According to news reporting from Shijiazhuang, People’s Republic of China, research stated, “Aldosterone regulates the initiation and development of atherosclerosis which is identified as a chronic inflammatory disease by promoting the generation of C-reactive protein in vascular smooth muscle cells.”
Our news correspondents obtained a quote from the research from Hebei University of Chinese Medicine: “Curcumin is the most active ingredient of turmeric with anti-inflammation and antioxidation effects. Here, the effect of curcumin on aldosterone-induced C-reactive protein generation in vascular smooth muscle and the molecular mechanisms involved were explored. Primary rat vascular smooth muscle cells and hyperaldosteronism model rats were used in this study. The amount of C-reactive protein, reactive oxygen species, and the signaling pathway-related molecules generated were estimated. We found that curcumin inhibited aldosterone-induced C-reactive protein generation in vascular smooth muscle cells by interfering with the reactive oxygen species-ERK1/2 signal pathway.”
According to the news reporters, the research concluded: “The results provide new evidence for the potential anti-inflammatory and cardiovascular protective effects of curcumin.”
Laval University (Quebec), August 26, 2020
According to news originating from Quebec City, Canada, research stated, “Recent data from randomized clinical trials (RCTs) suggest that DHA may have stronger anti-inflammatory effects than EPA. This body of evidence has not yet been quantitatively reviewed.”
Our news journalists obtained a quote from the research from Laval University, “The aim of this study was to compare the effect of DHA and EPA on several markers of systemic inflammation by pairwise and network meta-analyses of RCTs. MEDLINE, EMBASE, and The Cochrane Library were searched through to September 2019. We included RCTs of 7 d on adults regardless of health status that directly compared the effects of DHA with EPA and RCTs of indirect comparisons, in which the effects of DHA or EPA were compared individually to a control fatty acid. Differences in circulating concentrations of C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-a) and adiponectin were the primary outcome measures. Data were pooled by pairwise and network meta-analysis and expressed as mean differences (MDs) with 95% CIs. Heterogeneity was assessed (Cochran Q statistic) and quantified (I2 statistic) in the pairwise meta-analysis. Inconsistency and transitivity were evaluated in the network meta-analysis. The certainty of evidence was assessed using the GRADE (Grading of Recommendations Assessment, Development, and Evaluation) approach. Eligibility criteria were met by 5 RCTs (N=411) for the pairwise meta-analysis and 20 RCTs (N=1231) for the network meta-analysis. In the pairwise meta-analysis, DHA and EPA had similar effects on plasma CRP [MDDHA versus EPA=0.14 mg/L (95% CI: -0.57, 0.85); I2=61%], IL-6 [MDDHA versus EPA=0.10 pg/mL (-0.15, 0.34); I2=40%], and TNF-a [MDDHA versus EPA=-0.10 pg/mL (-0.37, 0.18); I2=40%]. In the network meta-analysis, the effects of DHA and EPA on plasma CRP [MDDHA versus EPA=-0.33 mg/L (-0.75, 0.10)], IL-6 [MDDHA versus EPA=0.09 pg/mL (-0.12, 0.30)], and TNF-a [MDDHA versus EPA=-0.02 pg/mL (-0.25, 0.20)] were also similar. DHA and EPA had similar effects on plasma adiponectin in the network meta-analysis.”
According to the news editors, the research concluded: “Results from pairwise and network meta-analyses suggest that supplementation with either DHA or EPA does not differentially modify systemic markers of subclinical inflammation.”
Common cold combats influenza
Yale University, September 4, 2020
As the flu season approaches, a strained public health system may have a surprising ally—the common cold virus.
Rhinovirus, the most frequent cause of common colds, can prevent the flu virus from infecting airways by jumpstarting the body's antiviral defenses, Yale researchers report Sept. 4 in the journal The Lancet Microbe.
The findings help answer a mystery surrounding the 2009 H1N1 swine flu pandemic: An expected surge in swine flu cases never materialized in Europe during the fall, a period when the common cold becomes widespread.
A Yale team led by Dr. Ellen Foxman studied three years of clinical data from more than 13,000 patients seen at Yale New Haven Hospital with symptoms of respiratory infection. The researchers found that even during months when both viruses were active, if the common cold virus was present, the flu virus was not.
"When we looked at the data, it became clear that very few people had both viruses at the same time," said Foxman, assistant professor of laboratory medicine and immunobiology and senior author of the study.
Foxman stressed that scientists do not know whether the annual seasonal spread of the common cold virus will have a similar impact on infection rates of those exposed to the coronavirus that causes COVID-19.
"It is impossible to predict how two viruses will interact without doing the research," she said.
To test how the rhinovirus and the influenza virus interact, Foxman's lab created human airway tissue from stem cells that give rise to epithelial cells, which line the airways of the lung and are a chief target of respiratory viruses. They found that after the tissue had been exposed to rhinovirus, the influenza virus was unable to infect the tissue.
"The antiviral defenses were already turned on before the flu virus arrived," she said.
The presence of rhinovirus triggered production of the antiviral agent interferon, which is part of the early immune system response to invasion of pathogens, Foxman said.
"The effect lasted for at least five days," she said.
Foxman said her lab has begun to study whether introduction of the cold virus before infection by the COVID-19 virus offers a similar type of protection.
Highly fluorinated chemicals can increase risk for diabetes and coeliac disease in children
Orebro University (Sweden), September 4, 2020
Tuulia Hyötyläinen and Matej Orešič, both researchers in biomedicine, have published two studies on the connection between highly fluorinated chemicals—per- and polyfluoroalkyl substances (PFASs) – and two diseases in children: type 1 diabetes and coeliac disease (US spelling celiac, or gluten intolerance). Both are autoimmune diseases, which arise from an abnormal immune response to the body's healthy cells or tissues.
The studies are based on a combination of comprehensive metabolomics (analysis of small molecules, i.e. metabolites, in a body), analysis of PFAS, and the system's biology approach to integrate complex data acquired in the study. The data comes from a group of expectant mothers and children.
Type 1 diabetes is one of the most common chronic diseases among children and younger people in the Nordic countries. Over the past decades, the number of cases has markedly increased. However, the incidence curve has flattened in recent years.
Some children are genetically predisposed for type 1 diabetes, but only a fraction of them, around one-tenth, develop the disease. It is clear that some environmental trigger is needed to initiate the progression to this autoimmune disease. For example, viral infections and diet are suspected to have an influence.
Tuulia Hyötyläinen and Matej Orešič show in this study, published in Environment International, how PFAS impacts lipid metabolism and risk of type 1 diabetes in new-born children. The study includes expectant mothers exposed to these harmful substances at various levels, which are then transferred from the expectant mother to the fetus.
Within the same study, these findings were further confirmed in another prospective clinical study involving children at-risk for type1 diabetes, as well as in two studies in mice (experimental models of type 1 diabetes).
"We show that children exposed to the high levels of PFAS during the prenatal stage have a certain lipid profile. We have previously identified this profile to be associated with an increased risk for type 1 diabetes and the development of the disease in children," explains Matej Orešič.
In another study published in Environment Research, Tuulia Hyötyläinen and Matej Orešič show a connection between PFAS and coeliac disease.
"These results show that high exposure to PFAS in the womb and in first years of life can accelerate the development of coeliac disease in children," says Tuulia Hyötyläinen.
PFAS consists of some 5,000 man-made chemical substances in extensive use in society. They are used in a wide range of products, such as coatings in clothing, furniture, adhesives and food packaging as well as in fire-fighting foam.
"Exposure to harmful chemicals in early life, including prenatally, may offer an explanation for the changing incidence of these autoimmune diseases in developed countries and can be connected to other health risks," says Matej Orešič.
The increase of type 1 diabetes has flattened in many industrial countries, especially in the Nordic countries. A possible explanation is the stricter PFAS regulation.
T cells need methionine
University of Michigan School of Medicine, September 2 2020.
Research reported on September 2, 2020 in Nature revealed a mechanism used by cancer cells to evade the immune system.
“Abnormal epigenetic patterns correlate with effector T cell malfunction in tumors, but the cause of this link is unknown,” Yingjie Bian of the University of Michigan School of Medicine and colleagues wrote. “Here we show that tumor cells disrupt methionine metabolism in CD8+ T cells, thereby lowering intracellular levels of methionine and the methyl donor S-adenosylmethionine (SAM) and resulting in loss of dimethylation.”
Dr Bian and colleagues sought to determine why immune cells known as T cells stop combatting tumors and other related questions. They found that low methionine levels were associated with T cell impairment.
Other research has investigated the effects of starving tumor cells of methionine. However, this also starves T cells of the amino acid, thereby diminishing their function. "You have competition between tumor cells and T cells for methionine,” explained senior author Weiping Zou, MD, PhD, who is a Professor of Surgery, Pathology, Immunology and Biology at the University of Michigan in Ann Arbor. “The T cells also need it. If you starve the tumor cells of methionine, the T cells don't get it either. You want to selectively delete the methionine for the tumor cells and not for the T cells."
Supplementing with methionine restored T cell immunity in tumor-bearing mice and colon cancer patients. "There are still a lot of mechanistic details we have not worked out, particularly the detailed metabolic pathways of methionine metabolism,” Dr Zou remarked. “We also need to understand how metabolism pathways may be different from tumor cells and T cells. We hope to find a target that is relatively specific to tumor cells so that we do not harm the T cells but impact the tumor."
