Hypotheses: Autoimmune Cross-targeting, Co-carcinogenesis, and Quorum complications : October 2014

Thursday, October 30, 2014

Spirochetes, the mitochondria, and Alzheimer's disease....is it really midichloria?

Alzheimer's I believe is a damaged mitochondria not an autoimmune disease. Damage can come from the herpes virus, diacytel, or Midochloria?

Borrelia spirochetes and Alzheimer's
http://www.ncbi.nlm.nih.gov/pubmed/15894409
http://www.ncbi.nlm.nih.gov/pubmed/15665404
http://www.ncbi.nlm.nih.gov/pubmed/8369471
http://www.ncbi.nlm.nih.gov/pubmed/18487847
http://www.ncbi.nlm.nih.gov/pubmed/21816039
http://www.ncbi.nlm.nih.gov/pubmed/7919164

Borrelia and primary biliary cirrhosis
http://www.ncbi.nlm.nih.gov/pubmed/16870516

anti-mitochondrial antibodies and biliary cirrhosis
http://www.ncbi.nlm.nih.gov/pubmed/14594130

You would think that I am trying to connect spirochetes and Alzheimer's but spirochetes don't damage mitochondrias. A bacteria that travels with them often does....

INSIDE the mitochondria infecting with lyme disease is Midichloria mitochondrii
http://forums.prohealth.com/forums/index.php?threads/bacteria-inside-mitochondria-in-lyme-tick.258328/

Is it spirochetes or is it really the bacteria midichloria that causes alzheimer's by damaging the mitochondria and making it unable to move?

My previous posts on Alzheimer's
http://angelabiggs.blogspot.com/2014/07/alzheimers-mitochondria-damage-from.html

Cross-targeting autoimmunity in parkinson's caused by Nocardia mycobacteria and a flu virus

Cross-targeting is when 2 infections target the immune system on one place and an autoimmune disease results. Parkinson's in this case is being considered an autoimmune disease.

Nocardia and parkinson's
http://articles.latimes.com/1990-05-17/news/mn-286_1_nocardia-infection
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC228573/
http://www.ncbi.nlm.nih.gov/pubmed/8420152
http://drbroxmeyer.netfirms.com/parkinsons.pdf
http://www.scielo.br/pdf/bjmbr/v37n4/5145.pdf
http://www.intechopen.com/books/mechanisms-in-parkinson-s-disease-models-and-treatments/filterable-forms-of-nocardia-an-infectious-focus-in-the-parkinsonian-midbrains

flu virus and parkinson's
http://www.ncbi.nlm.nih.gov/pubmed/21668692
http://www.ncbi.nlm.nih.gov/pubmed/22474298
http://www.ncbi.nlm.nih.gov/pubmed/23271861
http://www.parkinson.org/NationalParkinsonFoundation/files/6d/6dea0022-01a5-4d55-926c-42efa0084c18.pdf
https://www.michaeljfox.org/foundation/grant-detail.php?grant_id=711

http://www.stjude.org/stjude/v/index.jsp?vgnextoid=6dadedc5d21f2210VgnVCM1000001e0215acRCRD

Wednesday, October 22, 2014

Autoimmune Cross-targeting

The prevalence of autoimmune diseases continues to rise. The risk of celiac disease, type one diabetes, and autism have reached one in a hundred. What is happening?

We know that families can carry genetic dispositions for developing autoimmune diseases. The HLA gene is a risk factor for celiac disease but is not required for the development of the disease. The HLA gene is however a clue. HLAs are in essence the mailboxes for our Tcells to look for viral infections inside of cells. Seems logical to suspect a viral infection is involved in celiac disease.

We know that celiac patients tend to have a history of bladder infections so we could also suspect a bacterial infection. However when patients are examined the infection is often not present which suggests that these infection may merely be the triggers.

By definition an autoimmune disease is when the immune system attacks the patient's own body. How would the immune system confuse either of these infections with self? How are these infections triggers?

Cross-targeting. Two infections targeting one place.

My hypothesis is that cross-targeting occurs for all autoimmune diseases. This blog is dedicated to examining each autoimmune disease with their suspected infections and seeing if the pattern of cross-targeting exists.

Monday, October 13, 2014

IFN and strep

IF gluten and casein raise the IFN values too high then all infections that cross the BBB should be sensitive. Strep should be gluten and casein sensitive and IFN should appear in the meningitis forms and in the autoimmune associated diseases such as rheumatic fever and Sydenham chorea.

aging decreases beta IFN and people die from strep pneumoniae in lungs (stays in the lungs and macrophages are not triggered to eat the strep)
http://www.ncbi.nlm.nih.gov/pubmed/24670807

adherence of Strep to epithelial cells with IFN
http://www.ncbi.nlm.nih.gov/pubmed/7868244

Streptococcus pneumoniae meningitis
http://www.ncbi.nlm.nih.gov/pubmed/23071286

strep and ataxia
http://www.ncbi.nlm.nih.gov/pubmed/15814071

strep and pandas
http://pandasnetwork.org/strep-creates-inflammation-and-so-can-diet/

Pandas
http://www.foodsmatter.com/asd_autism/miscellaneous/articles/pandas.html

Gluten and Sydenham chorea
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3569904/

IFN goes down in Sydenham chorea? Is that true for most autoimmune diseases?
http://www.ncbi.nlm.nih.gov/pubmed/12620654

a different autoimmune disease and IFN is lower
http://www.ncbi.nlm.nih.gov/pubmed/25272942

so even with lower IFN the sensitivity to gluten remains?

Curcumin and IFN
http://www.ncbi.nlm.nih.gov/pubmed/25251395
http://www.ncbi.nlm.nih.gov/pubmed/17979888

curcumin and sydenham chorea

Friday, October 3, 2014

Autoimmune cross-targeting and Treg confusion ?

My Hypothesis:
Cross-targeting: the layering of 2 different infections on one target causes autoimmune disease. A viral infection marking the inside of the target then a bacterial, or fungal, or mycobacteria..etc.. infection marking the outside.

Tregs are T regulating cells with the "just right" goldilock's medium touch for looking into cells using the MHC mailboxes. The mailboxes hold up one piece at a time from inside. Tregs are not too weak or too strong when looking into the cells they spend just the right amount of time looking at the MHCs and they are conditioned to know all interior self proteins.

Specifically Tregs look into cells to see if they are infected with viruses or to protect any antibody labeled cells which are healthy and fine on the inside from being mistakenly killed as bacteria.

In suppressive mode the Tregs secrete il-10 creating tolerance. Il-10 is a cytokine that halts immune system attack. It is interesting to note that some viruses have developed evil il-10 homologs in order to stop the immune system from attacking. However under normal conditions the Treg expresses il-10 for tolerance when cross-reacting antibodies have marked a new area falsely because of molecular mimicry or the bad luck of a shared protein.

For example if e.coli breaks down red blood cells it creates bilirubin. The liver also breaks down red blood cells creating bilirubin. If antibodies against bilirubin show up as the immune system patrols your body the Treg would halt any attack on your liver by first checking the health of the marked liver cells and then secreting il-10.

Now considering cross-targeting: what if when the Treg arrives at the liver it finds that the liver cells are infected by a virus like betaretrovirus or hepatitis. The infection generating the antibodies bringing it here was actually from e.coli but now your treg won't secrete il-10. You have an overlap of infections causing autoimmunity because of confused Tregs. The Tregs have no idea what mode to go into. Is this possible?

Let us consider another example: George Eisenbarth found a latent period of type 1 diabetes where he could first see anti-islet antibodies until something triggered the rapid progression into autoimmunity. The flu and coxsackie are viruses that replicate in the pancreas. Both viruses have been implicated in diabetes because new cases of type 1 diabetes appear during outbreaks. Could these viruses be the rapid trigger Eisenbarth was looking for? Could this be cross-targeting and Treg confusion?

Celiac and treg
http://www.ncbi.nlm.nih.gov/pubmed/23874626

type 1 diabetes and treg
http://www.jimmunol.org/content/181/7/4516.full.pdf

Rheumatoid arthritis and treg
http://deepblue.lib.umich.edu/bitstream/handle/2027.42/55983/22415_ftp.pdf?sequence=1

Autoimmune liver disease and treg
http://www.hindawi.com/journals/jir/2013/607073/

e.coli and the liver primary biliary cirrhosis
http://www.ncbi.nlm.nih.gov/pubmed/24128311

betaretrovirus and primary biliary cirrhosis
http://www.pnas.org/content/100/14/8454

il-2 and tregs
http://www.jimmunol.org/content/172/7/3983.full

treg cells are antigen dependent
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2784904/

Fox and Treg
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3008159/

primary biliary cirrhosis and cross-targeting

My Hypothesis:
Cross-targeting: the layering of 2 different infections on one target causes autoimmune disease. A viral infection marking the inside of the target then a bacterial, or fungal, or mycobacteria..etc.. infection marking the outside.

e.coli and the liver primary biliary cirrhosis
http://www.ncbi.nlm.nih.gov/pubmed/24128311

betaretrovirus and primary biliary cirrhosis
http://www.pnas.org/content/100/14/8454

note that this group with e.coli would overlap celiac disease
while the mycoplasma group would overlap RA

the areas over autoimmune disease overlap my help elucidate the infections involved

Hypotheses: Autoimmune Cross-targeting, Co-carcinogenesis, and Quorum complications