Interesting research re genes+infection+injury=illness

[Chemar]

http://www.the-scientist.com/blog/display/.../#ixzz0ro14K3Au

 

very interesting!

One of the most detailed studies to date of how the interaction between genes and environment results in disease has demonstrated that an inflammatory bowel disease resembling human Crohn's needs a specific mutation, virus, and injury to develop in mice.................

 

and

 

"So really there were three environmental factors that were working together with the mutation: the viral infection, the composition of the microbiota (presumably induced by the viral infection), and a very specific inflammatory hit on the [intestinal lining]," Blumberg said.

 

What's more, Stappenbeck found that by treating the mice with a wide spectrum of antibiotics -- in effect killing the intestinal microbes -- the disease state was eliminated.

 

"This is a virally triggered [disease] that can be treated with antibiotics, which I think is really interesting," Stappenbeck said. "Normally viruses aren't susceptible to antibiotics, but because this [disease], which is triggered by a virus, requires the presence of normal microbes in the gut, you can stop it by wiping them out."

[Kay]

Thanks! forwarded this on to a friend, her daughter has crohns, I find it interesting that her daughter lived with me over the summer after graduating from high school, she shared a room with my daughter and both of them have ended up with similar issues. She with crohns and anxiety and my daughter with Pandas and stomach (digestive, ibs?) issues have played a big part with her as well. I am sure her mom will find it interesting research. thanks.

 

http://www.the-scientist.com/blog/display/.../#ixzz0ro14K3Au

 

very interesting!

One of the most detailed studies to date of how the interaction between genes and environment results in disease has demonstrated that an inflammatory bowel disease resembling human Crohn's needs a specific mutation, virus, and injury to develop in mice.................

and

 

"So really there were three environmental factors that were working together with the mutation: the viral infection, the composition of the microbiota (presumably induced by the viral infection), and a very specific inflammatory hit on the [intestinal lining]," Blumberg said.

 

What's more, Stappenbeck found that by treating the mice with a wide spectrum of antibiotics -- in effect killing the intestinal microbes -- the disease state was eliminated.

 

"This is a virally triggered [disease] that can be treated with antibiotics, which I think is really interesting," Stappenbeck said. "Normally viruses aren't susceptible to antibiotics, but because this [disease], which is triggered by a virus, requires the presence of normal microbes in the gut, you can stop it by wiping them out."

[trggirl]

Thanks! Very interesting! It's just so complicated, it makes me wonder if they will ever figure things out.

[Chemar]

the part that really caught my attention, if I am understanding it correctly, is that they felt the virus responded to the wide spectrum of antibiotics because of the all the gut bacteria also being killed off? Makes me wonder if that is why my son seems to react negatively re his Crohn's when using probiotics ie adding bacteria, albeit "good" ones? also wonder if maybe the virus "feeds" off the other microbes? so when they are gone......???

 

also of interest was the "toxic trigger"....

 

anyways, we will see where this research leads, but as Crohn's is autoimmune, inflammatory and likely microbe induced....I felt this study may also be of interest to PANDAS/PITAND patients

[Fixit]

the part that really caught my attention, if I am understanding it correctly, is that they felt the virus responded to the wide spectrum of antibiotics because of the all the gut bacteria also being killed off? Makes me wonder if that is why my son seems to react negatively re his Crohn's when using probiotics ie adding bacteria, albeit "good" ones? also wonder if maybe the virus "feeds" off the other microbes? so when they are gone......???

 

also of interest was the "toxic trigger"....

 

anyways, we will see where this research leads, but as Crohn's is autoimmune, inflammatory and likely microbe induced....I felt this study may also be of interest to PANDAS/PITAND patients

 

absolutley.......

thanks for posting this......so i wonder if you could figure out the right probiotic, if that would help in keeping the bacteria the it feeds on at bay.. and it wold in essence do the same thing as an abx would..

just to repost...here is the artilce that talks about bacteria and weight gain....

it seems more and more there is evidence of the gut and so many secondary issues....

now if they could just be so open to infections and secondary issues

 

http://www.time.com/time/health/article/0,...1969807,00.html

[Chemar]

bumping this up related to recent Crohn's thread here

[Iowadawn]

I know Dr. K is big on Florastor as a probiotic, as are we. It is a "good yeast" --saccharomyces boulardii lyo -- not good bacteria, as most probiotics are. The abx will not kill this. It creates an environment that doesn't allow bad yeast to set up shop. This might be good in that the good bacteria still get hit by the abx, but the Florastor keeps the gut functioning. Just thinking outloud. Very interesting research. Dawn

[kim]

This abstract regarding the work by Thaddeus Stappenbeck et al. (he's one of the researchers mentioned in the original article) kicked up some interesting things to think about! I have been looking for info on "leptin" because of the involvement in appetite regulation for quite a while now, and the info on "adiponectin" was new to me and interesting too. Cheri, isn't it nice to see some of our older research (toxins) and newer info come together? Thanks for posting this.

For those who don't like to weed thru this sort of info, there are some links at bottom for newer research on probiotics, and a crohn's/vit d article

 

 

http://www.ncbi.nlm.nih.gov/pubmed/18849966

 

Here we show that ATG16L1 is a bona fide autophagy protein. Within the ileal epithelium, both ATG16L1 and a second essential autophagy protein ATG5 are selectively important for the biology of the Paneth cell, a specialized epithelial cell that functions in part by secretion of granule contents containing antimicrobial peptides and other proteins that alter the intestinal environment. ATG16L1- and ATG5-deficient Paneth cells exhibited notable abnormalities in the granule exocytosis pathway.

and

 

revealed an unexpected gain of function specific to ATG16L1-deficient Paneth cells including increased expression of genes involved in peroxisome proliferator-activated receptor (PPAR) signalling and lipid metabolism, of acute phase reactants and of two adipocytokines, leptin and adiponectin, known to directly influence intestinal injury responses.

 

 

http://en.wikipedia.org/wiki/Autophagy_(cellular)

 

In cell biology, autophagy, or autophagocytosis, is a catabolic process involving the degradation of a cell's own components through the lysosomal machinery. It is a tightly-regulated process that plays a normal part in cell growth, development, and homeostasis, helping to maintain a balance between the synthesis, degradation, and subsequent recycling of cellular products. It is a major mechanism by which a starving cell reallocates nutrients from unnecessary processes to more-essential processes

 

and

 

it may help to prevent or halt the progression of some diseases such as some types of neurodegeneration and cancer,[3] and play a protective role against infection by intracellular pathogens; however, in some situations, it may actually contribute to the development of a disease.

 

and

 

During nutrient starvation, increased levels of autophagy lead to the breakdown of non-vital components and the release of nutrients, ensuring that vital processes can continue.

 

 

http://en.wikipedia.org/wiki/Leptin

 

Function

Leptin acts on receptors in the hypothalamus of the brain where it inhibits appetite by (1) counteracting the effects of neuropeptide Y (a potent feeding stimulant secreted by cells in the gut and in the hypothalamus); (2) counteracting the effects of anandamide (another potent feeding stimulant that binds to the same receptors as THC, the active ingredient of marijuana); and (3) promoting the synthesis of a-MSH, an appetite suppressant. This inhibition is long-term, in contrast to the rapid inhibition of eating by cholecystokinin (CCK) and the slower suppression of hunger between meals mediated by PYY3-36.

 

 

 

http://en.wikipedia.org/wiki/Adiponectin

 

Function

Adiponectin is a protein hormone that modulates a number of metabolic processes, including glucose regulation and fatty acid catabolism.[3] Adiponectin is exclusively secreted from adipose tissue into the bloodstream and is very abundant in plasma relative to many hormones. Levels of the hormone are inversely correlated with body fat percentage in adults,[4] while the association in infants and young children is less clear. The hormone plays a role in the suppression of the metabolic derangements that may result in type 2 diabetes,[4] obesity, atherosclerosis,[3] non-alcoholic fatty liver disease (NAFLD) and an independent risk factor for metabolic syndrome.[5]

 

this was interesting!

 

Berberine, an herbal folk medicine, has been shown to increase adiponectin expression[18] which partly explains its beneficial effects on metabolic disturbances.

 

 

* * * * * * * * *

 

http://www.medicalnewstoday.com/articles/176550.php

Promising Probiotic Treatment For Inflammatory Bowel Disease

 

http://www.medicalnewstoday.com/articles/190809.php

Symptoms Of Digestive Disorders Alleviated By Probiotic Found In Breast Milk

 

(pros and cons have been discussed before on this one

 

http://www.medicalnewstoday.com/articles/177447.php

Sufferers Of Crohn's Disease May Benefit From Vitamin D Supplements

Edited July 5, 2010 by kim