Association of Intestinal Dysbiosis Problem with Initiation and Development of Somatic Diseases

Abstract

Deficiency of solutions of key issues of initiation, development, prophylaxis and therapy of many somatic diseases results in the search for new external and internal causes of pathological processes manifestation in various functional systems of the organism. Recently researchers paid attention to internal - not external - cause of obesity, diabetes, atherosclerosis, cardiovascular syndrome, allergy, asthma, and neurodegenerative diseases development [1-4]. It was suggested that this trigger mechanism is localized in microbiota of human gastrointestinal tract [1]. This opinion is based on facts of pronounced dysbiosis and intestinal dysbacteriosis revealed in patients with these somatic diseases [14]. What is the initial cause - development of pathological processes in the intestine accompanied with initiation of somatic pathology or, alternatively, developing somatic pathology is accompanied with intestinal dysbiosis?Researchers' opinions divided, however more and more blame intestinal dysbiosis for initiation of somatic pathological processes [1,5]. The amount of microorganisms in the intestine is compatible with the amount of cells in human body and reaches 37 trillion units [1]. Therefore, the common genetic kit of microbiota and its unpredictable adaptive and sometimes aggressive abilities look quite impressive. Naturally, microbiota and human organism stay in harmony. Dysbiosis and dysbacteriosis are accompanied with violation of relationships between the host and microorganisms. Imbalance between aerobes and anaerobes in the intestine and change of amount and composition of certain pools of microorganisms - all these lead to appearance of conditions for translocation of natural intestinal endotoxins and metabolism products from intestinal lumen to bloodstream [1,5,6]. The emphasis is placed on negative consequences of dysbiosis development for functioning of endocrine organs, brain, kidneys, liver, heart and vessels, skeletal muscles [1,3,4]. Decarboxylation and deamination processes are disturbed in dysbiosis. These processes are naturally aimed at lysis of amino acids [1]. Excess of amino acids in the intestine serves as nutrients for rectal microflora. Bacterial enzymes break down excess of amino acids converting them into amines, phenols, indole, skatole, hydrogen sulphide and other poisonous for human organism substances. Phenol and cresol are formed from amino acid tyrosine, indole and skatole - from tryptophan. Scientists noticed that "drop" of certain amount of blood, for example in stress, from hepatic-portal system to systemic circulation is also accompanied with translocation of endotoxin, indole, skatole, phenol and cresol. Endotoxin (for example, E.coli lipopolysaccharide) binds with TLR4 and naturally activates immunity of host's organism through cascade of processes involving CD14 and proinflammatory cytokines (IL-1P, IL6, TNF) [1,7]. However, excessive endotoxin translocation into blood leads to fever development by proinflammatory cytokines together with local inflammatory process in "vulnerable" regions. Such local inflammatory processes are accompanied with formation of atherosclerotic plaques, disturbance of endocrine organs functioning and even malignant transformation of cells [1,8,9]. Integrity of negative events in the organism during dysbiosis development allowed us proposing the term - "syndrome of intestinal dysbiosis". The search for "intestinal and dysbiosis' and syndrome" in PubMed revealed only two articles on August 21, 2018 [10,11].

Authors and Affiliations

Kulchitsky Vladimir, Zamaro Alexandra, Huo Po, Li Junbo, ChenC Xinrui, Koulchitsky Stanislav

Keywords

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  • EP ID EP591022
  • DOI 10.26717/BJSTR.2018.08.001630
  • Views 187
  • Downloads 0

How To Cite

Kulchitsky Vladimir, Zamaro Alexandra, Huo Po, Li Junbo, ChenC Xinrui, Koulchitsky Stanislav (2018). Association of Intestinal Dysbiosis Problem with Initiation and Development of Somatic Diseases. Biomedical Journal of Scientific & Technical Research (BJSTR), 8(2), 6420-6422. https://europub.co.uk/articles/-A-591022