Journal of Hematology & Thromboembolic Diseases
Open Access
ISSN: 2329-8790
ISSN: 2329-8790
Short Communication - (2022)Volume 10, Issue 3
The ancient protein turn has an impact Nuclear Factor kappa B (NF-kB) is considered to be a regulator of innate immunity. Pathogenic signals and cellular danger signals are linked through the NF-B signaling pathway, which organizes cellular resistance to invading pathogens. NF-kB is now extensively expressed and plays a role in a variety of cellular processes, including growth, differentiation, and death. However, NF-kB is best recognized for modulating the actions of proinflammatory cytokines such as Tumors Necrosis Factor (TNF)-a and Interleukin (IL)-1b in the immune response. The NF-kB transcription factor is a dimer composed of two members of the Rel family, such as p50, p52, crel, and RelB. NF-kB is coupled to inhibitory proteins from the IkB family, such as IkB-a, -b, -g, BCL-3, p105, and p100, in the cytoplasm [1,2]. TNF-a and IL-1b trigger a kinase cascade that leads to IkB phosphorylation, which then targets IkB for ubiquitin-dependent destruction. When IkB is lost, unbound NF-kB is able to enter the nucleus and change the transcription of its target genes. Surprisingly, there is a lot of variation in how the various members of the Rel and IkB families interact.
Two lines of evidence have been used to prove the relationship between NF-kB and intestinal epithelial inflammation. First, inflammatory colonic tissue has been demonstrated to activate NF-kB. Second, anti-inflammatory drugs (glucocorticoids and salicylates) that are used to treat gastrointestinal inflammation are known to suppress NF-kB activity. Ketone bodies enemas, although not being commonly regarded of as an antiinflammatory medication, have been demonstrated to reduce mucosal inflammation in ulcerative and divert colitis. In colonic epithelial cells, butyrate has been demonstrated to suppress cytokine-mediated gene expression in vitro. Ketone bodies may decrease NF-kB activity in research of the human colon cancer cell line HT-29, based on this analysis [3]. They demonstrated that ketone bodies administration reduced nuclear NF-kB binding activity, specifically the p50 protein, using electrophoretic mobility shift experiments. Although the inability of NF-kB to translocate from the cytoplasm appeared to be the cause of the decrease in nuclear NF-kB activity, butyrate does not appear to inhibit IkB degradation [4].
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The discovery that numerous eukaryotic transcription factors and coactivators, like as CBP and P300, have histone acetyltransferase activity, has solidified this relationship in recent years. Furthermore, histone deacetylase activity has been demonstrated to be coordinated with the activity of a variety of transcriptional repressors and corepressors, such as mSin3A and nuclear receptors [5]. Thus, particular transcription factors appear to activate target genes by coordinating histone hyperacetylation with the transcriptional machinery, whereas histone hypoacetylation appears to suppress transcription. However, because posttranslational changes other than acetylation, like as phosphorylation and methylation, occur, the methods by which histones influence gene transcription appear to be considerably more complicated than previously imagined Each of these complicated, covalent histone modifications affects DNA-protein interactions and subsequent gene transcription, implying that they comprise a whole layer of control. Is ketone bodies activity on NF-kB truly due to its hyperacetylating effect on histones? trichostatin is a kind of trichostatin. As a consequence of the research, this appears to be the case. Although the current study used an in vitro model system, ketone bodies appears to have impacts on histones even in vivo. Ketone bodies are thought to function through altering histones, NF-kB, and, eventually, mucosal inflammation, through the intact intestinal lumen.
The effects of ketone bodies on NF-kB are either direct or indirect, which is an important question that has yet to be resolved. Ketone bodies may affect the expression of one or more genes that regulate NF-kB activation. If this is the case, medicines that prevent new RNA or protein production should be able to counteract the butyrate effects. Alternatively, the butyrate effects might be explained by a unique mechanism involving a more direct influence on the NF-kB pathway within the cytoplasm. Recently, it was discovered that transcription factors, such as the tumor suppressor protein p53, may be directly acetylated, modifying their function. Other posttranslational changes, most notably phosphorylation, can also influence transcription factors. It would indeed be interesting to see whether ketone bodies directly modify the NFkB protein complex, causing it to fail to translocate into the nucleus.
This tiny four-carbon molecule has tremendous impacts on intestinal epithelia, controlling numerous processes such as development, differentiation, apoptosis, and neoplasia, regardless of the particular mechanisms involved. Researchers now have a possible explanation for its anti-inflammatory properties in the stomach. The fact that ketone bodies is naturally present in the intestinal lumen and that its levels can be influenced by dietary fiber adds to the intrigue of such a research. Ketone bodies "treatment," whether dietary or pharmaceutical, appears to be beneficial to the gut, doing whatever it takes to preserve homeostasis.
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Citation: Ekkel E (2022) The Ketone Bodies Relationship in Regulating Intestinal NF-kB Immune Function. J Hematol Thrombo Dis. 10:482.
Received: 03-Mar-2022, Manuscript No. JHTD-22-17210; Editor assigned: 07-Mar-2022, Pre QC No. JHTD-22-17210 (PQ); Reviewed: 21-Mar-2022, QC No. JHTD-22-17210; Revised: 28-Mar-2022, Manuscript No. JHTD-22-17210 (R); Published: 04-Apr-2022 , DOI: 10.35248/2469-9837.22.10.482
Copyright: © 2022 Ekkel E. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.