Re: Downregulation of Cellular Metabolism During Environmental Stress: Mechanisms an

[Guest guest]

and all,

Do you have any studies that would suggest

that any of the tick-borne pathogens might disregulate stat 1?

a

Annu Rev Physiol.

1996;58:539-63. Related Articles, Links

Downregulation of cellular metabolism during environmental stress:

mechanisms and implications.

Hand SC, Hardewig I.

Department of EPO Biology, University

of Colorado, Boulder 80309-

0334, USA.

Survival time of organisms during exposure to environmental stresses

that limit energy availability is, in general, directly related to

the degree of metabolic depression achieved. The energetic cost

savings realized by the organism is a consequence primarily of the

ability to depress ion pumping activities of cells, macromolecular

synthesis, and macromolecular turnover. Evidence supporting the

concept of channel arrest-the reduction in ion leakage across cell

membranes during hypometabolic states-has highlighted the energetic

benefits of limiting ATP turnover related to cellular ion

homeostasis. Depression of protein synthesis results in substantial

bioenergetic savings. However, when protein synthesis is arrested,

the preservation of macromolecules becomes increasingly important as

the duration of quiescence is extended because the cellular capacity

for replenishing these components is reduced. It is likely that the

rate of macromolecular degradation is a key feature that sets the

upper time limit for survival during chronic environmental stress.

Publication Types:

Review

PMID: 8815808 [PubMed - indexed for MEDLINE]

[Guest guest]

> and all,

>

> Do you have any studies that would suggest that any of the tick-

borne

> pathogens might disregulate stat 1?

>

>

>

> a

No. Indeed, I havent seen many examples where the immune-derailing

molecular acts of bacteria have been fully uncovered.

For this reason, the new Yersinia molecule recently posted about here

is interesting.

Another known anti-immune molecule is CPAF, a protein secreted by

chlamydiae that cuts up a human protein that figures in immune

activation control.

But more of these things seem to be unknown than known. For example,

Zhong showed recently that chlamydiae actively prevent apoptosis of

the cells they infect, but so far he cant find the molecule that does

it. Presumably it is some protein that chlamydiae secrete into the

host cell.

Similarly, macrophages infected by M. tuberculosis arent as

immunoactivated as they should be. Mtb " soothes " them, which helps

Mtb survive. But no one knows exactly how Mtb accomplishes this.

I just started learning about the STAT1 stuff last week, and have

been discussing it with ne at cfs_research. I dont really know

enough to say whether the 91/84-STAT1 deficiency is " microbe-

directed " - ie, a result of an immune-system-blocking microbial

molecule. As far as I know (which is not very far at all), the STAT

deficiency conceivably could instead be a host-directed response to a

microbe (or to something else).