Day: September 10, 2025

Categories : Ageing RheumatologyTags : Leave a comment

Immune Ageing Found to Drive – Not Be Driven by – Rheumatoid Arthritis

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Rheumatoid arthritis. Credit: Scientific Animations CC4.0

Features of immune system ageing can be detected in the earliest stages of rheumatoid arthritis (RA), even before clinical diagnosis, a new study has found which provides at-risk individuals with hope for early intervention.

The research led by academics at the University of Birmingham, delivered through the National Institute for Health and Care Research (NIHR) Birmingham Biomedical Research Centre, and published in the journal eBioMedicine shows that individuals with joint pain or undifferentiated arthritis already exhibit signs of a prematurely aged immune system, suggesting that immune ageing may play a direct role in the development of RA.

The study involved 224 participants across various stages of RA development and was funded by FOREUM and the European League Against Rheumatism (EULAR). It represents one of the most comprehensive analyses of immune ageing in RA to date.

Researchers found that patients with early immune ageing features were more likely to develop RA. These findings could lead to the development of predictive tools that identify at-risk individuals and enable timely treatment.

“We’ve discovered that immune ageing isn’t just a consequence of rheumatoid arthritis—it may be a driver of the disease itself,” said Dr Niharika Duggal, senior author of the study and Associate Professor in Immune Ageing at the University of Birmingham. “We found that people in the early stages of rheumatoid arthritis ie, before a clinical diagnosis show signs of faster immune system ageing.

“These findings suggest we might be able to intercept the disease development in at-risk individuals and prevent it from developing by using treatments that slow ageing, such as boosting the body’s natural process for clearing out damaged cells (autophagy).”

Key Findings

  • Hallmarks of immune ageing, including reduced naïve T cells and thymic output, were observed in patients with early joint symptoms.
  • An elevated IMM-AGE score revealed accelerated immune ageing in patients before RA diagnosis.
  • Elevated levels of inflammatory markers (such as IL-6, TNFα, and CRP) were found in preclinical stages.
  • Advanced ageing features, including senescent T cells and inflammatory Th17 cells, appeared only after RA was fully established.

The study suggests that targeting ageing pathways could offer new strategies to prevent RA. Future research should determine whether geroprotective drugs such as spermidine (autophagy booster), senolytics (clearance of senescent cells) and metformin (attenuates inflammation and boosts autophagy) may help slow or halt disease progression in high-risk individuals.

Source: University of Birmingham

Categories : Metabolic DisordersTags : Leave a comment

Considering Sex Hormones Led to Better Identification of Genes Linked to Type 2 Diabetes

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Genomic and hormone study of white Europeans finds 22 additional disease-related variants

Ball and stick 3D model of testosterone. Source: Wikimedia CC0

Researchers identified almost two dozen previously unknown genetic variants linked to type 2 diabetes by including participants’ hormone levels in their analysis. Yan V. Sun of Emory University, USA, and colleagues reports these findings in the open-access journal PLOS Genetics.

Type 2 diabetes affects an increasing number of people worldwide, and more often affects men than women. The disease is caused by a mix of genetic and lifestyle factors, but little is known about how someone’s environment – both inside and outside the body – interacts with their genes to impact a person’s risk of developing the disease.

In the new study, researchers performed genome-wide interaction studies to investigate whether a person’s hormone levels interact with their genetic variants to affect their risk of developing type 2 diabetes. They grouped males and females independently and considered measurements of three types of sex hormones – total testosterone, bioavailable testosterone and sex-hormone binding globulin. The information came from white European participants in the UK Biobank, which contains biological samples and health data from half a million people.

The researchers used statistical analyses to identify relevant variants in the genomes of individuals with and without type 2 diabetes. By taking into account hormone levels, the analysis was able to identify 22 spots on the genome that increased a person’s risk for type 2 diabetes. These variants had not been reported previously in the most recent genomic study for type 2 diabetes.

The new study suggests that a person’s hormone levels may be interacting with their genes to increase their odds of having type 2 diabetes. For future studies, the researchers recommended that additional hormone measurements for each participant and more diverse cohorts should be included. They conclude that this approach, which includes environmental factors in genomic studies, may help us to identify additional disease-related genes and gain a better understanding of the mechanisms behind complex diseases.

The authors add, “We found that sex hormone levels contribute to differences in genetic risk factors for type 2 diabetes in men and women. By analyzing data for men and women separately, we identified new genetic associations with type 2 diabetes.”

The lead analyst, Amonae Dabbs-Brown notes, “I actually used to work at the CDC developing methods to measure some of these sex hormones. It’s really exciting to see what happens downstream. Maybe one day I’ll even get to see how these analyses are used in the clinic!”

Provided by PLOS

In your coverage, please use this URL to provide access to the freely available paper in PLOS Genetics: https://plos.io/3ViXDKH

Contact: Rob Spahr [rob.spahr@emory.edu]

Citation: Dabbs-Brown A, Liu C, Hui Q, Wilson PW, Zhou JJ, Gwinn M, et al. (2025) Identification of gene-sex hormone interactions associated with type 2 diabetes among men and women. PLoS Genet 21(9): e1011470. https://doi.org/10.1371/journal.pgen.1011470

Author countries: United States

Funding: This work is supported in part by funding from the National Institutes of Health (HL154996 to YVS, DK139632 to YVS, and HL156991 to YVS). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. YVS received salary support from the National Institutes of Health.

Competing interests: The authors have declared that no competing interests exist.

Categories : Diet and Nutrition GastrointestinalTags : Leave a comment

Red Meat Aggravates IBD by Altering the Gut Microbiome

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Photo by Jose Ignacio Pompe on Unsplash

Epidemiological studies have revealed a strong correlation between red meat consumption and the development of inflammatory bowel disease. In a new study published in Molecular Nutrition and Food Research that was conducted in mice, red meat consumption caused an imbalance of bacteria in the intestinal microbiota. 

Investigators fed mice various kinds of red meat, including pork, beef, and mutton, for two weeks, and then they induced colitis with 2.5% dextran sulfate sodium. Intake of these three red meat diets exacerbated colonic inflammation. Analyses revealed an overproduction of pro-inflammatory cytokines and infiltration of immune cells in the colon of mice fed red meat diets. 

These diets led to a marked decrease in the relative abundance of Streptococcus, Akkermansia, Faecalibacterium, and Lactococcus bacterial strains, coupled with an increase in Clostridium and Mucispirillum.  

“This study contributes to improving food innervation approaches for inflammatory bowel disease treatment and indicates a close crosstalk among diet, gut microbiota, and intestinal immunity,” said co–corresponding author Dan Tian, MD, PhD, of Capital Medical University, in China. 

Source: Wiley

Categories : AgeingTags : Leave a comment

Study Explains Why Influenza is More Deadly for Older People

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Photo by JD Mason on Unsplash

Scientists have discovered why older people are more likely to suffer severely from the flu, and can now use their findings to address this risk. In a new study published in PNAS, experts discovered that older people produce a glycosylated protein called apoplipoprotein D (ApoD), which is involved in lipid metabolism and inflammation, at much higher levels than in younger people. This has the effect of reducing the patient’s ability to resist virus infection, resulting in a more serious disease outcome.

The team established that highly elevated ApoD production with age in the lung drives extensive tissue damage during infection to reduce the protective antiviral type I interferon response.

The research was an international collaboration led by scientists from the China Agricultural University, University of Nottingham, Institute of Microbiology (Chinese Academy of Sciences), National Institute for Viral Disease Control and Prevention (Chinese Centre for Disease Control and Prevention) and the University of Edinburgh.

Aging is a leading risk factor in influenza-related deaths. Furthermore, the global population is aging at an unprecedented rate in human history, posing major issues for healthcare and the economy. So we need to find out why older patients often suffer more severely from influenza virus infection.”

Professor Kin-Chow Chang from the School of Veterinary Medicine and Science at the University of Nottingham, and co-author on the paper

In this new study, the team investigated the mechanisms behind increased severity of influenza virus infection with age using an aging-mouse model and appropriate donor human tissue sections.

They identified ApoD as an age-related cell factor that impairs the activation of the immune system’s antiviral response to influenza virus infection by causing extensive breakdown of mitochondria (mitophagy) resulting in greater production of virus and lung damage during infection. Mitochondria are essential for cellular production of energy and for induction of protective interferons.

ApoD is therefore a target for therapeutic intervention to protect against severe influenza virus infection in the elderly which would have a major impact on reducing morbidity and mortality in the aging population.

Professor Chang, added: “There is now an exciting opportunity to therapeutically ameliorate disease severity of the elderly from influenza virus infection by the inhibitory targeting of ApoD.”

Source: University of Nottingham

Categories : Cardiovascular DiseaseTags : Leave a comment

Heparin-induced Thrombocytopenia is Caused by a Single Antibody

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Disposable syringe of Clexane (enoxaparin), a low molecular weight heparin (LMWH). CC0

Researchers at McMaster University have discovered that a rare but dangerous reaction to heparin is caused by a single antibody – overturning decades of medical misunderstanding and opening the door to more precise ways of diagnosing and treating this medical complication.  

The study, published in the New England Journal of Medicine, focused on heparin-induced thrombocytopenia (HIT), a serious immune complication that affects approximately one per cent of hospitalised patients treated with the blood thinner heparin. Nearly half of those who develop HIT experience life-threatening blood clots, which can lead to strokes, heart attacks, amputations, and even death, making early detection and treatment critically important. 

Until now, scientists believed that the immune response causing HIT involved many different types of antibodies working together. But this research has revealed something surprising: in every patient studied, only one antibody was causing the disease, while the rest created what the researchers describe as a kind of “smokescreen,” making it harder to identify the true culprit. This discovery helps pinpoint the exact source of the problem, opening the door to more accurate diagnosis and better-targeted treatments. 

“This study not only challenges our existing understanding of HIT but also revolutionises how we think about the immune response overall,” said Ishac Nazy, senior author of the study and scientific director of the McMaster Platelet Immunology Laboratory and co-director of the Michael G. DeGroote Center for Transfusion Research (MCTR).   

“This work corrects decades of misunderstanding in HIT. This status quo was a key reason behind the high rate of false-positive test results and frequent misdiagnoses in HIT, which can lead to severe consequences for patients, including unnecessary treatment or avoidable complications. Our findings lay the groundwork for more accurate diagnostics and targeted treatments,” said Nazy, a professor in the Department of Medicine and the Department of Biochemistry and Biomedical Sciences at McMaster. 

The research team was comprised of scientists from the McMaster Platelet Immunology Laboratory (MPIL) within MCTR as well as collaborators from the University of Massachusetts Amherst. 

They analysed blood samples from nine patients diagnosed with HIT. In each case, they found that the antibodies targeting platelet factor 4 (PF4) – a protein involved in blood clotting – were monoclonal. This suggests that HIT may be driven by a highly specific immune reaction, rather than a generalised one. 

“This discovery could reshape how we diagnose HIT and eventually how we treat it,” said Jared Treverton, first author of the study and a PhD candidate at McMaster. “Knowing that HIT is caused by a monoclonal antibody will allow us to develop improved tests specific to patients with this disorder and design better targeted therapies. This is a major step towards making diagnostics more accurate and treatments much safer.” 

The findings are expected to have immediate relevance for haematologists, laboratory specialists, and researchers in immunology, as well as for patients receiving heparin in hospitals across Canada and around the world. 

Source: McMaster University