Low GSH may not allow the resolution of the inflammation

It seems that low GSH may not allow the resolution of the inflammation (as a process).

Prostaglandin E2 (PGE2) is initially pro-inflammatory. It’s synthesis requires GSH (see gene PTGES).

Next a quote from the review of inflammation process:

Resolution phase

This phase starts with the Eicosanoid Switch to resolution. When the PGE2 and/or PGD2 level is equal to the level of LTB4, the PMNs activate the switch from pro-inflammatory to anti-inflammatory eicosanoids production by limiting the production of LOX-5.

This switch is responsible for the production of anti-inflammatory lipoxins (LXs) from AA (R1)

My hypothesis

Insufficient rate of GSH synthesis may not allow elevation of PGE2/PGD2 to the required level, which leaves the local cells in the state of inflammation because they can’t switch to the next phase by design.

Also availability of Arachidonic acid is both important for initiation and resolution of the process because it’s the only precursor for PGE2 and other prostaglandins of that group.

Additionally, DHA and EPA from membrane phospholipids are involved as a precursor for “resolvins”.

Other quotes

The combined situation of AA deficiency together with a reduced intake of omega 3 fatty acids such as DHA and EPA (necessary for the flip flop reaction of LOX-5 and the Eicosanoid Switch), enable a perpetuation of the pro-inflammatory initiation phase and therefore of chronic inflammation. (R1)

Interesting note:

Theoretically, LA could be the source of a sufficient level of endogenous AA. However, higher intake of LA does not deliver increased levels of AA in comparison to low intake. (R1)

And also from other sources it becomes more evident that we do need to consume Arachidonic acid - it’s synthesis from abundant Linoleic acid is just not sufficient to support highly inflammatory life style.