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Posted

kind of a mix of info here, but I thought there were others who would be interested in some of these

 

 

 

http://www.ncbi.nlm.nih.gov/pubmed/1848536...ogdbfrom=pubmed

 

J Psychiatr Res. 2009 Jan;43(3):319-30. Epub 2008 May 15.

 

Age-related gene expression in Tourette syndrome.

Lit L, Enstrom A, Sharp FR, Gilbert DL.

 

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http://www.ncbi.nlm.nih.gov/pubmed/1935368...ogdbfrom=pubmed

 

Mov Disord. 2009 Jul 15;24(9):1267-79.

 

Immunopathogenic mechanisms in tourette syndrome: A critical review.

Martino D, Dale RC, Gilbert DL, Giovannoni G, Leckman JF.

 

Department of Neurological and Psychiatric Sciences, University of Bari, Italy. davidemartino@virgilio.it

 

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http://www.ncbi.nlm.nih.gov/pubmed/1942734...ogdbfrom=pubmed

 

 

Prog Neuropsychopharmacol Biol Psychiatry. 2009 Aug 31;33(6):967-71. Epub 2009 May 7.

 

A cytokine study in children and adolescents with Tourette's disorder.

Gabbay V, Coffey BJ, Guttman LE, Gottlieb L, Katz Y, Babb JS, Hamamoto MM, Gonzalez CJ.

 

NYU Child Study Center, Child and Adolescent Psychiatry, New York University School of Medicine, 577 First Avenue, New York, NY 10016, USA. vilma.gabbay@nyumc.org

 

************

 

http://www.ncbi.nlm.nih.gov/pubmed/1750347...ogdbfrom=pubmed

 

Am J Med Genet B Neuropsychiatr Genet. 2007 Oct 5;144B(7):958-63.

 

A subgroup of Tourette's patients overexpress specific natural killer cell genes in blood: a preliminary report.

Lit L, Gilbert DL, Walker W, Sharp FR.

 

Genetics Graduate Group, Department of Neurology, M.I.N.D. Institute, University of California at Davis, Sacramento, CA 95817, USA. Llit@ucdavis.edu

 

 

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Neurodevelopmental Disorders - Tourette Syndrome

56 min - May 1, 2008 -

2005 UC Davis MIND Institute Summer Series on Neurodevelopmental Disorders presents "Tourette Syndrome" by Frank Sharp, MD Series: MIND ...

 

 

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http://www.ncbi.nlm.nih.gov/pubmed/1930711...mp;ordinalpos=6

 

Prostaglandins Leukot Essent Fatty Acids. 2009 Apr;80(4):221-7.

 

Plasma fatty acid profiles in autism: a case-control study.

Wiest MM, German JB, Harvey DJ, Watkins SM, Hertz-Picciotto I.

 

Division of Epidemiology, Department of Public Health, University of California, Davis, CA 95616, USA. mwiest@uidaho.edu

 

*************

 

http://www.ncbi.nlm.nih.gov/pubmed/1913605...ogdbfrom=pubmed

 

Brain Behav Immun. 2009 Mar;23(3):389-95. Epub 2008 Dec 25.

 

Increased IgG4 levels in children with autism disorder.

Enstrom A, Krakowiak P, Onore C, Pessah IN, Hertz-Picciotto I, Hansen RL, Van de Water JA, Ashwood P.

 

***************

 

http://www.ncbi.nlm.nih.gov/pubmed/1934319...ogdbfrom=pubmed

 

Autism Res. 2008 Oct;1(5):275-83.

 

Reduced levels of immunoglobulin in children with autism correlates with behavioral symptoms.

 

Department of Medical Microbiology and Immunology, 2805, 50th Street, Wet lab building, Sacramento, CA 95817, USA.

Posted

WOW!!!!! on this one! Thank you, Kim...This confirms what my pediatrician thinks about my daughters autism and the PANDAS link...and you can get the full study for free! I'm going to print it out for him...he'll appreciate the research that reinforces his opinion, especially since he's getting so little support from specialists. This is so exciting!

http://www.ncbi.nlm.nih.gov/pubmed/1934319...ogdbfrom=pubmed

 

Autism Res. 2008 Oct;1(5):275-83.

 

Reduced levels of immunoglobulin in children with autism correlates with behavioral symptoms.

 

Department of Medical Microbiology and Immunology, 2805, 50th Street, Wet lab building, Sacramento, CA 95817, USA.

Posted

This one gives me pause, because although total IgG is below normal range for my child, IgGs 1,2,3 are in low normal range, while IgG4 is very below normal range.

 

http://www.ncbi.nlm.nih.gov/pubmed/1913605...ogdbfrom=pubmed

 

Brain Behav Immun. 2009 Mar;23(3):389-95. Epub 2008 Dec 25.

 

Increased IgG4 levels in children with autism disorder.

Enstrom A, Krakowiak P, Onore C, Pessah IN, Hertz-Picciotto I, Hansen RL, Van de Water JA, Ashwood P.

Posted

That's interesting... anyone look at it yet?

 

WOW!!!!! on this one! Thank you, Kim...This confirms what my pediatrician thinks about my daughters autism and the PANDAS link...and you can get the full study for free! I'm going to print it out for him...he'll appreciate the research that reinforces his opinion, especially since he's getting so little support from specialists. This is so exciting!
http://www.ncbi.nlm.nih.gov/pubmed/1934319...ogdbfrom=pubmed

 

Autism Res. 2008 Oct;1(5):275-83.

 

Reduced levels of immunoglobulin in children with autism correlates with behavioral symptoms.

 

Department of Medical Microbiology and Immunology, 2805, 50th Street, Wet lab building, Sacramento, CA 95817, USA.

Posted

It makes a strong correlation between low IgG levels and high Aberrant Behavior Checklist scores in the more severely autistic population. They also looked at apergers group who got lower ABC scores and IgG levels were not as low as the severe group, but still lower than typical kids.

  • 2 weeks later...
Posted

Someone mentioned recently that they were told that "strep" doesn't live in the gut. Here they were looking at the bacterial peptidoglycan, or the antigentic epitope.

It was interesting and scary to see strep and Crohn's mentioned.

 

http://www.ncbi.nlm.nih.gov/pubmed/7515336...p;ordinalpos=14

 

Clin Immunol Immunopathol. 1994 Jun;71(3):303-8.

 

The presence of peptidoglycan-polysaccharide complexes in the bowel wall and the cellular responses to these complexes in Crohn's disease.

 

Therefore, in this study the hypothesis that an enhanced immune responsiveness to bacterial antigens plays a pivotal role in the induction or the chronicity of CD was tested. As antigens, the peptidoglycan structures of intestinal bacteria (Eubacterium aerofaciens or fecal PPC) or of Streptococcus pyogenes, the 65-kDa heat shock protein and muramyl dipeptide (MDP), the smallest bioactive subunit of peptidoglycan, were used
.

 

and

 

At the inflammation site in active CD, the lymph nodes, the responses to most of the bacterial antigens were significantly higher than in the PB. In summary, the results show the presence of bacterial peptidoglycan in the bowel wall and the immune responsiveness, especially at the inflammation site, to these antigens in active CD and therefore present suggestive evidence for the role of peptidoglycan in the etiology and/or pathogenesis of CD.

 

 

 

 

http://www.ncbi.nlm.nih.gov/pubmed/1825012...mp;ordinalpos=1

 

Secreted enteric antimicrobial activity localises to the mucus surface layer.

 

RESULTS: The secreted antibacterial activity was largely confined to the layer of mucus, whereas only minute amounts of activity were noted in the luminal content. The extractable activity originating from either crypt/mucus/lumen compartments respectively (given as a percentage) was for Listeria monocytogenes, 48 (4)/44 (4)/8 (8); Enterococcus faecalis, 44 (10)/49 (3)/7 (7); Bacterium megaterium, 56 (4)/42 (3)/2 (1); Streptococcus pyogenes, 48 (4)/46 (3)/6 (6); Escherichia coli, 46 (4)/47 (3)/7 (7); and Salmonella enterica sv. Typhimurium, 38 (3)/43 (7)/19 (10). A spectrum of antimicrobial peptides was identified in isolated mucus, which exhibited strong and contact-dependent antibacterial activity against both commensal and pathogenic bacteria.

Posted

Wow - I have Crohn's myself. Always figured my PANDAS son inherited the "autoimmune vulnerability" from me.

 

Someday, I wonder if they'll discover that most of these disorders are post-infectious... and how many will be traced to strep in some way, shape, or form.

 

 

Someone mentioned recently that they were told that "strep" doesn't live in the gut. Here they were looking at the bacterial peptidoglycan, or the antigentic epitope.

It was interesting and scary to see strep and Crohn's mentioned.

 

http://www.ncbi.nlm.nih.gov/pubmed/7515336...p;ordinalpos=14

 

Clin Immunol Immunopathol. 1994 Jun;71(3):303-8.

 

The presence of peptidoglycan-polysaccharide complexes in the bowel wall and the cellular responses to these complexes in Crohn's disease.

 

Therefore, in this study the hypothesis that an enhanced immune responsiveness to bacterial antigens plays a pivotal role in the induction or the chronicity of CD was tested. As antigens, the peptidoglycan structures of intestinal bacteria (Eubacterium aerofaciens or fecal PPC) or of Streptococcus pyogenes, the 65-kDa heat shock protein and muramyl dipeptide (MDP), the smallest bioactive subunit of peptidoglycan, were used
.

 

and

 

At the inflammation site in active CD, the lymph nodes, the responses to most of the bacterial antigens were significantly higher than in the PB. In summary, the results show the presence of bacterial peptidoglycan in the bowel wall and the immune responsiveness, especially at the inflammation site, to these antigens in active CD and therefore present suggestive evidence for the role of peptidoglycan in the etiology and/or pathogenesis of CD.
http://www.ncbi.nlm.nih.gov/pubmed/1825012...mp;ordinalpos=1

 

Secreted enteric antimicrobial activity localises to the mucus surface layer.

 

RESULTS: The secreted antibacterial activity was largely confined to the layer of mucus, whereas only minute amounts of activity were noted in the luminal content. The extractable activity originating from either crypt/mucus/lumen compartments respectively (given as a percentage) was for Listeria monocytogenes, 48 (4)/44 (4)/8 (8); Enterococcus faecalis, 44 (10)/49 (3)/7 (7); Bacterium megaterium, 56 (4)/42 (3)/2 (1); Streptococcus pyogenes, 48 (4)/46 (3)/6 (6); Escherichia coli, 46 (4)/47 (3)/7 (7); and Salmonella enterica sv. Typhimurium, 38 (3)/43 (7)/19 (10). A spectrum of antimicrobial peptides was identified in isolated mucus, which exhibited strong and contact-dependent antibacterial activity against both commensal and pathogenic bacteria.

Posted

Worried Dad,

 

I wonder if what might be more important than the strep, is the condition of the mucosal barrier. See above where it says "muramyl dipeptide (MDP), the smallest bioactive subunit of peptidoglycan, were used?" A "muramyl dipeptide," here's what wiki say

 

Muramyl dipeptide is a peptidoglycan constituent of both Gram positive and Gram negative bacteria. It is composed of N-acetylmuramic acid linked by its lactic acid moiety to the N-terminus of an L-alanine D-isoglutamine dipeptide.

 

Ok, so what's N-acetylmuramic acid

 

N-Acetylmuramic acid, or MurNAc, is the ether of lactic acid and N-acetylglucosamine with a chemical formula of C11H19NO8. It is part of a biopolymer in the bacterial cell wall, built from alternating units of N-acetylglucosamine (GlcNAc) and N-acetylmuramic acid (MurNAc), cross-linked with oligopeptides at the lactic acid residue of MurNAc. This layered structure is called peptidoglycan.

 

MurNAc is a monosaccharide derivative of N-acetylglucosamine.

 

Chlamydial cell wall lacks muramic acid. This is relevant because it is an exception, most bacteria have muramic acid in their cell walls

 

 

The composition of our mucosal layer and the interaction with these structures, might be the bigger picture

 

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

http://en.wikipedia.org/wiki/N-acetylmuramic_acid

Posted

Very interesting. Thanks, Kim!

 

 

Worried Dad,

 

I wonder if what might be more important than the strep, is the condition of the mucosal barrier. See above where it says "muramyl dipeptide (MDP), the smallest bioactive subunit of peptidoglycan, were used?" A "muramyl dipeptide," here's what wiki say

 

Muramyl dipeptide is a peptidoglycan constituent of both Gram positive and Gram negative bacteria. It is composed of N-acetylmuramic acid linked by its lactic acid moiety to the N-terminus of an L-alanine D-isoglutamine dipeptide.

 

Ok, so what's N-acetylmuramic acid

 

N-Acetylmuramic acid, or MurNAc, is the ether of lactic acid and N-acetylglucosamine with a chemical formula of C11H19NO8. It is part of a biopolymer in the bacterial cell wall, built from alternating units of N-acetylglucosamine (GlcNAc) and N-acetylmuramic acid (MurNAc), cross-linked with oligopeptides at the lactic acid residue of MurNAc. This layered structure is called peptidoglycan.

 

MurNAc is a monosaccharide derivative of N-acetylglucosamine.

 

Chlamydial cell wall lacks muramic acid. This is relevant because it is an exception, most bacteria have muramic acid in their cell walls

 

 

The composition of our mucosal layer and the interaction with these structures, might be the bigger picture

 

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

http://en.wikipedia.org/wiki/N-acetylmuramic_acid

  • 4 weeks later...

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