Re: Cytokines

[Guest guest]

This sounds like very interesting information to have, i.e., one's cytokine

status, but I am wondering how those who have had this testing have been able

to apply the results in a practical way. In other words, if yer cytokines

are screwy, what do ya do then? Happy Holidays to All,

[Guest guest]

Cytokines web site, more than I can ever learn!

http://www.copewithcytokines.de/cope.cgi

Marcia

[Guest guest]

Sue,

Do you know if the results of this study were ever published. Was it

a cfs study. I've been intrigued by what little I have read on

cytokine reasearch and cfs.

> " I went from being totally disabled and bedridden to functioning

at an

> almost normal level, for the last 3 years. I have my own business

now, and

> am very successful and self supportive.

>

> I was part of a study 3 years ago, using IL2. It saved my life. "

>

>

[Guest guest]

> Sue,

>

> Do you know if the results of this study were ever published. Was

it

> a cfs study. I've been intrigued by what little I have read on

> cytokine reasearch and cfs.

>

>

>

> > " I went from being totally disabled and bedridden to functioning

> at an

> > almost normal level, for the last 3 years. I have my own business

There's a good article in the Western J of Med, about cytokines

generated by physical illnesses causing Depression:

http://www.ewjm.com/cgi/content/full/173/5/333?

maxtoshow= & HITS=10 & hits=10 & RESULTFORMAT= & titleabstract=cytokines%

2C+depression & searchid=QID_NOT_SET & stored_search= & FIRSTINDEX=0 & fdate=1

/1/1999 & journalcode=ewjm

I hope the above URL is good.

[Guest guest]

,

Cytokines are immune system messengers but are not all exclusive to the immune

system, they are a form of communication between cells and in most cases they

can directly influence the expression of certain genes. Most often, cytokines

are associated with being pro-inflammatory, but that is not true for all, some

actually counter-regulate the inflammatory ones, and most are able to manipulate

an immune response.

They are a hot area in autism research, and could explain sulphurtransferase

deficiencies [Dr Rosemary Waring reports low activity of this enzyme group and

has identified that the cytokineTumor Necrosis Factor alpha (TNF-a) for example

suppresses its activity]. The study below is an example of what is going on:

--------------------------------------------------------------------------

J Neuroimmunol 2001 Nov 1;120(1-2):170-9

Proinflammatory and regulatory cytokine production associated with innate and

adaptive immune responses in children with autism spectrum disorders and

developmental regression.

Jyonouchi H, Sun S, Le H.

Department of Pediatrics, University of Minnesota, MMC 610 FUMC, 420 Delaware

Street SE, Minneapolis, MN 55455, USA. jyono001@...

We determined innate and adaptive immune responses in children with

developmental regression and autism spectrum disorders (ASD, N=71),

developmentally normal siblings (N=23), and controls (N=17). With

lipopolysaccharide (LPS), a stimulant for innate immunity, peripheral blood

mononuclear cells (PBMCs) from 59/71 (83.1%) ASD patients produced >2 SD above

the control mean (CM) values of TNF-alpha, IL-1beta, and/or IL-6 produced by

control PBMCs. ASD PBMCs produced higher levels of

proinflammatory/counter-regulatory cytokines without stimuli than controls. With

stimulants of phytohemagglutinin (PHA), tetanus, IL-12p70, and IL-18, PBMCs from

47.9% to 60% of ASD patients produced >2 SD above the CM values of TNF-alpha

depending on stimulants. Our results indicate excessive innate immune responses

in a number of ASD children that may be most evident in TNF-alpha production.

PMID: 11694332 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------

This next bit probably goes a bit beyond your question, but if anyone is

interested then please read on.

The same parameters were measured in the study below, though in a different and

non-autistic cell line (fetal alveolar type II epithelial cells) but with the

effect of oxidative stress taken into account by disabling the

glutathione/antioxidant system in various ways:

--------------------------------------------------------------------------------

Inhibition of glutathione-related enzymes augments LPS-mediated cytokine

biosynthesis: involvement of an IkappaB/NF-kappaB-sensitive pathway in the

alveolar epithelium.

Haddad JJ, Safieh-Garabedian B, Saade NE, Lauterbach R.

Department of Anesthesia and Perioperative Care, University of California at San

Francisco, School of Medicine, 94143-0542, USA. haddadj@...

The regulation of lipopolysaccharide (LPS)-mediated pro-inflammatory cytokine

biosynthesis by reduction-oxidation (redox)-sensitive enzymes involved in

maintaining intracellular glutathione homeostasis was investigated in fetal

alveolar type II epithelial cells (fATII). Inhibition of glutathione-oxidized

disulfide reductase, which recycles GSSG --> 2GSH, by the action of

1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU) augmented LPS-dependent secretion

of interleukin (IL)-1beta, IL-6 and tumor necrosis factor (TNF)-alpha. BCNU

increased [GSSG] concentration at the expense of [GSH], thereby favoring

oxidation equilibrium. Inhibition of gamma-glutamylcysteine synthetase, the

rate-limiting enzyme in the biosynthesis of GSH, by the action of

L-buthionine-(S,R)-sulfoximine (BSO), potentiated LPS-induced IL-1beta, IL-6 and

TNF-alpha production. Similar to BCNU, BSO depleted [GSH] and induced the

accumulation of [GSSG]. BCNU and BSO reduced LPS-mediated phosphorylation of

inhibitory-kappaB (IkappaB-alpha), allowing its cytosolic accumulation. This

effect was associated with the inhibition of the nuclear translocation of

selective nuclear factor (NF)-kappaB subunits: NF-kappaB1 (p50), RelA (p65),

RelB (p68) and c-Rel (p75), but not NF-kappaB2 (p52). BCNU and BSO reduced

LPS-induced NF-kappaB activation as determined by the electrophoretic mobility

shift DNA-binding assay. Analytical analysis of the effect of modulating the

dynamic redox ratio ([GSH]+[GSSG])/[GSSG] revealed a novel role for GSSG as a

disulfhydryl compound which mediates an inhibitory effect on NF-kappaB

activation. It is concluded that selective modulation of redox-sensitive enzymes

has an immunopharmacological potential in regulating pro-inflammatory cytokines

and that the TkappaB-alpha/NF-kappaB pathway is redox-sensitive and

differentially involved in mediating redox-dependent regulation of cytokine

signaling.

PMID: 12433058 [PubMed - in process]

--------------------------------------------------------------------------------

The study below IMO serves to illustrate how possible it is that this system

might be involved in autism, chromosome 22q11.2 is home to the glutathione

transferases (GSTT1 & 2), and that the subsequent oxidative stress thus caused

might be able to enhance the cytokine profile upon challenge as outlined in the

first abstract. (credit for the ASD/22q11 & GSTT1 link goes to from the

abmd list BTW). In other words: Below is an actual living 'model' of a disabled

glutathione system which is what is described above. The one below is very

associated with ASD, ADHD and retardation.

--------------------------------------------------------------------------------

Genet Med 2001 Jan-Feb;3(1):79-84

Neuropsychiatric disorders in the 22q11 deletion syndrome.

Niklasson L, Rasmussen P, Oskarsdottir S, Gillberg C.

Department of Child and Adolescent Psychiatry, University of Goteborg, Queen

Silvia Children's Hospital, Sweden.

PURPOSE: This study was undertaken with a view to establishing the occurrence

of neuropsychiatric disorders in the 22q11 deletion syndrome. METHODS:

Thirty-two children and young adults with genetically confirmed 22q11

deletion were given comprehensive neuropsychiatric assessments. RESULTS:

Altogether, 56% had a neuropsychiatric disorder. Only 6% were of normal IQ

and free of physchiatric disorder. Attention-deficit/hyperactivity disorder

was diagnosed in 44% and 31% had an autism spectrum problem. In 16% criteria

for both these diagnoses were met. Fifty-three percent had mental

retardation, often with a test-profile suggesting a nonverbal learning

disorder. CONCLUSION: The findings imply that a majority of children and

adolescents with 22q11 deletion syndrome are in need of neuropsychiatric

assessment and intervention.

--------------------------------------------------------------------------------

Jon.

Cytokines

Can anyone explain cytokines to me? I've read many post on this list

about this and wanted to know more. Someone recently posted that

children may respond differently to treatment depending on what

cytokines are malfunctioning.

[Guest guest]

What's labs/tests show this???

From: Sheri Nakken <vaccineinfo@...>

Subject: cytokines

vaccinations

Date: Thursday, May 7, 2009, 8:33 PM

someone asked about cytokines

Here is some info on Wikipedia (not a fan of wikipedia but this is OK)

http://en.wikipedia .org/wiki/ Cytokines

and here

http://arthritis. about.com/ od/inflammation/ f/cytokines. htm

http://www.microvet .arizona. edu/courses/ MIC419/Tutorials /cytokines. html

http://www.scienced aily.com/ releases/ 2009/05/09050517 4547.htm

A cytokine storm

A cytokine storm occurs when the body's immune system over-reacts to

an intruder, such as a virus, by producing high levels of cytokines,

which are signaling chemicals that help mobilize immune cells capable

of removing infectious agents from the body. When too many cytokines

are produced, they can stimulate an inflammatory response in which

the accumulation of immune cells and fluid at the site of infection

may prevent affected tissues and organs such as the lungs from

functioning properly and may even cause death.

I would suggest that vaccines cause cytokine storms and inflammation

and on and on

I'll see if I can find more in relation to vaccines

Sheri

[Guest guest]

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See

bottom paragraph.  Perhaps if they asked some basic questions about vaccine

pathways, they might come up with other things which later are also said to be

blindingly obvious

 

http://www.the-scientist.com/blog/display/55678/

 

Home of immune memory found

Posted by Edyta

Zielinska

[Entry posted

at 7th May 2009 05:19 PM GMT]

View

comment(1) | Comment on this news

story   

New findings

overturn a major model of where immune memory is stored. Rather than circulating

throughout body, as researchers had thought, memory T-cells actually reside in a

comfortable niche in the bone marrow waiting for the next chance to fight

infection, according to a new

article publishing online in Immunity today (May 7th).

" It's very

exciting data, " said Lanzaveccia from the Institute for Research in

Biomedicine in Switzerland, who was not involved in the research. It would be

important to see " what the relationship is between these memory cells and other

memory cells that have been described, " he added.

s Radbruch from

the Charité German Rheumatology Center in Berlin and colleagues wanted to take a

closer look at T memory cells because in earlier studies they had found that

memory B-cells, which produce antibodies, reside in the bone marrow.

Immunologists have long believed that memory cells come from activated

effector T cells that have resigned their ability to fight, and simply remain in

circulation until they are re-activated a second time by the same pathogen they

initially attacked. Researchers have been able to easily isolate circulating

memory T-cells in human subjects, said Lanzaveccia, but accessing bone marrow is

much more difficult.

To test whether memory T cells stayed in

circulation or retreated to the bone marrow, Radbruch and first author Koji

Tokoyoda, also at the German Rheumatology Center, infected a mouse with a

pathogen, and then searched for the T-cells specific to that pathogen at

different time points. As expected, the specific T-effector cells at first

proliferated to fight the infection. Four days in, researcher detected the

memory cells mainly located in the lymphoid organs and spleen. But 3-8 weeks

after infection -- by which time the remaining cells would have turned into

memory cells -- the researchers searched again for those pathogen-specific cells

and found that more than 80% of them were now in the bone marrow. These cells

remained there for up to 134 days -- the length of time the researchers tested.

To make sure the cells they detected in the bone marrow were " true "

memory cells, Radbruch and colleagues characterized their surface molecules and

tested them for the characteristics of memory cells: lack of proliferation,

decreased gene expression, and the ability to reactivate upon re-infection with

the same pathogen they had initially encountered. The cells in the bone marrow

passed all three tests. The remaining 20% of cells not in the bone marrow

probably belonged to a subset of T-memory cells that had been reactivated or

were reacting to chronic infection, Radbruch suggested.

Radbruch and

colleagues wanted to find out what attracted the memory cells to the bone

marrow. The prime suspect: an adhesion molecule called alpha2 integrin. The

molecule showed increased expression on memory cells, and its ligand is

predominantly expressed in bone marrow tissue. Also, when the researchers

blocked alpha2 integrin with an antibody, the cells no longer homed to the bone

marrow.

Researchers went on to characterize the interaction between the

memory cells and their bone marrow niche. " What I find totally exciting about

this [paper], " said Lanzaveccia, is that " it has very nice and quantitative

data. " The researchers counted the number of memory cells in the bone marrow,

nestled in niches producing nurturing cytokines, to be as high as 5 million. The

authors hypothesize that the bone marrow offers memory cells an environment rich

in cytokines essential for their survival. IL-7, for example, richly present in

bone marrow, helps T-cells that aren't actively proliferating, survive.

The paper poses such a basic question in immunology, Radbruch

said, that one of his reviewers had asked why no one has thought to do such an

experiment before. " All the good papers are like that, " said Lanzaveccia: They

make an experimenter think, " Gosh I should have thought of that! "

 

From: Sheri Nakken <vaccineinfo@...>

Subject: cytokines

vaccinations

Date: Thursday, May 7, 2009, 8:33 PM

someone asked about cytokines

Here is some info on Wikipedia (not a fan of wikipedia but this is OK)

http://en.wikipedia .org/wiki/ Cytokines

and here

http://arthritis. about.com/ od/inflammation/ f/cytokines. htm

http://www.microvet .arizona. edu/courses/ MIC419/Tutorials /cytokines. html

http://www.scienced aily.com/ releases/ 2009/05/09050517 4547.htm

A cytokine storm

A cytokine storm occurs when the body's immune system over-reacts to

an intruder, such as a virus, by producing high levels of cytokines,

which are signaling chemicals that help mobilize immune cells capable

of removing infectious agents from the body. When too many cytokines

are produced, they can stimulate an inflammatory response in which

the accumulation of immune cells and fluid at the site of infection

may prevent affected tissues and organs such as the lungs from

functioning properly and may even cause death.

I would suggest that vaccines cause cytokine storms and inflammation

and on and on

I'll see if I can find more in relation to vaccines

Sheri

[Guest guest]

Register free for information.

http://www.the-scientist.com/

[Guest guest]

That is a glitch of some sort!

From: Katarina <kkatkov@...>

Subject: Re: cytokines

Vaccinations

Date: Friday, May 8, 2009, 8:44 AM

>

> Info from

>

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> o\:* {behavior:url(#default#VML);}

> w\:* {behavior:url(#default#VML);}

> .shape {behavior:url(#default#VML);}

Sorry, but what is all this?

------------------------------------

[Guest guest]

Also check out 's blog (one of our list members)... there's

several posts back in August of 08 that discuss cytokines and the

whole cellular immunity thing in detail. It's VERY well written and

one of my favorite pieces on the subject. I refer people to it

frequently:

http://unherdof.wordpress.com/2008/08/17/long-lost-cellular-immunity/

or

http://tinyurl.com/73oxpd

On Thu, May 7, 2009 at 7:33 PM, Sheri Nakken <vaccineinfo@...> wrote:

>

>

> someone asked about cytokines

>

> Here is some info on Wikipedia (not a fan of wikipedia but this is OK)

>

> http://en.wikipedia.org/wiki/Cytokines

>

> and here

> http://arthritis.about.com/od/inflammation/f/cytokines.htm

> http://www.microvet.arizona.edu/courses/MIC419/Tutorials/cytokines.html

>

> http://www.sciencedaily.com/releases/2009/05/090505174547.htm

> A cytokine storm

> A cytokine storm occurs when the body's immune system over-reacts to

> an intruder, such as a virus, by producing high levels of cytokines,

> which are signaling chemicals that help mobilize immune cells capable

> of removing infectious agents from the body. When too many cytokines

> are produced, they can stimulate an inflammatory response in which

> the accumulation of immune cells and fluid at the site of infection

> may prevent affected tissues and organs such as the lungs from

> functioning properly and may even cause death.

>

> I would suggest that vaccines cause cytokine storms and inflammation

> and on and on

>

> I'll see if I can find more in relation to vaccines

> Sheri