Mushroom from Wikipedia
Crimini mushrooms from world's healthiest foods
"The effects of whole mushrooms during inflammation" in BMC Immunology (2009)
"Whole mushrooms have a number of components that are potentially immuno-modulatory. The in vitro data show that whole mushroom extracts regulate macrophage and T cell production of cytokines in a way that is predicted to be beneficial for boosting anti-tumor immunity. In vivo, the immuno-regulatory functions of edible mushrooms are harder to detect. Following challenge with DSS [dextran sodium sulfate] there is a transient protection from colonic injury and a modest increase in TNF-α production locally in the colon. Whether the increase is an effect of known immuno-modulatory nutrient components or as a result of bacteria like the psuedomonads that are associated with mushroom cultivation is not known."
"Mushroom intolerance: a novel diet–gene interaction in Crohn's disease" in British Journal of Nutrition (2009)
"Carrying a functional single nucleotide polymorphism (L503F, c. 1672 C>T) in the gene for the Na-dependent organic cation transporter (OCTN1), increases the risk of Crohn's disease (CD) in some, but not all, populations. Case–control data on New Zealand Caucasians show no differences for CD risk between individuals carrying the L503F OCTN1 C-allele when compared with those carrying the variant T-allele. However, more of the New Zealand CD cases report intolerance to maize and mushrooms than those who report beneficial effects or no differences. The OCTN1 gene encodes a transporter for ergothionine, a fungal metabolite at high levels in mushrooms but not widely common in other dietary items. An inability to tolerate mushrooms showed statistically significant associations with the variant OCTN1 genotype. That is, among those individuals reporting adverse effects from mushrooms, there was a higher frequency of the variant T-allele when compared with the general population, or with CD patients overall. We believe that this is a novel gene–diet association, suggesting that individuals carrying the OCTN1 variant single nucleotide polymorphism may have an enhanced risk of adverse symptoms associated with consuming mushrooms. Nutrigenomic approaches to dietary recommendations may be appropriate in this group."
Showing posts with label macrophages. Show all posts
Showing posts with label macrophages. Show all posts
6.8.11
Does phytic acid influence Crohn's?
Phytic Acid on Wikipedia
"Phytic acid (known as inositol hexakisphosphate (IP6), or phytate when in salt form) is the principal storage form of phosphorus in many plant tissues, especially bran and seeds.[1] Phytate is not digestible to humans or nonruminant animals, however, so it is not a source of either inositol or phosphate if eaten directly. Morever, it chelates and thus makes unabsorbable certain important minor minerals such as zinc and iron, and to a lesser extent, also macro minerals such as calcium and magnesium. ...
Phytic acid may be considered a phytonutrient, providing an antioxidant effect.[1][21] Phytic acid's mineral binding properties may also prevent colon cancer by reducing oxidative stress in the lumen of the intestinal tract. ...
As a food additive, phytic acid is used as a preservative, as E391."
Phytic Acid: Tips for Consumers from Food Science
"Inhibition of chronic ulcerative colitis associated adenocarcinoma development in mice by inositol compounds" in Carcinogenesis (2006)
" Further mechanistic studies showed that the inhibition of UC-associated carcinogenesis by inositol compounds might relate to their function on the modulation of macrophage mediated inflammation, nitro-oxidative stress and cell proliferation in UC-associated carcinogenesis. This study indicates that inositol compounds may have the potential to serve as preventive agents for chronic inflammation-carcinogenesis." [Emphases mine.]
"Effect of Inositol Hexaphosphate on Lipopolysaccharide-Stimulated Release of TNF-α from Human Mononuclear Cells" [full text]
"This study also showed that at doses significantly exceeding IP6 cellular contents, it acted as an agonist up-regulating TNF-α secretion. Moreover, IP6 appeared to influence differentially the responsiveness of mononuclear cells to secondary stimulus. Up-regulation by IP6 of TNF-α release, referred to as priming, was observed under the influence of S. minnesota LPS [LipoPolySaccharide]. Priming is considered one of the regulatory mechanisms implicated in controlling immune cell responses. This event improves the ability of immune cells to locate and kill invading microorganisms and hence may be critical to effective neutrophil functions. In this connection, IP6 can take part in the defense against invasive bacteria, such as S minnesota species. On the other hand, priming is implicated in neutrophil- and lymphocyte-mediated tissue injury both in vitro and in vivo. In this context, IP6 by down-regulating TNFα release from cells stimulated with D. desulfuricans and E. coli LPSs which showed higher potency compared to S. minnesota LPS in this study, may diminish the tissue damage caused by lymphocytes. Thus, the effects of IP6 released from necrotic cells at an inflammatory focus may be beneficial for a variety of inflammatory diseases, including septic shock.
...
In conclusion, the present findings demonstrate an extracellular role for IP6, which in this study has appeared to act as a bi-functional modulator of TNF-á release from mononuclear cells in response to bacterial challenge. The enhancing or diminishing effects of IP6 may control the level of activation states and subsequent responses of mononuclear cells, depending on the particular Gramnegative bacteria’ endotoxins."
"Phytic acid (known as inositol hexakisphosphate (IP6), or phytate when in salt form) is the principal storage form of phosphorus in many plant tissues, especially bran and seeds.[1] Phytate is not digestible to humans or nonruminant animals, however, so it is not a source of either inositol or phosphate if eaten directly. Morever, it chelates and thus makes unabsorbable certain important minor minerals such as zinc and iron, and to a lesser extent, also macro minerals such as calcium and magnesium. ...
Phytic acid may be considered a phytonutrient, providing an antioxidant effect.[1][21] Phytic acid's mineral binding properties may also prevent colon cancer by reducing oxidative stress in the lumen of the intestinal tract. ...
As a food additive, phytic acid is used as a preservative, as E391."
Phytic Acid: Tips for Consumers from Food Science
"Inhibition of chronic ulcerative colitis associated adenocarcinoma development in mice by inositol compounds" in Carcinogenesis (2006)
" Further mechanistic studies showed that the inhibition of UC-associated carcinogenesis by inositol compounds might relate to their function on the modulation of macrophage mediated inflammation, nitro-oxidative stress and cell proliferation in UC-associated carcinogenesis. This study indicates that inositol compounds may have the potential to serve as preventive agents for chronic inflammation-carcinogenesis." [Emphases mine.]
"Effect of Inositol Hexaphosphate on Lipopolysaccharide-Stimulated Release of TNF-α from Human Mononuclear Cells" [full text]
"This study also showed that at doses significantly exceeding IP6 cellular contents, it acted as an agonist up-regulating TNF-α secretion. Moreover, IP6 appeared to influence differentially the responsiveness of mononuclear cells to secondary stimulus. Up-regulation by IP6 of TNF-α release, referred to as priming, was observed under the influence of S. minnesota LPS [LipoPolySaccharide]. Priming is considered one of the regulatory mechanisms implicated in controlling immune cell responses. This event improves the ability of immune cells to locate and kill invading microorganisms and hence may be critical to effective neutrophil functions. In this connection, IP6 can take part in the defense against invasive bacteria, such as S minnesota species. On the other hand, priming is implicated in neutrophil- and lymphocyte-mediated tissue injury both in vitro and in vivo. In this context, IP6 by down-regulating TNFα release from cells stimulated with D. desulfuricans and E. coli LPSs which showed higher potency compared to S. minnesota LPS in this study, may diminish the tissue damage caused by lymphocytes. Thus, the effects of IP6 released from necrotic cells at an inflammatory focus may be beneficial for a variety of inflammatory diseases, including septic shock.
...
In conclusion, the present findings demonstrate an extracellular role for IP6, which in this study has appeared to act as a bi-functional modulator of TNF-á release from mononuclear cells in response to bacterial challenge. The enhancing or diminishing effects of IP6 may control the level of activation states and subsequent responses of mononuclear cells, depending on the particular Gramnegative bacteria’ endotoxins."
14.6.11
What is the primary defect in CD?
"New insights into the pathogenesis of Crohn's disease: are they relevant for therapeutic options?" in Swiss Med Wkly (2009)
"Data on NOD2/CARD15 expression suggest that macrophages and epithelial cells could be the locus of the primary pathophysiological defect and that T-cell activation might just be a secondary effect inducing chronification of the inflammation, perhaps as backup mechanism to insufficient innate immunity."
"Data on NOD2/CARD15 expression suggest that macrophages and epithelial cells could be the locus of the primary pathophysiological defect and that T-cell activation might just be a secondary effect inducing chronification of the inflammation, perhaps as backup mechanism to insufficient innate immunity."
What are macrophages and why are they important to CD?
"New insights into the pathogenesis of Crohn's disease: are they relevant for therapeutic options?" in Swiss Med Wkly (2009)
"Data on NOD2/CARD15 expression suggest that macrophages and epithelial cells could be the locus of the primary pathophysiological defect and that T-cell activation might just be a secondary effect inducing chronification of the inflammation, perhaps as backup mechanism to insufficient innate immunity."
"Revisiting Crohn's disease as a primary immunodeficiency of macrophages" in Journal of Experimental Medicine (2009)
"Despite two decades of mouse immunology and human genetics studies, the pathogenesis of Crohn's disease (CD) remains elusive. New clinical investigations suggest that CD may be caused by inborn errors of macrophages. These errors may result in impaired attraction of granulocytes to the gut wall, causing impaired clearance of intruding bacteria, thereby precipitating the formation of granulomas. This theory paves the way for a macrophage-based Mendelian genetic dissection of CD."
"Data on NOD2/CARD15 expression suggest that macrophages and epithelial cells could be the locus of the primary pathophysiological defect and that T-cell activation might just be a secondary effect inducing chronification of the inflammation, perhaps as backup mechanism to insufficient innate immunity."
"Revisiting Crohn's disease as a primary immunodeficiency of macrophages" in Journal of Experimental Medicine (2009)
"Despite two decades of mouse immunology and human genetics studies, the pathogenesis of Crohn's disease (CD) remains elusive. New clinical investigations suggest that CD may be caused by inborn errors of macrophages. These errors may result in impaired attraction of granulocytes to the gut wall, causing impaired clearance of intruding bacteria, thereby precipitating the formation of granulomas. This theory paves the way for a macrophage-based Mendelian genetic dissection of CD."
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