Showing posts with label IP-10. Show all posts
Showing posts with label IP-10. Show all posts

7.6.12

Does ginseng supplementation improve Crohn's symptoms?

Ginseng from Wikipedia

"Bioactivity-guided identification and cell signaling technology to delineate the immunomodulatory effects of Panax ginseng on human promonocytic U937 cells" in Journal of Translational Medicine (2009)
"Ginseng roots contain multipleactive constituents including ginsenosides, polysaccharides, peptides, polyacetylenic alcohols and fatty acids that have been shown to have different effects on carbohydrate and lipid metabolism as well as on the function of neuroendocrine, immune, cardiovascular and central nervous systems in humans [1,2]. Previous studies have shown that ginseng and its active components are potent immunomodulators. Their immunomodulatory effects are mostly due to its regulation of cytokine production and phagocytic activities of monocytes/macrophages and dendritic cells, as well as activation of T- and B-lymphocytes [3-8].
In addition, ginseng has been shown to have potent regulatory effects on the inflammatory cascade. Ginsan, a polysaccharide extract from ginseng, enhances the phagocytic activity of macrophages in mice infected with Staphylococcus aureus [9]. Ginsan also inhibits the production of proinflammatory cytokines including tumour necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, IL-12, IL-18 and interferon-γ (IFN-γ) by suppressing the activity of mitogen activated protein kinases (MAPK) including MAPK and JNK, and the transcription factor nuclear factor-kappaB (NF-κB). The ginseng root extract stimulates the inducible nitric oxide synthase (iNOS) activity in RAW264.7 murine macrophages.
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In conclusion, the results of this study provide evidence that ginseng can suppress TNF-α-inducible cytokines and signalling proteins in promonocytic cells. The suppressive effect of the reconstituted mixture of individual ginsenosides on TNF-α induced-CXCL-10 [Interferon gamma-induced protein 10 (IP-10) or small-inducible cytokine B10] transcription was comparable to that of the PGSE [Panax ginseng extract] treatment. Moreover, ginseng down regulated CXCL-10 expression by suppressing TNF-α-induced ERK1/2 activation. Thus, ginseng may exert its anti-inflammatory properties by targeting at different levels of the TNF-α signalling pathways. Further studies will be needed to examine the potential beneficial effects of ginsenosides in the management of acute and chronic inflammatory diseases in humans."

10.5.12

Does increasing lactocepin reduce Crohn's symptoms?

"Lactocepin Secreted By Lactobacillus Exerts Anti-Inflammatory Effects By Selectively Degrading Proinflammatory Chemokines" in Cell Host and Microbe (2010)
"The intestinal microbiota has been linked to inflammatory bowel diseases (IBD), and oral treatment with specific bacteria can ameliorate IBD. One bacterial mixture, VSL#3, containing Lactobacillus, Bifidobacterium, and Streptococcus, was clinically shown to reduce inflammation in IBD patients and normalize intestinal levels of IP-10, a lymphocyte-recruiting chemokine, in a murine colitis model. We identified Lactobacillus paracasei prtP-encoded lactocepin as a protease that selectively degrades secreted, cell-associated, and tissue-distributed IP-10, resulting in significantly reduced lymphocyte recruitment after intraperitoneal injection in an ileitis model. A human Lactobacillus casei isolate was also found to encode lactocepin and degrade IP-10. L. casei feeding studies in a murine colitis model (T cell transferred Rag2−/− mice) revealed that a prtP-disruption mutant was significantly less potent in reducing IP-10 levels, T cell infiltration and inflammation in cecal tissue compared to the isogenic wild-type strain. Thus, lactocepin-based therapies may be effective treatments for chemokine-mediated diseases like IBD."