According to the recently published research, an infection may trigger myocardial infarction. Using a range of advanced methodologies, the research found that, in coronary artery disease, atherosclerotic plaques containing cholesterol may harbor a gelatinous, asymptomatic biofilm formed by bacteria over years or even decades. Dormant bacteria within the biofilm remain shielded from both the patient's immune system and antibiotics because they cannot penetrate the biofilm matrix.

A viral infection or another external trigger may activate the biofilm, leading to the proliferation of bacteria and an inflammatory response. The inflammation can cause a rupture in the fibrous cap of the plaque, resulting in thrombus formation and ultimately myocardial infarction.

Professor Pekka Karhunen, who led the study, notes that until now, it was assumed that events leading to coronary artery disease were only initiated by oxidized low-density lipoprotein (LDL), which the body recognizes as a foreign structure.

"Bacterial involvement in coronary artery disease has long been suspected, but direct and convincing evidence has been lacking. Our study demonstrated the presence of genetic material -- DNA -- from several oral bacteria inside atherosclerotic plaques," Karhunen explains.

The findings were validated by developing an antibody targeted at the discovered bacteria, which unexpectedly revealed biofilm structures in arterial tissue. Bacteria released from the biofilm were observed in cases of myocardial infarction. The body's immune system had responded to these bacteria, triggering inflammation which ruptured the cholesterol-laden plaque.

The observations pave the way for the development of novel diagnostic and therapeutic strategies for myocardial infarction. Furthermore, they advance the possibility of preventing coronary artery disease and myocardial infarction by vaccination.

The study was conducted by Tampere and Oulu Universities, Finnish Institute for Health and Welfare and the University of Oxford. Tissue samples were obtained from individuals who had died from sudden cardiac death, as well as from patients with atherosclerosis who were undergoing surgery to cleanse carotid and peripheral arteries.

The research is part of an extensive EU-funded cardiovascular research project involving 11 countries. Significant funding was also provided by the Finnish Foundation for Cardiovascular Research and Jane and Aatos Erkko Foundation.

The research article "Viridans Streptococcal Biofilm Evades Immune Detection and Contributes to Inflammation and Rupture of Atherosclerotic Plaques" was published in the Journal of the American Heart Association.

The global prevalence of myopia is rising, especially in East Asia, and it's predicted that around half of the world's population will be affected by 2050, note the researchers.

Risk factors are thought to include excessive screen time and too little time spent outdoors, as well as inherited susceptibility, they explain.

Omega-3 polyunsaturated fatty acids (ω-3 PUFAs), which can only be obtained from the diet, are thought to improve/prevent several chronic eye conditions, including dry eye disease and age-related macular degeneration. But whether they can help ward off myopia isn't clear as studies to date have been experimental and haven't included people.

To explore this further, the researchers drew on 1005 Chinese 6-8 year olds, randomly recruited from the population based Hong Kong Children Eye Study, which is tracking the development of eye conditions and potential risk factors.

The children's eyesight was assessed and their regular diet measured by a food frequency questionnaire, completed with the help of their parents. This included 280 food items categorized into 10 groups: bread/cereals/pasta/rice/noodles; vegetables and legumes; fruit; meat; fish; eggs; milk and dairy products; drinks; dim sum/snacks/fats/oils; and soups.

Intakes of energy, carbohydrate, proteins, total fat, saturated fats, monounsaturated fats, PUFAs, cholesterol, iron, calcium, vitamins A and C, fiber, starch, sugar and nutrients were then calculated, based on the questionnaire responses.

The amount of time the children spent outdoors in leisure and during sports activities, reading and writing, and on screens during weekdays and at the weekend was calculated from validated questionnaire responses.

In all, around a quarter of the children (276; 27.5%) had myopia. Higher dietary intake of omega-3 fatty acids was associated with a lower risk of the condition.

Axial length -- measurement of the eye from the cornea at the front to the retina at the back, and an indicator of myopia progression -- was longest in the 25% of children with the lowest dietary intake of omega-3 fatty acids, after accounting for influential factors, including age, sex, weight (BMI), the amount of time spent in close work and outdoors, and parental myopia.

It was shortest in the 25% of children with the highest dietary intake of omega-3 fatty acids.

Similarly, cycloplegic spherical equivalent (SE), which measures refractive error, such as the degree of nearsightedness, was highest in those with the lowest omega-3 fatty acid intake and lowest in those with the highest intake.

But these findings were reversed for the 25% of children with the highest saturated fat intake, compared with the 25% of those with the lowest. None of the other nutrients was associated with either measure or myopia.

This is an observational study, and as such, can't establish causal and temporal factors. And the researchers acknowledge that food frequency questionnaires rely on recall and only provide a snapshot in time of diet. Nor was there objective evidence of nutritional intake from blood samples.

The prevalence of myopia in Hong Kong is also among the highest in the world. And whether the findings might apply to other ethnic groups with different lifestyles and less myopia remains to be verified, they add.

But omega-3 fatty acids may suppress myopia by increasing blood flow through the choroid, a vascular layer in the eye, responsible for delivering nutrients and oxygen, and so staving off scleral hypoxia -- oxygen deficiency in the white of the eye and a key factor in the development of nearsightedness, they suggest.

And they conclude: "This study provides the human evidence that higher dietary ω-3 PUFA intake is associated with shorter axial length and less myopic refraction, highlighting ω-3 PUFAs as a potential protective dietary factor against myopia development."

Scientists have long understood how injected allergens -- like those in lab tests or insect stings -- trigger anaphylaxis. But researchers have puzzled over how anaphylaxis begins in the gut after eating a food allergen.

Now, Arizona State University researchers, in collaboration with a team led by Yale University and other partners, have pinpointed a surprising culprit: specialized immune cells in the intestine that produce powerful chemical messengers.

These chemical messengers can cause muscles in the airways and gut to contract, increase mucus production and boost inflammation. They're already known to play a role in asthma attacks. This study shows they are also key drivers of severe food allergy reactions that start in the gut.

The findings, published in the current issue of Science, reveal that reactions to allergens in the gut are fundamentally different from reactions to allergens entering the bloodstream directly.

"Until now, we assumed that anaphylaxis followed the same pathway regardless of where allergens entered the body, with histamine from mast cells as the main driver," says ASU researcher Esther Borges Florsheim. "Our study shows that when allergens are ingested, a specialized set of mast cells in the gut don't release histamine -- instead, they produce lipid-based molecules called leukotrienes. These molecules, rather than histamine, trigger anaphylaxis in the gastrointestinal tract."

Florsheim is a researcher with the Biodesign Center for Health Through Microbiomes and assistant professor with the School of Life Sciences at ASU.

Different path to the same dangerous outcome

In both food and systemic allergies, immune cells called mast cells play a central role. When these cells detect an allergen via antibodies called immunoglobulin E, or IgE, they burst open, releasing chemicals that cause swelling, low blood pressure and other symptoms.

In the bloodstream, the most important of these chemicals is histamine, which is why antihistamines can help in some allergic situations. However, the new research shows that when an allergen is ingested, mast cells in the intestinal lining respond differently. They make relatively little histamine. Instead, they ramp up production of cysteinyl leukotrienes, a family of inflammatory lipids already known to constrict airways in conditions like asthma.

In the gut lining, intestinal mast cells take cues from nearby epithelial cells. These cues shift the cells' activity, so they make more leukotrienes and less histamine. Detailed genetic and chemical analyses showed that intestinal mast cells come in several subtypes. Compared to mast cells elsewhere in the body, mast cells in the gut were primed to make leukotrienes.

Previous research found that blocking the IgE pathway -- either by removing IgE antibodies or the receptor they bind to on mast cells -- protected against developing severe symptoms.

A new way to prevent food allergy emergencies

To test whether leukotrienes were truly driving the reaction, the team used zileuton, an FDA-approved drug used to treat asthma, which blocks a crucial enzyme needed to make leukotrienes.

The results showed the drug reduced allergy symptoms and provided protection from a dangerous drop in body temperature -- a hallmark of anaphylaxis.

Importantly, the same drug did not prevent reactions caused by allergens injected into the bloodstream. That finding showed that the gut pathway is different from the whole-body allergic pathway and has its own chemical drivers.

Current emergency treatments for severe allergic reactions, such as epinephrine, are aimed at quickly reversing symptoms once anaphylaxis starts. Antihistamines can help in mild reactions, but they are far less effective for preventing severe events -- especially those triggered by food.

The new findings suggest that targeting leukotrienes could offer a new preventive or therapeutic approach for food-triggered anaphylaxis.

More research is still needed to test whether the results from this study can be applied to humans. However, drugs that block leukotriene production (like zileuton) or leukotriene receptors (such as montelukast, also commonly used for asthma) are already approved for other uses, which could speed up testing for food allergy applications.

More than just a gut reaction

Beyond the potential clinical applications, the work changes how scientists think about allergic reactions. It shows that how an allergen gets into the body -- through the skin, bloodstream or gut -- can shape the type of immune response involved.

"This finding highlights the gut as unique in how it senses allergens and potentially other harmful environmental challenges, such as food additives," Florsheim says. "It also helps explain a long-standing puzzle: why levels of food-specific antibodies, especially IgE, do not reliably predict the risk of food allergy."

The researchers plan to follow up by studying whether similar mast cell populations and leukotriene-driven pathways exist in human intestines, and whether blocking them can reduce or prevent severe reactions in people with life-threatening food allergies.