development of which depends on the causative SARS-CoV-2 variant, and the number of vaccination doses received. Long COVID has been reported more commonly post-SARS-CoV-2 Omicron BA.2 subvariant infections.
Based on the review findings, long COVID is a multiorgan disease that has debilitated several lives worldwide, for which diagnostic and therapeutic options are inadequate. The findings underscored the need for future studies, clinical trials, improved education, mass communication campaigns, policies, and funding to reduce the future burden of long COVID.
The microbes in the human gastrointestinal tract, known as the gut microbiome, have a significant impact on out health and well-being. Scientists have begun to learn more about the complex relationships between diet, gut microbes, and disease. New research has now revealed that an nutrient and additive commonly found in the diet, called ergothioneine (EGT), can promote the survival of a microbe that can promote cancer development. EGT appears to shield the microbes from a natural phenomenon called oxidative stress, which is caused by an excess of free radicals, or reactive oxygen species (ROS).
Antioxidants like EGT can protect cells from oxidative stress, and excessive oxidative stress is a common feature of disease. Immune cells can release ROS on purpose to kill bacteria, and bacteria have ways to prevent damage caused by ROS – they can use antioxidants too. In this case, the microbes are using EGT from the diet. The findings have been reported in Cell.
The study authors determined that bacteria can take up EGT, which is naturally found in grains, beans, and mushrooms, to survive longer.
The pathogenic microbe Helicobacter pylori, which is associated with gastric cancer development, outcompeted other microbes for survival in a host, using EGT to do so. The researchers used mass spectrometry and a new tool they called “reactivity-guided metabolomics” to identify specific molecules in complex environments, to show the microbes had ingested the EGT from the diet.
“We were excited to discover an unconventional mechanism that enables bacteria to withstand oxidative stress during infection,” said senior study author Stavroula Hatzios, an assistant professor at Yale University.
Bacteria take up EGT in a different way than human cells, so it could be possible to develop a specific drug that can inhibit the uptake of this nutrient by microbes in the gut, she added.
Human cells can take up dietary EGT, which has been shown to be an anti-inflammatory molecule that can prevent disease. Reduced EGT levels have been associated with a wide variety of diseases, including autoimmune and cardiovascular disorders. Bacterial uptake of EGT could have a significant influence on human health.
