Monday, November 13, 2017

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

Mycobacteria Asthma


bipolar and type 2 diabetes

bipolar, metabolic disorder, and autoimmune disorder

older post with 2 types of bipolar:

CMV with schizophrenia and this bipolar 1 which is autoimmune while the mycob. is not?

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

cGMP and asthma

 asthma and metabolic syndrome

high cholesterol and asthma

cGMP is inhibited at night

Is this the nighttime asthma?

Fungal Asthma

Baker's asthma and rhinitis

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

vitamin D and p450

p450 causes vasodilation issues

exercise in cold air normally induces vasodilation

vit D and exercise asthma

asthma, hypothyroid, and noncardiogenic pulmonary edema

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?

note that staph does not like aspirin

the quorum of MARSA is phenol-soluble modulin (not in normal staph)

high phenols where found in the urine of asthma patients but were assumed to be that of pesticides

phenols induce wine

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

Aspirin induced asthma

Samters triad: asthma, polyps, aspirin allergy

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

COPD increases the risk of infection

gerd (gastric reflux ) and asthma

asthma and COPD overlap


COPD and h.pylori? questionable

h.pylori and adult onset asthma (it is protective in children)

COPD and peptic ulcers

smoking and peptic ulcers

smoking, peptic ulcers, and H.pylori

H.pylori and bronchitis

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

almond milk and GERD

Pine nut oil as a cure for peptic ulcers

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

ataxia, h.pylori and Stomach problems

could this cause the fish allergy?

histamine fish poisoning ???

h.pylori and histamine ????

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

Castleman's disease and HHV8

HHV8 is the Kaposi's sarcoma virus

vaccine against follicular lymphoma

Tattoo ink as the carcinogen of the lymph nodes

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

HHV8 and the alpha estrogen receptor

alpha estrogen receptor is a marker for follicular dendritic cells

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.

Knudson's 2 hit RB cancer gene is the lynch pin to the cell division cycle start
(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

Albumin and IgG: the Fc receptor binds both

Fc receptors on Follicular dendritic cells

HIV infects FDC cells

HIV is a retrovirus. Retroviruses infect using LH/albumin binding receptors (my hypothesis). Could HIV infect using the Fc receptors?

human serum albumin alone binds bacterial products

albumin and the immune system

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

peyer's patches removed caused higher albumin

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?

Sunday, November 5, 2017

T.gondii infections and the immune system response

T. gondii

Host ER and mitochondria are attacked by  T.gondii

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

il-21 activates the NK

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

perforin: is similar to c9. They creates transmembrane holes

Perforin is released by NK and CTLs

t.gondii and TH17

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)

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

T.gondii and il-23

t.gondii and il-17

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

Oddly il-27 seems to counter the il-17 during a T.gondii infection

il-27 and abnormal growth of tumors and cancer

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

TH17 and mycoplasmas

TH17 and chlamydia

TH17 and candida / salmonella

TH17 and herpes zoster (mitochondria)

TH17 and HIV (nucleus)

TH17 and EBV (nucleus)

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)

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

perforin is released by NK and CTLs

il-21 activates the NK

il-17 and il-22 together trigger il-20

mitochondrias could have evolved from mycobacterias

mycobacterias destroy the mitochondria during infection

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)

( TLR-9 I had linked to being the net of the mitochondria )

il-26 and herpes viruses

il -26 is often expressed with il-22

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


salmonella nests inside of cells in vacole near golgi

Golgi and il-24 with melanoma (supporting connection)

golgi and ER relationship....IFNgamma

ifn gamma and tnf with salmonella


Chlamydia moves inside of cells to replicate

gonorrhoeae replicates in the cytosol of host cells

mmp-9, vacuolar degeneration, the intestine

mmp-9 increases with chlamydia infection

leishmania and vacuoles

HIV collects in vacuoles too

HIV and il-23

CMV and il-23

CMV and vacuoles

H.pylori and il-23

H.pylori replicates in vacuoles

Endoplasmic Reticulum:

ER and il-18

mycoplasmas and the ER (electron microscope images)

polyomavirus and il-18

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

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


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

P53 review:  haulting growth, repair, apoptosis (so low levels are common)

50% of cancers have lost the P53 gene (mutation or inactivation)

The cancers with p53 may be the "chemo-resistant" cancers

In breast cancer the p53 mutation appears with the most aggressive forms

Triple negative Breast cancer and p53 mutations

Methylation of p53 in ovarian cancer

methylation of p53 decreases its ability to arrest the cell cycle

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

SV40 (polyomavirus) inhibits P53 completely or mutates it

HPV (human papilloma virus)  inhibits P53

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