autism and antibiotics - fyi

[pr40]

article I saw today. I hope this is for real.

 

http://www.natureworldreport.com/2015/03/25/autistic-child-improves-on-antibiotics-raises-question-of-autism-gut-bacteria-connection/

[kim]

pr40

 

That is the same article we have been just discussing on another thread (fecal transplant).

 

I'm sure this has been posted on this forum before, but can't hurt to leave it again

 

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0101257
Antibiotic Treatment Attenuates Behavioral and Neurochemical Changes Induced by Exposure of Rats to Group A Streptococcal Antigen

 

People who are using the search feature may be more likey to find under your heading

[dasu]

Interesting article. Its been interesting yet painful to see the slow process mainstream medicine has made on connecting bacteria to mental health.

 

Another key takeaway I have from reading the article is to keep better notes. '“Careful parental observations can be crucial,” said Dr. Frye.'

Edited March 25, 2015 by dasu

[kim]

from the link above

http://journals.plos...al.pone.0101257
Antibiotic Treatment Attenuates Behavioral and Neurochemical Changes Induced by Exposure of Rats to Group A Streptococcal Antigen

 

Both the immunomodulatory and the neuroprotective effects of antibiotics may be achieved directly or by their effects on the GI microbiota, which is essential for the normal development and functioning of the host immune system [43]–[47], as well as brain development and function [48], [49]. Previous studies in animals have shown that introduction of specific bacteria or elimination of others can lead to behavioral and neural changes, including among others, changes in depressive- and anxiety-like behaviors and alterations in the production, release and metabolism of neurotransmitters and the expression of receptors (for review see: [50]). Interestingly, a recent study has demonstrated that introduction of the gram negative bacteria B. fragilis to a mice model of autism spectrum disorders ameliorated deficits in communicative, stereotypic, sensorimotor, and anxiety-like behaviors, including a reduction in marble burying

 

 

 

More on B. fragilis

 

http://www.thedoctorwillseeyounow.com/content/autoimmune/art3294.html

 

The presence of polysaccharide A increases the activity of T-regulatory (treg) cells, which in turn causes suppression of a pro-inflammatory immune cell called Th17. By shutting down local Th17 cells, B. fragilis is spared from immune attack and is left free to colonize the colon and keep it healthy.

 

 

http://www.caltech.edu/article/13412

04/21/2011
Learning to Tolerate Our Microbial Self

 

excerpt underlined by me

From that vantage point, the bacteria are able to orchestrate control over the immune system—and, specifically, over the behavior of immune cells known as regulatory T cells, or Treg cells. The normal function of Treg cells is to prevent the immune system from reacting against our own tissues, by shutting down certain immune responses; they therefore prevent autoimmune reactions (which, when uncontrolled, can lead to diseases such as multiple sclerosis, type 1 diabetes, lupus, psoriasis, and Crohn's disease).

Bacteroides fragilis has evolved to produce a molecule that tricks the immune system into activating Treg cells in the gut, but in this case, Mazmanian says, "the purpose is to keep the cells from attacking the bugs. Beautiful, right?"

In their Science paper, Mazmanian and colleagues describe the entire molecular pathway that produces this effect. It starts with the bacteria producing a complex sugar molecule called polysaccharide A (PSA). PSA is sensed by particular receptors, known as Toll-like receptors, on the surfaces of Treg cells, thus activating those cells specifically. In response, Treg cells suppress yet another type of cell, the T helper 17 (Th17) cells. Normally, Th17 cells induce pro-inflammatory responses—those that would result, for example, in the elimination of foreign bacteria or other pathogens from the body. By shutting those cells down, B. fragilis gets a free pass to colonize the gut. "Up until now, we have thought that triggering of Toll-like receptors resulted solely in the induction of pathways that eliminate bacteria," says Round. "However, our studies suggest that multiple yet undiscovered host pathways allow us to coexist with our microbial partners."

Edited September 1, 2015 by kim

[kim]

http://www.nih.gov/news/health/aug2015/nei-18.htm

In uveitis, bacteria in gut may instruct immune cells to attack the eye

 

So how do bacteria in the gut activate T cells against cells in the eye? The researchers theorize that bacteria in the gut produce a molecule that, to T cells, looks similar to a protein in the retina. This gives the T cells marching orders to look for that retinal protein and attack it. Consistent with this idea, the researchers found that they could activate retina-specific T cells by exposing them to a soup of bacterial proteins extracted from mouse intestines. When those activated T cells were injected into normal mice (not prone to uveitis), the mice developed uveitis.

“Given the huge variety of bacteria in our intestines, if they can mimic a retinal protein, it is conceivable that they could also mimic other self-proteins in the body. So we believe that normally harmless bacteria in the gut could be involved in promoting other autoimmune diseases as well,” Dr. Caspi said.

 

[dasu]

Thanks for posting this info.