Re: Tumor necrosis factor-alpha (TNF-A)

[Guest guest]

Hi KC, this is a good article, so very interesting reading. but there

was debate on what causes opoptosis and necrosis,tnf. I did alit of

research on this awhile back. the way I understood it is that

neutrophils are called on to fight toxins and necrosis,tnf is

supposed to rid our body of dead neutrophils. where opoptosis happens

after attack of non-toxic assults.I dont think tnf goverens this

function but I'd have to go back and refresh my memory to be sure.

may find something under opoptosis vs. necrosis

--- In , " tigerpaw2c " <tigerpaw2c@...>

wrote:

>

> SYNONYMS

> Lymphotoxin B, Cachectin.

>

>

http://www.bio.davidson.edu/courses/immunology/Students/spring2000/wo

> lf/tnfalpha.html

>

>

> --------------------------------------------------------------------

-

> -----------

>

> FUNCTION

> Tumor necrosis factor-alpha (TNF-A) is a pleiotropic inflammatory

> cytokine. It was first isolated by Carswell et al. in 1975 in an

> attempt to identify tumor necrosis factors responsible for necrosis

> of the sarcoma Meth A (Carswell et al., 1975). Most organs of the

> body appear to be affected by TNF-A, and the cytokine serves a

> variety of functions, many of which are not yet fully understood.

> The cytokine possesses both growth stimulating properties and

growth

> inhibitory processes, and it appears to have self regulatory

> properties as well. For instance, TNF-A induces neutrophil

> proliferation during inflammation, but it also induces neutrophil

> apoptosis upon binding to the TNF-R55 receptor (Murray, et al.,

> 1997). The cytokine is produced by several types of cells, but

> especially by macrophage. Tracey and Cerami suggest two beneficial

> functions of TNF-A which have lead to its continued expression

> (1990). First, the low levels of the cytokine may aid in

> maintaining homeostasis by regulating the body's circadian rhythm.

> Furthermore, low levels of TNF-A promote the remodeling or

> replacement of injured and senescent tissue by stimulating

> fibroblast growth.

>

> Additional beneficial functions of TNF-A include its role in the

> immune response to bacterial, and certain fungal, viral, and

> parasitic invasions as well as its role in the necrosis of specific

> tumors. Lastly it acts as a key mediary in the local inflammatory

> immune response. TNF-A is an acute phase protein which initiates a

> cascade of cytokines and increases vascular permeability, thereby

> recruiting macrophage and neutrophils to a site of infection. TNF-

A

> secreted by the macrophage causes blood clotting which serves to

> contain the infection. Without TNF-A, mice infected with gram

> negative bacteria experience septic shock (Janeway et al., 1999).

>

> The pathological activities of TNF-A have attracted much

attention.

> For instance, although

>

[Guest guest]

apoptosis vs. necrosis/chart

http://www.qub.ac.uk/cm/pat/undergraduate/Basiccancer/necrosis_v_apoptos

is.htm

this is how I look at this

apoptosis-non-toxic irritants,fungi/mold fragments,ect.

necrosis-mycotoxins and chemical toxins,bacterial and viral toxins,ect.

severe/prolonged mycotoxin exposure is known to cause aplastic anemia

aplastic anemia is little or no neutrophils produced by bone marrow

neutrophils are called on to attack toxins that are attacking mucosa

lineings.