Sunday, February 26, 2017

Infected macrophages, TNF alpha, mast cells, and Neutrophils

M. fermatans infection lowers TNF alpha 60%
http://www.nature.com/cdd/journal/v11/n11/full/4401482a.html

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
https://www.ncbi.nlm.nih.gov/pubmed/22502799

the histamine secreted by the mast cells induce exocytosis by macrophages
http://www.jimmunol.org/content/jimmunol/166/6/4083.full.pdf
(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
https://www.ncbi.nlm.nih.gov/pubmed/25727365

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
https://www.ncbi.nlm.nih.gov/pubmed/22752117

T. gondii and suicide
https://www.ncbi.nlm.nih.gov/pubmed/20010026

TLRs and t.gondii
http://www.nature.com/nri/journal/v14/n2/fig_tab/nri3598_F1.html

TLR11 binds profolin of T.gondii (a protein that polymerizes actin during the formation of tails)
https://www.ncbi.nlm.nih.gov/pubmed/18312842

There is a brain-derived-factor connected to suicide which is known to bind tropomyosin-related kinase B (TrkB)
http://www.hdbp.org/psychiatria_danubina/pdf/dnb_vol25_sup2/dnb_vol25_sup2_341.pdf

Tropomyosin is an actin binding regulator of the cytoskeleton
https://www.ncbi.nlm.nih.gov/pubmed/26315888

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

The brains of suicide : disrupted cytoskeletons
https://www.researchgate.net/figure/234000212_fig3_Figure-3-The-protein-network-of-altered-cytoskeleton-proteins-in-the-brains-of-suicide


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
https://www.ncbi.nlm.nih.gov/pubmed/9248995

T.gondii induces apoptosis via ER stress pathway
https://www.ncbi.nlm.nih.gov/pubmed/24612639

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)
http://abstracts.eurospe.org/hrp/0086/hrp0086P2-P308.htm

Are we giving these patients the cataracts?

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

Cortisone induced cataracts
http://www.medhelp.org/posts/Eye-Care-Archive/What-is-a-cortisone-induced-cataract/show/371756

I had previous looked at cataracts and the cortisol levels possibly raised by spirochete infections.
http://angelabiggs.blogspot.com/2016/04/anterior-cingulate-cortex-hoarding.html

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

Panic attacks and cortisol
http://www.ncbi.nlm.nih.gov/pubmed/10698825

Anxiety disorder and cortisol
http://www.ncbi.nlm.nih.gov/pubmed/26934635

Insulin injections have been linked to possibly causing panic attacks in some patients
http://www.factmed.com/report-OPTICLIK%20(INSULIN%20INJECTION%20PEN)-causing-PANIC%20ATTACK.php

Pregnant women with diabetes also have an increased risk of having a child with a cleft palate
https://www.ncbi.nlm.nih.gov/pubmed/11716256

cortisone has been linked to causing cleft palate
http://dev.biologists.org/content/develop/5/2/201.full.pdf







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
     http://angelabiggs.blogspot.com/2017/02/tam-receptors-and-ifns.html

TAM stands for : TYRO3, AXL, and MER

IFN alpha, MER, and TLR7 /TLR9 (mitochondria and nucleus)
https://arthritis-research.biomedcentral.com/articles/10.1186/ar4517

IFN beta, TYRO3, and TLR3 (cytosol)
https://www.ncbi.nlm.nih.gov/pubmed/26085147

IFN gamma, AXL, and natural killer cells (also TLR8 which is the ER)
https://www.ncbi.nlm.nih.gov/pubmed/18840707

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 cell...no 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.
https://www.ncbi.nlm.nih.gov/pubmed/18607390

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
https://www.ncbi.nlm.nih.gov/pubmed/15582201

Coffee and tea interact with Vit D receptor !!!
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3478213/

vit D levels and tea
https://www.vitamindcouncil.org/tea-and-coffee-consumption-linked-to-vitamin-d-status/

Vit D3 promotes Foxp3 expression
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3358577/

ECGC induces Foxp3 expression
http://www.sciencedirect.com/science/article/pii/S0165247811001258

(FOXp3 suppresses the viral Tcell response)

ALS and a fungal infection that has an aflatoxin like compound
http://angelabiggs.blogspot.com/2016/10/amyotrophic-lateral-sclerosis-hla-c.html

aflatoxin binds the Vit D receptor
https://www.citeab.com/publication/1455664-25483621-toxicity-of-aflatoxin-b1-towards-the-vitamin-d-rece

ECGC and ALS?? mouse models?
https://www.ncbi.nlm.nih.gov/pubmed/16356650

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
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4425186/

vit D in atopic dermatitis, asthma, and allergic disease
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2914320/

ECGC inhibited Th1 and Th17
https://portal.nifa.usda.gov/web/crisprojectpages/0220019-green-tea-egcg-and-t-cell-function-in-autoimmune-inflammation.html

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?
https://www.ncbi.nlm.nih.gov/pubmed/10211990

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?
https://www.ncbi.nlm.nih.gov/pubmed/11358719

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

THF alpha and parkinson's
https://www.ncbi.nlm.nih.gov/pubmed/8015728

THF alpha and multiple sclerosis
http://www.medscape.com/viewarticle/583080_9

TNF alpha and psoriasis
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2924720/

TNF alpha and type 2 diabetes
https://www.ncbi.nlm.nih.gov/pubmed/12532159/
http://www.nature.com/ijo/journal/v27/n1/full/0802187a.html

Increased TNF alpha has also been linked to IBD and major depression
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4229361/
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
https://www.ncbi.nlm.nih.gov/pubmed/8832967

Sendai virus infecting macrophages
https://www.ncbi.nlm.nih.gov/pubmed/168154

flu viruses and macrophages
http://www.futuremedicine.com/doi/pdf/10.2217/fvl.14.65
https://www.ncbi.nlm.nih.gov/pubmed/22894921
https://www.ncbi.nlm.nih.gov/pubmed/26423941


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
https://www.ncbi.nlm.nih.gov/pubmed/19047095 (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
https://www.ncbi.nlm.nih.gov/pubmed/25495515

Green tea attacks the mycobacteria that are inside macrophages
https://www.ncbi.nlm.nih.gov/pubmed/16352457


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
http://angelabiggs.blogspot.com/2015/12/mycobacterias-possible-connection-to.html

Mycobacteria use cGMP as a quorum when establishing biofilms to hold them in place
https://www.ncbi.nlm.nih.gov/pubmed/25546058

mycobacteria hide in white adipose tissue
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1762355/

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

cholesterol is stored as white adipose tissue
http://www.jlr.org/content/15/5/491.full.pdf

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