| Autor: |
Ktsoyan ZA; Institute of Molecular Biology of National Academy of Sciences of Republic of Armenia Yerevan, Armenia., Mkrtchyan MS; Institute of Molecular Biology of National Academy of Sciences of Republic of Armenia Yerevan, Armenia., Zakharyan MK; Institute of Molecular Biology of National Academy of Sciences of Republic of Armenia Yerevan, Armenia., Mnatsakanyan AA; Clinical Hospital of Infectious Diseases Nork, Ministry of Health of Republic of Armenia Yerevan, Armenia., Arakelova KA; Institute of Molecular Biology of National Academy of Sciences of Republic of Armenia Yerevan, Armenia., Gevorgyan ZU; Clinical Hospital of Infectious Diseases Nork, Ministry of Health of Republic of Armenia Yerevan, Armenia., Sedrakyan AM; Institute of Molecular Biology of National Academy of Sciences of Republic of Armenia Yerevan, Armenia., Hovhannisyan AI; Institute of Molecular Biology of National Academy of Sciences of Republic of Armenia Yerevan, Armenia., Arakelyan AA; Institute of Molecular Biology of National Academy of Sciences of Republic of Armenia Yerevan, Armenia., Aminov RI; School of Medicine and Dentistry, University of Aberdeen Aberdeen, UK. |
| Jazyk: |
angličtina |
| Zdroj: |
Frontiers in microbiology [Front Microbiol] 2016 May 24; Vol. 7, pp. 776. Date of Electronic Publication: 2016 May 24 (Print Publication: 2016). |
| DOI: |
10.3389/fmicb.2016.00776 |
| Abstrakt: |
Gut microbiota-produced short chain fatty acids (SCFAs) play an important role in the normal human metabolism and physiology. Although the gradients of SCFAs from the large intestine, where they are largely produced, to the peripheral blood as well as the main routes of SCFA metabolism by different organs are known well for the healthy state, there is a paucity of information regarding how these are affected in disease. In particular, how the inflammation caused by infection or autoinflammatory disease affect the concentration of SCFAs in the peripheral venous blood. In this work, we revealed that diseases caused either by infectious agents (two Salmonella enterica serovars, S. Enteritidis, and S. Typhimurium) or by the exacerbation of an autoinflammatory disease, familial Mediterranean fever (FMF), both result in a significantly elevated systemic concentration of SCFAs. In the case of salmonellosis the concentration of SCFAs in peripheral blood was significantly and consistently higher, from 5- to 20-fold, compared to control. In the case of FMF, however, a significant increase of SCFAs in the peripheral venous blood was detected only in the acute phase of the disease, with a lesser impact in remission. It seems counterintuitive that the dysbiotic conditions, with a reduced number of gut microorganisms, produce such an effect. This phenomenon, however, must be appraised within the context of how the inflammatory diseases affect the normal physiology. We discuss a number of factors that may contribute to the "leak" and persistence of gut-produced SCFAs into the systemic circulation in infectious and autoinflammatory diseases. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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