Sunday, February 26, 2017

Infected macrophages, TNF alpha, mast cells, and Neutrophils

M. fermatans infection lowers TNF alpha 60%

RA has anti-TNFalpha

TNF alpha is released by macrophages when they are infected

Mycoplasmas, mycobacterias, and viruses do infect macrophages. (in the case of RA mycoplasmas are the suspects)

The mast cells respond to TNF alpha from infected macrophages with histamine and il-8 secretions

the histamine secreted by the mast cells induce exocytosis by macrophages
(sort of requesting them to throw-up what they have and let the neutrophils take over)

the il-8 calls the neutrophils which are smaller than macrophages and are not APC

the tiny multilobed nucleus of the neutrophils barely function

Since the macrophages keep getting infected themselves the Neutrophils replace them. Neutrophils lack the complete transcriptional and translational machinery which in theory prevents the infection from using the cells resources. (limited functions) Hopefully trapping the infections inside if not destroying them.

Unfortunately this also means that the neutrophils are unable to be APC (antigen presenting cells)

Friday, February 24, 2017

Suicide, t.gondii tails, profolin, and the cytoskeleton

The suicidal tendencies of those infected with T.gondii could be caused by the parasite building it's flaggellum or tail from actin.

 T. gondii and suicide attempts in Denmark mothers

T. gondii and suicide

TLRs and t.gondii

TLR11 binds profolin of T.gondii (a protein that polymerizes actin during the formation of tails)

There is a brain-derived-factor connected to suicide which is known to bind tropomyosin-related kinase B (TrkB)

Tropomyosin is an actin binding regulator of the cytoskeleton

Could profolin like the brain-derived-factor disrupt the tropomyosin?

The brains of suicide : disrupted cytoskeletons

Tangent thoughts about T.gondii

T.gondii's infect macrophages and cause TNF to be released

Host cells's ER is used by T.gondii

T.gondii induces apoptosis via ER stress pathway

Dysfunction of the ER causes the IFNgamma to be expressed

Thursday, February 23, 2017

Insulin, Cortisol, and Cataracts

Cortisol raises blood sugar while insulin lowers it which means when we inject ourselves with insulin our body would respond with an increase in cortisol.

Insulin tolerance tests reveal that the bodies response to high insulin levels is the production of cortisol (through ACTH)

some patients develop cataracts after insulin treatments (after 3 months)

Are we giving these patients the cataracts?

Are the cataracts caused by the high waves of cortisol after injection?

Cortisone induced cataracts

I had previous looked at cataracts and the cortisol levels possibly raised by spirochete infections.

In this post I had looked at panic and anxiety attacks in regard to cortisol

Panic attacks and cortisol

Anxiety disorder and cortisol

Insulin injections have been linked to possibly causing panic attacks in some patients

Pregnant women with diabetes also have an increased risk of having a child with a cleft palate

cortisone has been linked to causing cleft palate

Wednesday, February 22, 2017

Types of macrophages (reviewing)

The types of macrophages

M1 the classically activated macrophage (CAM) which participates in the Th1 pathway (IgG, IgM, and IgA...non hidden infections)

M2 the alternatively activated macrophage (AAM) which participates in the Th2 pathway (IgE hidden infections)  triggered by Il-4

TAM macrophages which have the TAM arms and are involved in the viral pathway

TAM stands for : TYRO3, AXL, and MER

IFN alpha, MER, and TLR7 /TLR9 (mitochondria and nucleus)

IFN beta, TYRO3, and TLR3 (cytosol)

IFN gamma, AXL, and natural killer cells (also TLR8 which is the ER)

MDSC are considered M2-like. Myeloid- Derived Suppressor Cells are triggered by the Natural killer pathway. They are not true macrophages. This pathway is triggered by the destruction of ER  by a virus within the markers are available at the infected cell's surface and these "naked" cells will be destroyed.

IFN gamma is critical in activating MDSC to suppress.

Note that the IFN gamma also suppresses the Th2 pathway where infectious pathogens are hiding (like parasitic worms) as well as stimulating the AXL hands of the TAM macrophages.

IFN gamma is made by TLR8 the nets of infected ER or Natural Killer cells....when surface proteins are not available to bind with AXL and very little HLA-C mailboxes will make it to the surface because the ER of the cell has a virus infection.   

Sunday, February 19, 2017

Vit D receptor, Aflatoxin, ECGC (green tea), FoxP3 expression and ALS

black tea and aflatoxin

Coffee and tea interact with Vit D receptor !!!

vit D levels and tea

Vit D3 promotes Foxp3 expression

ECGC induces Foxp3 expression

(FOXp3 suppresses the viral Tcell response)

ALS and a fungal infection that has an aflatoxin like compound

aflatoxin binds the Vit D receptor

ECGC and ALS?? mouse models?

I need to look at these models

Vit D inhibits Th1 and Th17 yet favors Th2...the route to the IgE response of allergic reaction

vit D in atopic dermatitis, asthma, and allergic disease

ECGC inhibited Th1 and Th17

People can have allergic responses to ECGC (green tea factory workers) and people can have allergic responses to vit D3

Friday, February 17, 2017

Pondering TNF alpha

How do mycobacterias increase the THF alpha?

Adding TNF alpha decreased mycobacteria?

Is this because the mycobacteria are "hiders" moving into macrophages and embedding into white adipose tissue? The macrophages are favoring the Th17 route of hidden pathogens by increasing THF alpha?

Macrophages take up mycobacterias but then the mycobacterias survive inside the macrophage?

Looking at the diseases I have linked to mycobacterias they all appear to have increased TNF alpha

THF alpha and parkinson's

THF alpha and multiple sclerosis

TNF alpha and psoriasis

TNF alpha and type 2 diabetes

Increased TNF alpha has also been linked to IBD and major depression
those on anti-TNF for the IBD developed depression

TNF alpha blockers have been shown to worsen TB. Use of blockers made the illness worse. Is this because the macrophages are hiding?

Hypothesis: Macrophages release TNF at high rates when they themselves have become infected by mycobacterias or viruses

TNF and viruses

Sendai virus infecting macrophages

flu viruses and macrophages

RA patients taking TNF blockers develop something that looks like psoriasis

High TNF alpha also seems to be involved in skin tumors.

HPV which uses cannabinoid receptors causes tumors.

Cannabinoid receptors can cause an increase in TNF alpha (is this the same for skin cells?)

Green tea's EGCG seems to inhibit mycobacteria growth. How does that work?

Green tea's ECGC inhibits mycobacteria cell growth

Green tea attacks the mycobacteria that are inside macrophages

Further EGCG would help nerve growth....Less TNF alpha and more nerve growth factor.

Nerve growth factor/ TNF alpha receptors are on nerve endings and these receptors are in the same "family" of receptors

Tuesday, February 14, 2017

mycobacteria and white adipose tissue

Previous blog connect Fatty liver disease and type 2 diabetes to the cGMP of mycobacteria

Mycobacteria use cGMP as a quorum when establishing biofilms to hold them in place

mycobacteria hide in white adipose tissue

Are they, mycobacterias, picking white because brown would use the mycobacteria's signal cGMP ?

cholesterol is stored as white adipose tissue

Which means this state of high cholesterol causes not just obesity but lots of places for mycobacteria.