A recent study has found that by eating dietary fiber, the infection reduces the infection by influenza virus by reducing the inflammation of respiratory tissue and increasing the antiviral immune response.
Differences in sensitivity
Influenza virus, which causes influenza, is infected and 5 to 15% of the world population is infected every year. The most common medical symptoms of infection are nasal discharge, throat pain, fever and general massage, but this response of the virus varies considerably from one person to another. Some have been devastated by the virus and have to sleep for a few days, while others are more tolerant and show moderate symptoms of infection.
It seems that these differences in sensitivity are due to inflammation arising in response to the virus: In patients, it is a genetic and strain response that is mainly involved in the production of inflammatory molecules which are activated mainly, whereas the immune people are rather jeans, which enable active-inflammatory and antioxidant response. Which is active(1). Identifying the factors responsible for these different responses can be very interesting to reduce the negative impact of influenza on health.
One of the most important known modules of inflammation is food, especially dietary fiber is present in high concentrations in most plants. Intestinal microbes (millions of billions of bacteria in our grassy colonies) feed on fermentation through these fibers, which make many short-chain fatty acids such as acetate, proprioanate and bureaucrat that act on immune cells. And reduce inflammation. Some studies suggest that this anti-inflammatory activity of short-chain fatty acids can play a very important role in preventing the immune system from racing and produces numerous reactions that hurt the tissues or promote the development of automated diseases. (Allergy, type 1 diabetes, lupus).
Recent studies suggest that anti-inflammatory action of short-chain fatty acids also plays an important role in the antiviral response to influenza viruses.(2). A group of Australian researchers have shown that animals that use inhaler-rich food (abundant soluble fiber in some plants, such as articos, garlic, asparagus and banana) were more resistant to infection. There are fewer lung wounds due to the use of influenza and fewer lung viruses. Detailed analysis shows that this protection was caused by two main events:
- Decreased intrusion into white blood cells (neutrophils) in the airways, which reduces lung tissue loss due to these immune cells.
- Increase in activity of CD8 lymphocytes, killer cells are specialized in removing the virus.
In other words, high fiber diet optimizes the response of the virus by increasing antibody immunity and increasing inflammation that can damage the lungs.
These positive effects are associated with a significant change in the microbial composition of models: Inelin supplementation increases bifidobacterium bacteria and shorter chains increase fatty acid levels significantly, especially in bautaries. Interestingly, the addition of butaturated water to models consumed by models is enough to justify the anti-influenza defense provided by high-fiber diet, it confirms that it is actually a product of short-chain fatty acids. Chains by intestinal microbial which are responsible for the change in immune function.
In this way preventing influenza can be added to many previously known effects of dietary fiber for the prevention of cardiovascular diseases and certain types of cancers (especially colon). Currently, North American is very low in normal food fiber (10-15 grams daily instead of 30 to 40 grams), and the best way to lift this condition is to increase the total plant use, for example, grapes, grains (especially whole grains) ), Nuts, fruits and vegetables.
(1) Huang Y et al. The host distinguishes the dynamics of response to molecular responses and disinfectant influenza. PLoose Genet. 2011; 7: E 1002234
(2) Trumpet A. et al. Dietary fiber protects Ly6c-by-massing monocyte hematopoiesis and CD8 + T cell metabolism. Immune system 2018; 48: 992-1005