Monday, November 13, 2017

4 possible types of asthma from fungal, mycobacteria, staph, and H.pylori infections?

Mycobacteria Asthma

SERT and cGMP
http://www.ncbi.nlm.nih.gov/pubmed/19656393
http://www.jneurosci.org/content/27/40/10878.full

bipolar and type 2 diabetes
http://www.ncbi.nlm.nih.gov/pubmed/22621171

bipolar, metabolic disorder, and autoimmune disorder
http://www.ncbi.nlm.nih.gov/pubmed/25237732

older post with 2 types of bipolar:
http://angelabiggs.blogspot.com/2015/07/is-bipolar-disorder-autoimmune-disorder.html

CMV with schizophrenia and bipolar..is this bipolar 1 which is autoimmune while the mycob. is not?
http://www.ncbi.nlm.nih.gov/pubmed/24083998

Mycobacteria's cGMP : asthma, type 2 diabetes, and metabolic syndrome

cGMP and asthma
http://www.ncbi.nlm.nih.gov/pubmed/6258958

 asthma and metabolic syndrome
http://www.ncbi.nlm.nih.gov/pubmed/25789301

high cholesterol and asthma
http://www.ncbi.nlm.nih.gov/pubmed/16754527

cGMP is inhibited at night
http://www.jneurosci.org/content/23/20/7543.full.pdf

Is this the nighttime asthma?

Fungal Asthma

Baker's asthma and rhinitis
http://www.ncbi.nlm.nih.gov/pubmed/0009847440

female athletes were found to have worse asthma when the cycle had high progesterone which effects smooth muscles

https://books.google.com/books?id=HY9PiQL3kQMC&pg=PA394&lpg=PA394&dq=exercise+induced+asthma+thyroid&source=bl&ots=ahNvkskYXH&sig=BBdmHlRXtcEbwh7UTKaFdsgaBcE&hl=en&sa=X&ved=0ahUKEwiFsOSal4fKAhUB6WMKHRPDBDsQ6AEIQzAF#v=onepage&q=exercise%20induced%20asthma%20thyroid&f=false

vitamin D and p450
http://www.ncbi.nlm.nih.gov/pubmed/23564710

p450 causes vasodilation issues

exercise in cold air normally induces vasodilation

vit D and exercise asthma
https://www.researchgate.net/publication/47755411_Serum_vitamin_D_levels_and_exercise-induced_bronchoconstriction_in_children_with_asthma

asthma, hypothyroid, and noncardiogenic pulmonary edema
http://www.ncbi.nlm.nih.gov/pubmed/25866647

Second generation anti-histamines are substrates or modulators of p450

Are fungal infections the cause of exercise induced asthmas?


Staph asthma

eczema was connected to indoor allergies

is this the aspirin sensitive asthma?
http://www.ncbi.nlm.nih.gov/pubmed/23564710

note that staph does not like aspirin
http://dartmed.dartmouth.edu/winter03/html/vs_aspirin.shtml

the quorum of MARSA is phenol-soluble modulin (not in normal staph)
https://en.wikipedia.org/wiki/Phenol-soluble_modulin

high phenols where found in the urine of asthma patients but were assumed to be that of pesticides
http://www.medpagetoday.com/MeetingCoverage/AAAAI/37516

phenols induce vasodilation...red wine
http://www.ncbi.nlm.nih.gov/pubmed/15967426

 chronic urticaria can also be triggered by aspirin and has good response to second generation antihistamines

Aspirin induced asthma
https://en.wikipedia.org/wiki/Aspirin-induced_asthma

Samters triad: asthma, polyps, aspirin allergy


H. pylori/ Campylobacteria with asthma or it really COPD ?

COPD increases the risk of infection
https://www.ncbi.nlm.nih.gov/pubmed/15534156
https://www.ncbi.nlm.nih.gov/pubmed/21175903

gerd (gastric reflux ) and asthma
http://www.mayoclinic.org/diseases-conditions/asthma/expert-answers/asthma-and-acid-reflux/faq-20057993

asthma and COPD overlap
https://www.ncbi.nlm.nih.gov/pubmed/25712010
https://www.ncbi.nlm.nih.gov/pubmed/28283854

GERD and COPD
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4574848/

COPD and h.pylori? questionable
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4261373/
https://www.ncbi.nlm.nih.gov/pubmed/15733502

h.pylori and adult onset asthma (it is protective in children)
https://link.springer.com/article/10.1007%2Fs10096-017-2972-1

COPD and peptic ulcers
https://www.ncbi.nlm.nih.gov/pubmed/22348540
https://www.jwatch.org/jg201203090000003/2012/03/09/copd-associated-with-increased-risk-peptic-ulcer

smoking and peptic ulcers
https://www.ncbi.nlm.nih.gov/pubmed/3053883

smoking, peptic ulcers, and H.pylori
https://www.ncbi.nlm.nih.gov/pubmed/10958211

H.pylori and bronchitis
https://www.ncbi.nlm.nih.gov/pubmed/16565595

Fish allergy
Tree nut allergy not involving peanuts : walnuts, pecans
Cat hair allergy

almond milk and GERD
http://www.aaaai.org/ask-the-expert/food-reaction-gerd

Pine nut oil as a cure for peptic ulcers
https://www.linkedin.com/pulse/get-rid-peptic-ulcers-good-pine-nut-oil-janice-rosenthal/

http://www.sacredearthnetwork.net/group/medicinewheelnaturesremediesandrecipeslotionsandpo/forum/topics/siberian-pine-nut-oil-how-a-folk-remedy-found-its-way-into-scient

Does h.pylori and campylobacteria not like something in tree nuts?

Bacteria ulcers are a common fish problem.  Could this cause the fish allergy somehow?


ataxia and GERD
https://www.ehealthme.com/cs/gerd/ataxia/

ataxia, h.pylori and Stomach problems
https://healthunlocked.com/ataxia-uk/posts/134618233/ataxia-stomach-problems-and-lycopene

could this cause the fish allergy?

histamine fish poisoning ???
https://emedicine.medscape.com/article/1009464-overview

h.pylori and histamine ????
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC496809/






Follicular dendritic lymphoma and Co-carcinogenesis

Co-carcinogenesis: a virus and a carcinogen together cause cancer. Taking Francis Peyton Rous’ hypothesis further, the carcinogen is a polymerase inhibitor which binds the viral polymerase with higher affinity. Thus the DNA methylation state has been changed but the virus is no longer viable.  DNA damage does not cause most cancers, the interaction of carcinogens and viruses do.  Further these cancers wear the receptors that the virus that triggered it used to enter and the characteristics of the cancer will be from the receptor's pathways.

follicular lymphoma
http://www.cancerresearchuk.org/about-cancer/follicular-dendritic-cell-fdc-sarcoma/about

Castleman's disease and HHV8
https://en.wikipedia.org/wiki/Castleman%27s_disease

HHV8 is the Kaposi's sarcoma virus
https://en.wikipedia.org/wiki/Kaposi%27s_sarcoma-associated_herpesvirus

vaccine against follicular lymphoma
https://www.news-medical.net/news/2005/11/09/14390.aspx

Tattoo ink as the carcinogen of the lymph nodes
https://www.researchgate.net/publication/230570212_Tattoo_Pigment_Lymphadenopathy_Mimicking_Metastasis_in_Vulvar_Cancer

With the current popularity of Tattoos will this form of cancer increase?

HHV8 and the alpha estrogen receptor
http://d-scholarship.pitt.edu/13517/

alpha estrogen receptor is a marker for follicular dendritic cells
https://www.ncbi.nlm.nih.gov/pubmed/14507640

In order for Cancer to occur the virus must trigger the cell division cycle.  Knudson's Retinoblastoma protein genes are the target of nuclear viral proteins.
http://www.nature.com/onc/journal/v25/n38/full/1209621a.html

Knudson's 2 hit RB cancer gene is the lynch pin to the cell division cycle start
http://angelabiggs.blogspot.com/2017/10/knudsons-heredity-2-hit-cancer-compared.html
(this form does not involve a viral start but most cancers will need a virus to pull this lynch pin)

Thursday, November 9, 2017

TNF and Follicular Dendritic Cells Review thoughts

TNF beta (lymphotoxin-alpha)  Is expressed by Bcells to stimulate Follicular Dendritic Cells

TNF C (lympotoxin-beta) Is expressed by macrophages and dendritic cells to stimulate Follicular Dendritic Cells

B cells, macrophages and dendritic cells are Antigen presenting molecules

FDC are not really dendritic cells; they are non migratory cells at the lymph nodes involved in the development of Bcells

TNF alpha Is secreted when macrophages, dendritic cells, or B cells are infected.  Almost as if to say....the immune system can't go tell the FDC cells....panic now and call the NK cells.

TNF alpha and TNF beta have 74% homology

FDC cells take up antigens through complement receptors and FC receptors. FC receptors take up antigens attached to antibodies and antigens on albumin?


Tuesday, November 7, 2017

Follicular dendritic cells, the Fc receptor, and albumin antigen binding

Follicular dendritic cells

Review paper of FDC
https://www.ncbi.nlm.nih.gov/pubmed/12163300

Albumin and IgG: the Fc receptor binds both
https://www.frontiersin.org/articles/10.3389/fimmu.2014.00682/full

Fc receptors on Follicular dendritic cells
https://www.ncbi.nlm.nih.gov/pubmed/10843680
https://www.ncbi.nlm.nih.gov/pubmed/14634109

HIV infects FDC cells
https://www.ncbi.nlm.nih.gov/pubmed/12163303

HIV is a retrovirus. Retroviruses infect using LH/albumin binding receptors (my hypothesis). Could HIV infect using the Fc receptors?
http://angelabiggs.blogspot.com/2017/03/albumin-binding-receptors-and.html

human serum albumin alone binds bacterial products
http://www.sciencedirect.com/science/article/pii/S0168827814002657

albumin and the immune system
http://www.scopemed.org/?mno=10124


FDC have high levels of C3 complement receptors and they display the antigen carried by them or from antibodies taken in by Fc receptors.

Could FDC also be taking in albumin with antigens bound to them using the Fc receptor?

TNF alpha increased plasma albumin
https://www.ncbi.nlm.nih.gov/pubmed/9513905

peyer's patches removed caused higher albumin
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1554968/

the lymph fluid contains albumin as well...think of albumin as an protein sponge collecting things

How do follicular dendritic cells collect antigens for display? Can FDC collect antigens from albumin?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3023135/

Sunday, November 5, 2017

T.gondii infections and the immune system response

T. gondii

Host ER and mitochondria are attacked by  T.gondii
https://www.ncbi.nlm.nih.gov/pubmed/9378762

When the ER malfunctions proteins do not make it to the surface of the cell: IFN gamma is involved

TNF alpha means macrophages are infected as well as regular cells.

Il-21 is found with the infections too large for macrophages to consume like fungal infections these t. gondii infections would also require il-21

il-21 and t.gondii
https://www.ncbi.nlm.nih.gov/pubmed/23667536

il-21 activates the NK
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2433320/

NK comes and drops "perforin" which helps breakdown large infections

perforin: is similar to c9. They creates transmembrane holes
https://en.wikipedia.org/wiki/Perforin

Perforin is released by NK and CTLs

t.gondii and TH17
http://iai.asm.org/content/80/4/1437.full

Previously called the TH17 the "second popping" because it is responsible for opening up things within the Host cells (host cell popped and then more needs to be popped)
http://angelabiggs.blogspot.com/2017/10/th17-called-for-second-popping-of.html

The damage to the host ER sets of the il-23

T.gondii and il-23
http://jem.rupress.org/content/206/13/3047

t.gondii and il-17

http://iai.asm.org/content/73/1/617.full
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3757499/
https://academic.oup.com/jid/article/202/3/427/830922/Interleukin-17-Receptor-Signaling-Is-Deleterious

il-17 is seen when infections infect or reach the mitochondria or nuclear regions of host cells

T.gondii actually pulls close the hosts mitochondria and enlarges them
http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1001846

Oddly il-27 seems to counter the il-17 during a T.gondii infection
https://www.ncbi.nlm.nih.gov/pubmed/16906166?dopt=Abstract&holding=npg

il-27 and abnormal growth of tumors and cancer
https://www.hindawi.com/journals/mi/2017/3958069/

Is this il-27 because of the abnormal growth of the mitochondria?


Tuesday, October 31, 2017

TH17 Called for a "second popping of membranes" then the cytokines that signify where

TH17 are called with the infections is too huge for macrophages to consume or if the infections are hiding inside cells where a second popping of membranes is required.

TH17 and mycobacteria
https://www.hindawi.com/journals/mi/2015/854507/

TH17 and mycoplasmas
https://www.ncbi.nlm.nih.gov/pubmed/27240139

TH17 and chlamydia

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0162445

TH17 and candida / salmonella
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3652671/

TH17 and herpes zoster (mitochondria)
http://www.globethesis.com/?t=2284330488484866

TH17 and HIV (nucleus)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2886291/

TH17 and EBV (nucleus)
http://www.bloodadvances.org/content/1/17/1324

Now lets look at the cytokines to help identify where in the cell the infections are

il-19 il-24 and filarial infections (round worms)
https://www.ncbi.nlm.nih.gov/pubmed/26486636

il-18 mycoplasmas nesting in the ER

il-17 viral/ bacterial infection disruption of mitochondria or nucleus

il-21 fungal outside of cell which needs to be cut down

il-22 mycobacteria in cytosol

il-23 chlamydia/ gonorrhoeae/ h.pylori in vacuoles

il-24 salmonella in the golgi

perforin: like c9 they creates transmembrane holes
https://en.wikipedia.org/wiki/Perforin

perforin is released by NK and CTLs

il-21 activates the NK
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2433320/

il-17 and il-22 together trigger il-20
https://www.ncbi.nlm.nih.gov/pubmed/19731362

mitochondrias could have evolved from mycobacterias
https://academic.oup.com/jmicro/article-abstract/6/1/47/1014811?redirectedFrom=PDF

mycobacterias destroy the mitochondria during infection
https://www.ncbi.nlm.nih.gov/pubmed/14507307

which is why il-22 of the cytosol and il-17 of the mitochondria are both expressed in mycobacteria infections triggering il-20

TH17 make a pore

il-26 PORE (used for a second popping of membranes like the mitochondria and nucleus or internalized infections)
https://www.nature.com/articles/ni.3211

( TLR-9 I had linked to being the net of the mitochondria )
http://angelabiggs.blogspot.com/2017/01/tlrs-toll-like-receptors-summary.html

il-26 and herpes viruses
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0070281

il -26 is often expressed with il-22
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2997847/

which makes sense if mycobacterias trigger il-22 and mycobacterias' damage the mitochondria


Golgi:

salmonella nests inside of cells in vacole near golgi
https://www.ncbi.nlm.nih.gov/pubmed/18778407

Golgi and il-24 with melanoma (supporting connection)
https://www.ncbi.nlm.nih.gov/pubmed/15126330

golgi and ER relationship....IFNgamma
https://www.ncbi.nlm.nih.gov/pubmed/10712678

ifn gamma and tnf with salmonella
https://www.karger.com/Article/Pdf/163643

Vacuoles:

Chlamydia moves inside of cells to replicate
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4886739/

gonorrhoeae replicates in the cytosol of host cells
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3129011/

mmp-9, vacuolar degeneration, the intestine
http://www.nature.com/modpathol/journal/v16/n2/full/3880724a.html

mmp-9 increases with chlamydia infection
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1230927/

leishmania and vacuoles
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1360340/

HIV collects in vacuoles too
https://books.google.com/books?id=uV3sCAAAQBAJ&pg=PA252&lpg=PA252&dq=hiv+vacuoles&source=bl&ots=0nyQZ4WAnZ&sig=AZ9vsBc-EhL_yZjId1XoTVu3FHs&hl=en&sa=X&ved=0ahUKEwiG7YCJipvXAhUL5WMKHRWzC2AQ6AEIYDAO#v=onepage&q=hiv%20vacuoles&f=false

HIV and il-23
http://www.croiconference.org/sites/all/abstracts/245.pdf

CMV and il-23
https://bmcimmunol.biomedcentral.com/articles/10.1186/s12865-016-0175-7

CMV and vacuoles
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC149787/

H.pylori and il-23
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3342083/

H.pylori replicates in vacuoles
http://iai.asm.org/content/78/10/4157.full

Endoplasmic Reticulum:

ER and il-18
http://www.jimmunol.org/content/196/1_Supplement/207.1

mycoplasmas and the ER (electron microscope images)
https://www.ncbi.nlm.nih.gov/pubmed/25651334
http://www.tandfonline.com/doi/pdf/10.1080/00087114.1970.10796399
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4325531/

polyomavirus and il-18
https://www.ncbi.nlm.nih.gov/pubmed/26863474

polyomaviruses infect the ER

il-18 acts on TH1 cells to make IFN gamma

Note that when the ER is infected self proteins do not make it to the surface which means there will be no self proteins to be recognized.  An ER infected cell will look like a foreign cell which explains why IFNgamma is the default.  Kill anything that doesn't have self proteins on the outside.


Immunology Review paper
https://manugowdagn.files.wordpress.com/2016/01/kuby-immunology-7th-edition-2013.pdf

Think of the surface of infections:

Staph has a fairly flat surface and the antibodies of complement work well.

Strep has sugars sticking up making it harder for antibodies to touch but the lectin-mannose pathway works.

E.coli has a furry mess of a surface making it next to impossible for things to collect on the surface so the alternative pathway is followed.

Then you have the TH17 infections.  These are the infections that are too large or moving inside of the host cells.  Which means a second wave of membrane breaking must occur.

I believe that some cytokines help coordinate where the infections are.



Tuesday, October 24, 2017

p53

What about p53?

P53 is a transcription factor.  P53 would end a cancer cell if functional. (but it doesn't start the cancer) This would be one of the most critical defense genes against cancer.

P53 regulates cell cycle and pushes cells from stem to differentiated
http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1001268
https://www.ncbi.nlm.nih.gov/pubmed/1614522

P53 review:  haulting growth, repair, apoptosis (so low levels are common)
http://www.bioinformatics.org/p53/introduction.html

50% of cancers have lost the P53 gene (mutation or inactivation)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3756401/
http://www.nature.com/onc/journal/v26/n15/full/1210280a.html

The cancers with p53 may be the "chemo-resistant" cancers
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3756401/

In breast cancer the p53 mutation appears with the most aggressive forms
https://breast-cancer-research.biomedcentral.com/articles/10.1186/bcr426

Triple negative Breast cancer and p53 mutations
https://www.futuremedicine.com/doi/abs/10.2217/bmt.13.59?journalCode=bmt

Methylation of p53 in ovarian cancer
https://www.ncbi.nlm.nih.gov/pubmed/22855178

methylation of p53 decreases its ability to arrest the cell cycle
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2762123/

The methylated version is with the slower cancers

In order for viruses to replicate in the nucleus they must control the P53....seems confusing

EBV (herpes virus) and P53
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3754062/

SV40 (polyomavirus) inhibits P53 completely or mutates it
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1560412/
https://www.ncbi.nlm.nih.gov/pubmed/9129663

HPV (human papilloma virus)  inhibits P53
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC236349/

But in co-carcinogenesis the virus polymerase has been bound by the carcinogen and the viral proteins are not made. 

But there is a difference between viruses. Some infect using receptors that methylate DNA while others use receptors that would demethylate.

Herpes viruses which are connected to estrogen receptors methylate.
HPVs which are connected to cannabinoid receptors demethylate.

EBV has been associated with Ovarian and estrogen positive breast cancer.
HPV has been associated with TNBC and cervical.

P53, HPV, and cervical cancer
https://www.ncbi.nlm.nih.gov/pubmed/21672450