Monday, October 28, 2013

Gluten and Schizophrenia? T.gondii's pvm is thread-like and gluten sensitive? or is the gluten sensitive group the tumor/mycobacteria group?

Newer posts have decided that morphology does not connect to gluten and casein. Rather what all these infections have in common is the ability to cross barriers: the intestine and the Blood brain barrier. 
http://angelabiggs.blogspot.com/2015/03/infections-that-break-tight-junction.html

Several autoimmune diseases have gluten and casein sensitivities.  This could be due to morphology shifting. For fungus that means yeast to mold. For bacteria:  rod to string like lengths.

Schizophrenia and t.gondii
http://www.ncbi.nlm.nih.gov/pubmed/24413543

T. gondi has the LON enzyme http://www.uniprot.org/uniprot/B6K9X1
I didn't find t. gondi to have morphology switching so I do not know what we are looking at.

Schizophrenia has the gluten sensitivity: http://www.ncbi.nlm.nih.gov/pubmed/22446142
So something is happening:

T. gondii morphology may not be altered by LON rather the ability of it and other parasites to invade cells. Here is a paper talking about serine proteases and cystene proteases inhibition preventing cell invasion: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1797762
http://aac.asm.org/content/43/6/1358.full 

What I am considering is the PVM, parasitiophorous vauole membrane, is a threadlike extension that T.gondii creates during infection. Could this thread like system be sensitive to gluten and casein like the mold form of a fungus?  Is the LON enzyme involved here?

The PVM appears to be the specialized invasion tool
http://www.ncbi.nlm.nih.gov/pubmed/18512349

LON is casein sensitive (and I believe with the similar amino acid sequence gluten sensitive too).  This could explain the gluten sensitive of schizophrenia.  The parasite is inhibited by gluten...and may react.


T.gondii appears to cross the blood brain barrier.
http://www.ncbi.nlm.nih.gov/pubmed/13678858

Lets consider that maybe it doesn't cross the BBB.  what if it is only when the antibodies get across the BBB when a mycobacteria or strep creates a hole? but then...if you read on...i had previously found that gluten sensitive occur after mice were infected with t. gondi.  If only t.gondi was dimorphic...then this would make sense to me.

By antibodies i am referring to my earlier post of pan/apple domains and receptors. http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030169 

THE OTHER POSSIBILITY:
There exists more then one type of schizophernia. The Ovarian teratoma tumor form generates NMDA receptor antibodies just like t.gondii but the tumor's antibodies can't cross the BBB (blood brain barrier) unless another infection which is gluten and casein sensitive does.

So autoimmune schizophrenia has these possibilities:
t.gondii followed by a virus like herpes virus 8
or
tumor with BBB crossing-infection then the herpes virus
This could be why all cases are not gluten casein sensitive. The most likely infection would be mycobacterias because some schizophrenia has been associated with MS and psoriasis...which i have linked to mycobacterias!
http://asdresearchinitiative.wordpress.com/2014/02/22/schizophrenia-greater-risk-of-other-autoimmune-diseases/

Mycobacterias are gluten and casein sensitive. Changing morphology with them. 

Previous thoughts on Schizophrenia:
Here are the references and thoughts I have on Schizophrenia.

First schizophrenia can be autoimmune in that antibodies generated against the NMDA receptor of the brain can cause Hallucinations

ref: Antibody mediated encephalitis: a treatable cause of schizophrenia
British Journal of Psychiatry 2012
200:92-94

The bacteria infection T. gondii can be linked to the NMDA receptor through pan/apple domains.

 T. gonii has pan/apple on it. 

ref: A novel pan/apple domain containing protein for Toxoplasma gondii: characterization and receptor indentification 
PLoS

Schizophrenia has T. gondi antibodies

ref: Antibodies to Toxoplasma gondii in patients with Schizophrenia.
schizophrenia bulletin vol 33 no 3 pp 729-736

In our body when blood clots are degraded, plasminogen which has the PAN sequence in  it, is activated by tPA (tissue plasminogen activator)

t-PA binds not just plasminogen but the NMDA receptor.   Does this mean the NMDA receptor has a PAN/apple domain?

ref: t-PA is a new ligand of NMDA receptor
JBC papers Sept 23. 2004

If antibodies develop against T.gondii included the pan/apple domain does this mean the antibodies might also bind the NMDA receptor? 

Now I can apply my autoimmune hypothesis to it.  A dimorphic infection triggers an autoantibody precursor stage which then progresses into the the disease following a viral infection cross targeting event.

The strain ME49 of T.gondi contains more then one morphology. Both spherical vesicles and tubular elements are found.

The change in morphology might be just like e.coli using LON.  T.gondii appears to trigger a gluten response....but perhaps in this case gluten is inhibiting the "root like" PVM?

ref: Anti-gluten immune response following toxoplasma gondii infection in mice.
PLo S Nov 29 2012 , 7 (11)e50991

Schizophrenia has been associated with gluten and casein

ref. The gluten connection: the association between schizophrenia and celiac disease.
Acta Psychiatr Scand 2006 Feb: 113(2): 82-90

ref: Specific IgA antibody increases in Schizophrenia
1995 society of biological psychiatry 

So we have the bacteria creating the antibodies where the immune system is looking at the neuron's receptor but then we need the cross-targeting virus. The virus would infect the inside of the neurons bearing these receptors thus causing the immune system to have verification of the neuron as a target.  Cross targeting would push one into attacking one's self....making schizophrenia an autoimmune disease. 

Retroviruses were linked to schizophrenia patients in 2001in Germany.  An example of a retroviruses is the Borna virus...a virus which infects the central nervous system.

OR a herpes which infects nerves could be involved.  Herpes virus 8 and 2 are suspects. Could the this virus trigger the cross targeting? The t.gondii antibodies marking the outside of the neuron and the herpesvirus 8 marking the inside of the neurons?

herpes 2
http://www.ncbi.nlm.nih.gov/pubmed/15319094
herpes 8
http://www.ncbi.nlm.nih.gov/pubmed/24560611

Only after cross-targeting would the autoimmune form of schizophrenia develop...but this is a hypothesis and this is just something to consider. It is not proven.

Schizophrenia, infections, and autoimmune disease genetic predisposition (evidence schizophrenia is autoimmune like celiac disease and autism?)
http://www.ncbi.nlm.nih.gov/pubmed/24557043
http://www.ncbi.nlm.nih.gov/pubmed/22193673
http://www.ncbi.nlm.nih.gov/pubmed/16513876






Polyarteritis Nodosa and autoimmune cross-targeting? Linked with autoimmune liver disease?

 Hypothesis: The cross-targeting of infections at the same tissue causes autoimmune disease.  One infection marks the outside while another marks the inside...only then does the immune system become confused and attack. A virus marks the inside of the liver while an infections marks the outside.....in this case instead of at the liver it occurs in the blood vessels....maybe starting near the liver?


Polyarteritis nodosa is known to have active Hepatitis B
http://www.ncbi.nlm.nih.gov/pubmed/20605819 
http://www.ncbi.nlm.nih.gov/pubmed/11059878

 Polyarteritis nodosa could be caused by cross-targeting involving e.coli because I have previous linked the dimorphic e.coli of bladder infections to autoimmune hepatitis and celiac disease.

Polyarteritis nodosa connected to bladder infections and autoimmune hepatitis.
http://www.ncbi.nlm.nih.gov/pubmed/21119556
but the infection would have to get to the arteries or make antibodies against them.  

Mycoplasmas infecting most organs over time.  This would mean that polyarteritis may more commonly be linked with lupus?
http://www.ncbi.nlm.nih.gov/pubmed/21763578
http://lup.sagepub.com/content/4/6/494.abstract

Because mycoplasmas and e.coli infect the bloodstream...it makes sense how this once started could occur all over. 







Thursday, October 10, 2013

Stiffman's syndrome and cross-targeting autoimmunity

 Hypothesis: The cross-targeting of infections at the same tissue causes autoimmune disease.  One infection marks the outside while another marks the inside...only then does the immune system become confused and attack. A virus marks the inside of the kidney while an infections marks the outside.


antibodies to GAD precursor to GABA (nerves are the focus of the cross-targeting)
http://europepmc.org/articles/PMC1753919/pdf/v061p00939.pdf
causes lower back pain 

mycoplasmas and nerves (they can infect them)
http://www.ncbi.nlm.nih.gov/pubmed/16914976
http://www.ncbi.nlm.nih.gov/pubmed/3100660

Lupus and stiffman  (lupus, type 1 diabetes and graves i have previously connected with mycoplasmas)
http://lup.sagepub.com/content/13/3/215.extract
http://onlinelibrary.wiley.com/doi/10.1002/mds.22942/abstract
http://www.ncbi.nlm.nih.gov/pubmed/20537445

Type 1 diabetes and stiffman
http://www.ncbi.nlm.nih.gov/pubmed/10460456
http://www.ncbi.nlm.nih.gov/pubmed/19828214

Graves and stiffman
http://www.ncbi.nlm.nih.gov/pubmed/17712846
http://www.medscape.com/viewarticle/508849_2

Herpes  B and stiffman (rare herpes virus)
http://www.ncbi.nlm.nih.gov/pubmed/15999237
Monkeys as pets risk
http://www.ncbi.nlm.nih.gov/pubmed/9452406

Herpes vaccine and stiffman (genital herpes)
http://patientsville.com/vaccines/hpv4/stiff-man-syndrome-hpv-gardasil-2009.htm

mycoplasmas infect the nerve and then the herpes exposure causes cross-targeting on nerves by the immune system?

This page is still under construction and  may change.

Berger's disease and cross-targeting autoimmunity (NOT Buerger's)

Berger's disease is an autoimmune disease of the Kidney

Hypothesis: The cross-targeting of infections at the same tissue causes autoimmune disease.  One infection marks the outside while another marks the inside...only then does the immune system become confused and attack. A virus marks the inside of the kidney while an infection marks the outside.

Tonsillitis
http://www.ncbi.nlm.nih.gov/pubmed/16566197

Viruses of the Tonsils that have respiratory infections
RSV Respiratory Syncytial Infection  therefore the most likely culprit

RSV of the Kidney (the virus replicates in the kidney not just the tonsils & lungs) The kidney is the cross-target focus.
http://link.springer.com/article/10.1007%2FBF00862085 

duration of RSV virus secretion (IgM and IgA...IgA lasts around 30 days)
http://www.ncbi.nlm.nih.gov/pubmed/9406652
http://www.ncbi.nlm.nih.gov/pubmed/10830453

boys more likely to have RSV detected
http://www.ncbi.nlm.nih.gov/pubmed/15198187
Note that males are more likely to have Berger's then females.

These diseases are connected: Henoch-Schönlein purpura and Berger
http://www.ncbi.nlm.nih.gov/pubmed/10392263  the emphasis is on IgA antibody levels


Now Looking for the non viral infection:

infections possible...
http://www.ncbi.nlm.nih.gov/pubmed/10392263
Bowel angina...might connect bladder infection e.coli and celiac
Arthritis would connect mycoplasmas

NOTE that the either mycoplasmas or e.coli could be the culprit for cross-targeting with the RSV virus at the kidney.

Gluten (e.coli/celiac)
http://www.ncbi.nlm.nih.gov/pubmed/12046028
http://www.ncbi.nlm.nih.gov/pubmed/1582590
http://www.ncbi.nlm.nih.gov/pubmed/3113643


Antiphospholipids and the kidney (mycoplasmas/lupus)
http://www.uptodate.com/contents/antiphospholipid-syndrome-and-the-kidney
http://www.uptodate.com/contents/antiphospholipid-syndrome-and-the-kidney/abstract/2


Wednesday, October 9, 2013

churg-strauss and cross-targeting autoimmunity

Hypothesis: The cross-targeting of infections at the same tissue causes autoimmune disease.  One infection marks the outside while another marks the inside...only then does the immune system become confused and attack.

Churg-strauss syndrome: nasal polyps, asthma, rhinitis

staph or aspergillus?

Churg-strauss and rheumatoid
http://www.ncbi.nlm.nih.gov/pubmed/12589235...rheumatoid factor was there and staph was too

Note that in the past  had made associations of Aspergillus with Churg-strauss:
http://angelabiggs.blogspot.com/2013/04/churg-strauss-autoimmune-vasculitis.html

Churg-stauss and hepatitis B
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2845776/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1752586/
http://www.ncbi.nlm.nih.gov/pubmed/11791655

interesting especially after my other posts:
http://www.ncbi.nlm.nih.gov/pubmed/11361200

Takayasu: mycobacteria & hepatitis B
Churg-stauss: aspergillus & hepatitis B

Also keep in mind that I have connected Hashimoto's thyroid to fungal infections which means that Churg-strauss should have connections to Hashimoto's.

If the walls of the blood vessel become surface infected by staph or mycobacteria and then the cells themselves become infected with  a virus I believe autoimmune cross-targeting can occur.

The infections can be different in triggering the autoimmune cross-targeting....because it is the target that is significant. 



CPPD with high cholesterol, and mycobacteria or is it gout, staph, and septic arthritis? 2 types?

 Is Gout is connected to mycoplasmas but  CPPD is connected to mycobacterias?

http://www.rheumatology.org/I-Am-A/Patient-Caregiver/Diseases-Conditions/Calcium-Pyrophosphate-Deposition-CPPD

 metabolic syndrome,
http://rheumatology.oxfordjournals.org/content/48/suppl_2/ii2.full 
(i have type 2 diabetes connected to mycobacteria )

psoriasis,
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2426549/
http://archderm.jamanetwork.com/article.aspx?articleid=543012
(note that I have connected psoriasis to mycobacteria on other blog posts and that psoriasis is gluten sensitive)

asthma,
http://www.nejm.org/doi/pdf/10.1056/NEJM185903100600602

Gout and crohn's? is this really CPPD?
not high numbers: http://www.ehealthme.com/cs/crohn%27s+disease/gout
http://www.gout-pal.com/gout-pal-forum/please-help-my-gout/gout-and-crohns-disease/
so maybe this is also genetic susceptibility on top of the mycobacteria or not real?  or it is a mycobacteria related to psoriasis but not crohn's...the type of mycobacteria?

Testimonials of gout and gluten:
http://health.usnews.com/health-news/family-health/pain/articles/2009/02/27/gout-quiz-how-much-do-you-know-about-gouty-arthritis/comments (not celiac disease but gluten sensitive..causes the mycobacteria to morphology switch like I think e.coli can in celiac disease?)


mycobacteria grows on uric acid
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC217648/
http://www.faculty.biol.vt.edu/falkinham/Articles/JB36.pdf

Maybe in these genetically susceptible people their response to a mycobacteria eating their uric acid is to increase the amount of uric acid they make?  No feedback loop occurring so their bodies ramp up production?  (the Hyperuricaemia seen in the first reference)

Gout and high cholesterol
http://www.livestrong.com/article/490117-what-is-the-relation-between-high-levels-of-cholesterol-uric-acid

Cholesterol and mycobacteria
http://www.ncbi.nlm.nih.gov/pubmed/19634704
http://www.ncbi.nlm.nih.gov/pubmed/18334639
 http://www.ncbi.nlm.nih.gov/pubmed/18505807

 cholesterol as part of the immune system
http://onlinelibrary.wiley.com/doi/10.1111/j.1348-0421.2009.00203.x/full

Note that green tea inhibits the growth of mycobacteria
http://www.sciencedirect.com/science/article/pii/S1357272505003778

Green tea could help the symptoms of gout (by inhibiting the growth?)
http://goutandyou.com/gout-and-green-tea/

Are there 2 types of gout? the uric acid type that green tea might help versus the calcium phosphate type that cherries would help?  Mycobacteria versus mycoplasma type? which group do cherries help?

When gout is connected to RA then cherries and peaches seem to remedy it.
http://www.webmd.com/arthritis/news/20101110/cherries-may-cut-risk-of-gout-flare-ups

RA I have connected to mycoplasmas.
http://angelabiggs.blogspot.com/2013/04/lupus-and-ra-leukemia-and-mycoplasmas.html

Peaches, nectarines, and cherries are constantly battling mycoplasmas. 
http://ohioline.osu.edu/hyg-fact/3000/pdf/HYG_3206_08.pdf

cherries do seem to lower uric acid
http://www.ncbi.nlm.nih.gov/pubmed/12771324

is this gout verse CPPD connection correct?

staph can move in with fungal or mycoplasma biofilms

 Is gout, uric acid, connected to staph infections?
septic arthritis and gout have connections
http://rheumatology.oxfordjournals.org/content/42/9/1062.long

eczema has been found to have high uric acid concentrations
http://archinte.jamanetwork.com/article.aspx?articleid=534273

Tuesday, October 8, 2013

Takayasus caused by autoimmune cross-targeting?

Hypothesis: The cross-targeting of infections at the same tissue causes autoimmune disease.  One infection marks the outside while another marks the inside...only then does the immune system become confused and attack.


Takayasu and lupus?are these actually Kawasaki patients?
http://www.ncbi.nlm.nih.gov/pubmed/1351317
http://link.springer.com/article/10.1007%2Fs00296-009-1133-y#page-1
http://www.ncbi.nlm.nih.gov/pubmed/10380843
http://www.ncbi.nlm.nih.gov/pubmed/14986087

Takayasu's and mycobacteria
TA and tuberculosis are chronic granulomatous diseases
http://www.ncbi.nlm.nih.gov/pubmed/8839810
http://www.ncbi.nlm.nih.gov/pubmed/10371844 

type 2 diabetes patients with Takayasu (therefore the virus cannot be common)
http://www.ehealthme.com/cs/type+2+diabetes+mellitus/takayasu%27s+arteritis

confusing review (more common in women...dimorphic supports mycobacteria)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3232509/

crohn's and Takayasu (strong association implicates mycobacteria)
http://www.ncbi.nlm.nih.gov/pubmed/12746644
http://www.ncbi.nlm.nih.gov/pubmed/11907362
http://www.ncbi.nlm.nih.gov/pubmed/33869
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2722706/
http://practicalgastro.com/pdf/March09/JudahArticle.pdf
http://www.jmedicalcasereports.com/content/2/1/87

The BCG vaccine? (mycobacteria vaccine)
http://www.ncbi.nlm.nih.gov/pubmed/7901414 (erythema nodosum induced too?)
http://www.ncbi.nlm.nih.gov/pubmed/8569543


erythema nodosum and mycobacteria
http://www.ncbi.nlm.nih.gov/pubmed/23650522

looking for virus now: maybe this is not autoimmune?

the genetic susceptibility  found for Takayasu involve the t-cell mail box the HLA?
http://www.news-medical.net/news/20130730/Researchers-uncover-genetics-behind-what-makes-some-people-susceptible-to-Takayasu-arteritis.aspx      That would indicate a virus because HLA tells the t-cell what is inside...if a virus infects a piece would end up in the mailbox...huh.

found it!  Hepatitis B and Takayasu
http://www.ncbi.nlm.nih.gov/pubmed/11361200
http://www.ncbi.nlm.nih.gov/pubmed/7901414

Kawasaki is it autoimmune Cross-targeting triggered? Bcells infected by mycoplasmas?

 Hypothesis: The cross-targeting of infections at the same tissue causes autoimmune disease.  One infection marks the outside while another marks the inside...only then does the immune system become confused and attack.

Kawasaki is autoimmune:
http://link.springer.com/article/10.1007%2Fs00296-013-2770-8

Mycoplasma pneumonia and kawasaki
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1511717/
http://www.ncbi.nlm.nih.gov/pubmed/21042274
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3120998/
http://www.hindawi.com/crim/medicine/2011/606920/
http://onlinelibrary.wiley.com/doi/10.1111/j.1651-2227.2001.tb00810.x/abstract

Lupus and Kawasaki (lupus could be red blood cells infected by mycoplasmas see earlier posts)
http://www.ncbi.nlm.nih.gov/pubmed/22868216
http://www.ncbi.nlm.nih.gov/pubmed/3379628
http://treato.com/Kawasaki+Disease,Lupus/?a=s

The infection of Bcell lines by mycoplasmas (Lymph nodes are the hubs for Bcells)
http://www.ncbi.nlm.nih.gov/pubmed/16054780

Kawasaki and hepatitis B
http://www.ncbi.nlm.nih.gov/pubmed/14677029
http://www.ncbi.nlm.nih.gov/pubmed/14521027
http://cpj.sagepub.com/content/early/2015/01/29/0009922815569206

Kawasaki and other polyomaviruses
http://www.ncbi.nlm.nih.gov/pubmed/9622713

EBV virus (mono) and Kawasaki
http://jid.oxfordjournals.org/content/162/5/1215.extract
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC499744/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2687726/
http://www.ncbi.nlm.nih.gov/pubmed/7871990
http://pediatrics.aappublications.org/content/73/3/413 

I am considering a separate Kawasaki with Yersinia.....to be continued.  This would have reactive arthritis, graves based thyroiditis (the enlarged thyroid), and  mesenteric lymphadenitis.

Note that I think it is the target that is more relevant then the infection...both Yersinia and mycoplasmas can cause the disease...with EBV.


cogan's syndrome and autoimmune cross-targeting

Hypothesis: The cross-targeting of infections at the same tissue causes autoimmune disease.  One infection marks the outside while another marks the inside...only then does the immune system become confused and attack.

cogan's syndrome is autoimmune
http://www.ncbi.nlm.nih.gov/pubmed/22846458

 Chlamydia pneuoniae appears in the case history of several Cogan's syndrome patients.
http://www.ncbi.nlm.nih.gov/pubmed/15904966

Looking for the virus culprit now.  Considering the pinkeye connection.

Pinkeye and conjuctivitis
http://www.ncbi.nlm.nih.gov/pubmed/17457917

Looking at Coxsackie B and the ear
Coxsackie B has been implicated in tinnitus
http://www.ncbi.nlm.nih.gov/pubmed/17984924

Board under construction.