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Immunology Update - November 2019

Welcome to the next instalment of our regular update where we report on research from the world of immunology, highlighting work from BSI members that has hit the headlines over the past month.

Measles infection compromises immune memory

New research published in Science Immunology shows that infection with the measles virus deletes the immune system’s memory, resulting in vulnerability to other infections.

Scientists at the Wellcome Sanger Institute and their collaborators used blood samples of unvaccinated children before and after a measles infection. They discovered that after measles infection, the naïve B cell pool changed and became immunologically immature, making it more difficult for the immune system to respond to a new infection. They also found that memory B cell clones present before infection were depleted after infection, meaning the immune system failed to remember pathogens previously confronted.

Dr Velislava Petrova, lead author of the study and BSI member, said, “This study is a direct demonstration in humans of ‘immunological amnesia’, where the immune system forgets how to respond to infections encountered before. We show that measles directly causes the loss of protection to other infectious diseases.”

To test this directly, researchers used ferrets that were vaccinated against flu and then infected with a measles-like virus. After infection, the ferrets had diminished flu antibodies, resulting in increased susceptibility to a new flu infection with more severe symptoms. This suggests measles infection leads to the loss of vaccine-acquired immunity.

These crucial findings highlight the importance of the MMR vaccine to eliminate the risk of catching measles in the first place. This is highly relevant as the UK lost its World Health Organization (WHO) ‘measles-free’ status recently.  

Read the press release here.

Read the full article here: Petrova et al. 2019 Science Immunology DOI: 10.1126/sciimmunol.aay6125   

Adding probiotics to milk improves premature babies’ gut health

Research led by the Norfolk and Norwich University Hospital shows that since their Neonatal Intensive Care Unit (NICU) introduced live probiotic bacteria to babies’ milk, cases of necrotising enterocolitis (NEC) and late-onset sepsis declined.

The study, published in Archives of Diseases in Childhood, found that adding live Lactobacillus and Bifidobacterium probiotic bacteria to milk given daily to high-risk babies more than halved the rate of NEC. NEC is a leading cause of mortality in premature babies and abnormal gut microbiota is an important predisposing risk factor. Additionally, the cases of sepsis fell from 22.6% to 11.5%. This suggests a beneficial effect of this combination of probiotics in reducing the rate of gut disease and should encourage more NICUs in the UK to start giving probiotics to protect babies.

Dr Lindsay Hall, BSI member from the Quadram Institute and one of the co-authors of the research, said, “This work highlights how modulating the preterm gut microbiota with beneficial bacteria like Bifidobacterium can result in real improvements in health outcomes in these fragile and at-risk babies. The next stage is to understand how this type of supplementation modulates the wider microbial community and the mechanisms behind these beneficial effects.”

Read the press release here.

Read the full article here: Robertson et al. 2019 Archives of Disease in Childhood DOI: 10.1136/archdischild-2019-317346


The role of lactate in chronic inflammation

Research published in Cell Metabolism reports on a potential new therapeutic target in chronic inflammatory diseases, such as rheumatoid arthritis.

The study, led by researchers at the University of Birmingham, found that human immune cells altered their metabolism in response to accumulation of lactate in inflamed tissue. High levels of lactate, a molecule produced by most tissues in the body, indicates greater severity of a disease or condition. This research begins to understand lactate, not as a marker of health, but as an active driver of inflammation.

The increased lactate directly caused human CD4+ T cells to adopt a pro-inflammatory response through persisting in the inflamed tissue and enhancing their release of the IL17 cytokine. Additionally, in a mouse model of arthritis, blocking lactate transport into cells by a targeted antibody against the sodium-coupled lactate transporter SLC5A12, improved disease severity.

Author and BSI member, Dr Claudio Mauro of the University of Birmingham’s Institute of Inflammation and Ageing, said, “We identified the pathway initiated by lactate build-up in inflamed tissue that exacerbates the inflammatory response. We also now can provide evidence that molecules made by immune cells to transport sodium lactate – the sodium salt of lactic acid – could be a target for treatment to stop this lactate build-up in chronic inflammatory disorders.”

Further research is needed on other animal models of chronic inflammatory disease and additional testing of other antibodies to target SLC5A12.

Read the press release here.

Read the full article here: Pucino et al. 2019 Cell Metabolism DOI 10.1016/j.cmet.2019.10.004