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Crohn's disease associated AIEC adhesion is enhanced by exposure to dietary polysaccharide Maltodextrin.

kiny

Well-known member
FULL: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0052132

Kourtney P. Nickerson, Christine McDonald

Department of Molecular Medicine, Cleveland

December 12, 2012

Crohn's Disease-Associated Adherent-Invasive Escherichia coli Adhesion Is Enhanced by Exposure to the Ubiquitous Dietary Polysaccharide Maltodextrin







Abstract

Crohn's disease (CD) is associated with intestinal dysbiosis evidenced by an altered microbiome forming thick biofilms on the epithelium. Additionally, adherent-invasive E. coli (AIEC) strains are frequently isolated from ileal lesions of CD patients indicating a potential role for these strains in disease pathogenesis. The composition and characteristics of the host microbiome are influenced by environmental factors, particularly diet. Polysaccharides added to food as emulsifiers, stabilizers or bulking agents have been linked to bacteria-associated intestinal disorders. The escalating consumption of polysaccharides in Western diets parallels an increased incidence of CD during the latter 20th century. In this study, the effect of a polysaccharide panel on adhesiveness of the CD-associated AIEC strain LF82 was analyzed to determine if these food additives promote disease-associated bacterial phenotypes. Maltodextrin (MDX), a polysaccharide derived from starch hydrolysis, markedly enhanced LF82 specific biofilm formation. Biofilm formation of multiple other E. coli strains was also promoted by MDX. MDX-induced E. coli biofilm formation was independent of polysaccharide chain length indicating a requirement for MDX metabolism. MDX exposure induced type I pili expression, which was required for MDX-enhanced biofilm formation. MDX also increased bacterial adhesion to human intestinal epithelial cell monolayers in a mechanism dependent on type 1 pili and independent of the cellular receptor CEACAM6, suggesting a novel mechanism of epithelial cell adhesion. Analysis of mucosa-associated bacteria from individuals with and without CD showed increased prevalence of malX, a gene essential for MDX metabolism, uniquely in the ileum of CD patients. These findings demonstrate that the ubiquitous dietary component MDX enhances E. coli adhesion and suggests a mechanism by which Western diets rich in specific polysaccharides may promote dysbiosis of gut microbes and contribute to disease susceptibility.





 
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kiny

Well-known member
Knew this about AIEC biofilm formation a while ago, didn't know this about other pathogens as mentioned in the discussion section. It's mostly in soups and anything 'diet' as an artificial sweetener and to bulk food.

I have seen MDX in some probiotics and some EN for crohn, which is deplorable since they know damn well about these studies. People should demand the maltodextrin is taken out.

It's also often in powders to add taste, it's in some protein powder.

It's in Ensure of course, like it wasn't bad enough that the stuff is full of milk fat from their low quality casein, which is positively associated with crohn, that they have to throw in maltodextrin too. How is that garbage even allowed on the market as a medical food. I mean why stop there, why don't you put the bacteria directly in your Ensure to being with?
 
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I basically assume all those preservatives, flavorings, emulsifiers, stabilizers, coating materials or bulking agents are aggravating--if not causing--symptoms, but it's good to know functionally just how this happens.

It raises the question, in my mind, just how "good" polysaccarides (epicor, aloe extracts, mushroom extracts, etc. see book: Sugars that Heal) do their thing, to counter such effects like adherence of pathogens to gut walls.

This also leads me to question how good kefir water may be, since the (?unknown? + L. Brevia) yeasts change sugar into mannitol. Kombucha mainly leaves glucose as the sugar leftover from yeast fermentation.

"These polysaccharides are generally recognized as safe (GRAS) by the Food and Drug Administration (FDA) and include additives such as carboxymethyl cellulose (CMC), modified starches, carrageenan, pectin, and xanthan gum."--Weird, I always thought pectin was good for you? Maybe it is, since it isn't included in their studies. They were apparently just disclosing all, good and bad, additives in this class.
 
The question might be does the MDX escape digestion in the stomach. They also make
a resistant to digestion MDX,also known as resistant starch.
Old Mike
 

kiny

Well-known member
Hi all. Do ppl recommend cutting it out of ur diet if u have crohns? Soulds like a challenge but may be worth while. Anyone?
Why not, I try to avoid it.

Especially for people, like me, who respond to antimicrobial agents. Recolonisation of AIEC or mycobacteria will be hampered by reducing MDX, they're incredibly nasty pathogens and biofilms makes them that much more powerful.
 
i discovered that maltodextrin makes me worse, it was in a chicken boullion flavoring for soup/flavoring. its probably in alot of manufactured food products.
 

kiny

Well-known member
Short Chain Fatty Acids and Bile Salts Modulate the Growth of Crohn's-
Associated Adherent and Invasive E. coli (AIEC)


Deepali Herlekar, Katrina Stewart, Belgin Dogan, Craig Altier, Ellen J. Scherl, Kenneth W.
Simpson

Background: Adherent invasive Escherichia coli (AIEC) have been consistently isolated from the inflamed ileum of people with Crohn's disease (CD) and murine models of IBD, but are infrequently isolated from inflamed or healthy colon (Gastroenterology, 2004, 127:412). Differences in the chemical composition of the enteric microenvironment of the colon vs. the ileum, and the inflamed vs. the healthy ileum could account for the differential isolation of AIEC.

Aim: Assess the impact of short chain fatty acids (SCFA) and bile acids on the growth of CD associated AIEC.

Methods: The growth of ileal CD AIEC strains 541-15, 541-1, LF82 and 576-1 (phylogroups A, B1, B2 and D respectively) and E. coli DH5-alpha (control) was evaluated in a Bioscreen apparatus for 24 hrs at 37°C, with OD600 read every 15 mins. For bile salt experiments E. coli was grown in HEPES-LB pH7.4 supplemented with Na-salts of cholic, taurocholic, glycocholic, chenodeoxycholic and deoxycholic acid (0-10mM). NaCl was used to control for osmolality. For SCFA experiments E. coli was grown in media designed to simulate ileal (LB-HEPES, pH7.4, acetate 8 mM,propionate 1.5 mM,butyrate 2.5 mM) or colonic conditions (LB-MOPS, pH6.7, acetate 65 mM,propionate 29 mM,butyrate 29 mM). Control media was supplemented with NaCl at 13 or 123 mM. Maximal OD600 and time to half-maximal OD600 (T0.5) were evaluated by paired statistical analysis.

Results: Growth of AIEC and DH5-alpha in SCFA-colonic conditions (T0.5= 669±95 mins mean±SE) was slower (P<0.01) than in control media without SCFA (339±38 mins). Growth of AIEC and DH5-alpha in SCFA-ileal conditions (T0.5 357±37mins) was similar to growth in control media without SCFA (357±36 mins). There was no difference in maximal OD600 in colonic or ileal conditions. Growth (T0.5) of AIEC was stimulated by sodium salts of cholic (2-5mM, 258±13 vs control 311±22 mins, P<0.05), taurocholic (1- 5 mM, 225±12 vs control 281±19 mins, P<0.05) and glycocholic (2-5 mM, 240±12.3 vs. control 296±14 mins, P<0.01), but not deoxycholic (236±17 vs control 200±36 mins, P= 0.07) or chenodeoxycholic acid (218±14 vs. control 221±12.8 mins, P=0.39). In contrast, T0.5 for DH5-alpha was similar in bile salt-supplemented and control media, with the exception of Na-deoxycholate which suppressed growth.

Conclusions: Our results indicate that SCFA at proportions, concentrations and pH reported in the colon, but not the ileum, suppress the growth of AIEC and DH5-alpha. Conversely, free and conjugated salts of cholic acid at concentrations similar to those anticipated in the inflamed, bile salt malabsorbing distal ileum, stimulate the growth of AIEC, but not DH5-alpha. Our results support the concept that differences in the enteric microenvironment of the colon vs. the ileum, and the inflamed vs. the healthy ileum may account for the differential isolation of AIEC.
 

kiny

Well-known member
can't be bothered to find the source of the above even if I had access to it, it's an abstract from a 2012 journal, in a PDF amongst a bunch of other stuff that has nothing to do with crohn, jesus. It is hard enough for me that I have to read this in another language.

I kind of feel these things are useless because you put them in 200 different journals, it becomes useful once the crohn's disease public has access to them.

There are sites like PlosOne that let you publish for free or with a low upfront cost, please publish in places that are accessible to all, even in schools access to journals is often limited, which limits the exposure of your study.

2014 is the cutoff date in England where all studies are posted in full, online, accessible to all. As it should be. Won't be long before the EU enforces it.

Please stop using Elsevier.

http://thecostofknowledge.com/
 

kiny

Well-known member
I talked to Nutricia about maltodextrin (I know many use their EN or other products). There are some that contain maltodextrin, but their EN elemental 028 Extra neutral does not, it uses dried glucose syrup.

They were very friendly and straightforward.

This is their response that I translated in English, I left out a number of other things like a list of ingredients etc.

Dear xxx,

Thank you for your question about dextrine-maltose in Elemental O-28 Extra when used for nutritional therapy for crohn's disease.

You point to research by Nickerson en McDonald. This research shows the mechanism of dextrine-maltose, it is unknown to us how this affects other carbohydrates. The use of Elemental O-28 Extra Neutral should not cause any issues because it does not contain dextrine-maltose, but glucose syrup.

We understand the worries related to this study.

With friendly greetings, Nutricia Advanced Medical Nutrition.
If you want to avoid maltodextrin, make sure you use the type with dried glucose syrup.
 
I just noticed the lactose free trail mix I was giving my daughter was full of high maltose corn syrup. I cant believe I missed that. it is actually the second ingredient before the nuts..
thanks for this thread Kiny.

My question is this? Is the Maltose/maltodextrine similar to lactose, in that the bacteria feed off of it?
 
You know what's really really frustrating is that my IBD dietician prescribed me to go on fortisip a while ago, and I told her about my concerns with maltodextrin, she assured me that the nutrition I'd get would be worth whatever potential negatives that could come from it, grrr, medical professionals should be forced to research things like this, but unfortunately mine was just doing her 9-5 gig with no real interest in my health
 
Why not, I try to avoid it.

Especially for people, like me, who respond to antimicrobial agents. Recolonisation of AIEC or mycobacteria will be hampered by reducing MDX, they're incredibly nasty pathogens and biofilms makes them that much more powerful.
I'm one of those people that respond well to antimicrobials, too. The best CD remission I've ever had was while I was on a two week course of Clindamycin and Flagyl. I take S. Boulardii yeast to help keep bacteria levels in check, and while it helps greatly, it pales in comparison to a course of antibiotics.

I really appreciate you posting the maltodextrin information. I'll do anything I can to keep the microbe levels in check without having to resort to antibiotics. I'm scratching maltodextrin off my diet list right now.

Kiny, your research abilities are phenomenal. If you get a chance, you might want to search out the studies on Sachromyces Boulardii yeast and its effects on Inflammatory Bowel Disease.
 
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