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Why Doesn’t Our Immune System Attack The Beneficial Bacteria In Our Gut?

Diseases caused by the interaction of beneficial bacteria in our intestines with the immune system and the disruption of this interaction are one of the most popular topics of recent times. The question we will address is: how do we live amicably with microbes built into our gut?

Contrary to thought, not all types of bacteria are dangerous, but rather some are beneficial to our health. Diseases that arise as a result of the mutual effect of beneficial bacteria in our intestines with the immune system and the deterioration of this effect are one of the issues with the eye that have been in recent times. The question we will address is: how do we live amicably with microbes embedded in our gut?

What Is Gut Microbiota?
Did you know that the number of bacteria in our intestines is greater than the number of stars in our galaxy? While there are 100-400 million stars in the Milky Way, each person carries 100 trillion microbes that live in large numbers.(1) that is, our intestines are the host of this large microbiota, consisting of creatures too small to see with the naked eye. Bacteria make up most of the microbiota. Gut microbes; host immune development, immune response and inflammatory bowel disease, influencing susceptibility to diseases such as Type 2 diabetes and obesity is increasing evidence that Conversely, microbes, host factors also can affect the awareness of this disease and the key to change.

How Does The Immune System Work?

Our immune system is alarmed in the event of danger and initiates inflammation burn to maintain our strength. There is a very delicate balance in the regulation of the immune system. Our immune cells must be reined in to meet the factors that pose a threat to our power, but there is no threat. Because the immune system has effective weapons to fight enemies, and the appearance of these weapons when there is no danger can damage our own cells and tissues. Cytokines are the main agents of immunity. The immune system consists of many different components that interact with each other:

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Our immune system is divided into two main titles according to their structure and function, to be” natural immune “and” Acquired Immune”. Our natural immune power is always stimulating to protect us from enemies and prevents microbes from entering our power, destroying those who manage to enter. In other words, the first protective barrier against infections is formed. The structures of natural donations consist of epithelial layers, cells in tissues (macrophages, dendir cells and others), natural killer cells and plasma proteins.

If microbes cross the epithelial barrier and move to lymphoid organs, t and B lymphocytes, which are acquired immune cells, are effective. It comes into play more slowly, but provides a freer and more effective defense against infections. B cells destroy microbes outside the cell through antibodies. Cytotoxic T cells are active with antigens presented by dendritic cells and kill microbes for the cell. Auxiliary T cells secrete cytokines, which provide the effectiveness of cells effective in killing the ISE microbe.

There are two important characteristics that distinguish acquired immunity from natural immunity: specificity and certain. The specificity map describes the response that targets different antigens. Certain features of ISE the same anti-generation again results in a faster and stronger connection response in encounters.

What Is Intestinal Homeostasis?

Our immune system acts to perceive pathogenic (disease-making) bacteria as thoughts and destroy them. It ignores-tolerates the bacteria that live in our gut. Don’t ignore it, tammen, doesn’t mean closing your eyes. The donation system keeps the native microbiota under constant surveillance. Excessive multiplicity of a large number of microbes and damage to donor tissue are prevented. This condition, called donor homeostasis, is real with numerous different mechanisms. These mechanisms can be divided into two main headings as defense and tolerance mechanisms.(2)

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Epithelial cells are primarily involved in defense mechanisms. Our epithelial cells, with the tightened bonds between them, are a physical barrier between the bacteria in the donor Lumen and our tissues. Among the donor epithelial cells, there are some specialized cells. These cells secrete mucus and antimicrobial proteins, preventing the entry of pathogenic and over-proliferated bacteria into the tissue. Acquired donation is as effective as natural donation in preserving donor tissue. B cells provide additional defense by producing Immunoglobulina (IGA). Dendritic cells deliver proteins associated with bacteria to T cells, causing differences in T cells that play a role in defense.

So, why don’t our immune cells attack the beneficial bacteria in our donors? Cells involved in defense mechanisms are also involved in tolerance mechanisms. Host-germ effects in the donor environment can be seen in the direction of decreased inflammatory responses. Native bacteria in our intestines are detected through receptors located on the connective cells and secrete anti-inflammatory cytokines such as IL-10, TGF-β, and retinoic acid. However, because the same cell receptors detect and activate pathogenic microorganisms, they secrete cytokines that cause inflammation. How immune cells distinguish pathogens and beneficial bacteria is not known with certainty. Native donor bacteria proteins presented to T cells by dendritic cells cause a difference to regulatory T cells, which has an effect that limits inflammation.

ILC cells destroy T cells that have the potential to attack beneficial bacteria
Loss of natural lymphoid cell – 3 (ILC3) in donation and consequent reduction of IL-22 production were seen to negatively affect donor microbiota and the importance of host-microbiota effects of ILC-3 cells was understood. (3)

ILC3S act with various immune cells to prevent the publication of native bacteria in donation, as well as to limit excessive immune responses that may occur against these bacteria: (4)

  • For example, ILC3S can activate B cells and trigger IGA production. (Defense Mechanization)
  • In addition, ILC3S can restrict T-cell responses that will occur independently against resident bacteria. (Tolerance Mechanization)

One of the important characteristics of the immune system can be separated from the self and the alien. In this way, it does not attack its host cells. This condition, called immunological tolerances, involves the training of immune cells. For example, in the thymus, T cells are presented with proteins that are our strength. Then, as we circulate in our power to function, our response remains as we recognize the essence proteins. T cells react to their own proteins, resulting in the death of the T cell or its suppression by regulatory T cells. If these mechanisms fail, the ISE immune system can attack its own cells and tissues, and autoimmune diseases can occur in the environment. It was found that a similar location could also apply to the gut microbiota.

ILC3 cells deliver proteins associated with bacteria living in our bonds to T cells. In this way, T cells learn not to attack bacteria that are useful to trainers. In the researchers ‘ work using mice, they discovered that ILCs destroy T cells that have the potential to attack beneficial bacteria, and that disruption of ILC functioning leads to severe intestinal inflammation. (5)

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Finally, I want to talk about the effect of protecting the bacterial species involved in the microbiota. Bacteroides species are one of the dominant groups of bacteria that live in human bonds. In one study, the genomes of Bacteroides species were examined and an interesting result was obtained. Many Bacteroides species refer to a protein that has a small part in common with a human protein. The researchers concluded that this immune microbial protein mimics our own proteins and protects our immune microbiota and our powers from autoimmune attacks. (6)

1-microbiota-Ed Yong syf. 310

2-Abraham, C. And Medzhitov, R. (2011). Interactions between host innate immune system and microbes in inflammatory bowel diseases. Gastroenterology, 140 (6), 1729-1737. DOI: 10.1053 / j. gastro.2011.02.012

3-Thaiss, C. A., Zmora, N., Levy, M. And Elinav, E. (2016). Microbiome and innate immunity. Nature, 535 (7610), 65-74. DOI: 10.1038 / nature18847

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4-Artis, D., & Spits, H. (2015). Biology of innate lymphoid cells. Nature, 517 (7534), 293-301. DOI: 10.1038 / nature14189

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6-Hebbandi Nanjundappa, R., Ronchi, F., Wang, J., Clemente-Casares, X., Yamanouchi, J., Sokke Umeshappa, C., … Santamaria, P. (2017). An intestinal microbial imitation that takes over diabetogenic Autoreactivity to suppress colitis. Cell, 171 (3), 655-667.e17. DOI: 10.1016 / j.cell.2017.09.022

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