I don't see the sense in this. Phagocytes probably do not work well in a high salt solution but eating more salt does not give you high salt solution in the body - you just pee out more salt each day and the sodium level stays the same. All the stuff about inflammation sounds half-baked.
Biology is not my thing but are there implications with the nanoneedle and their use of salt as a stressor?
This looks different to ME? Isn't complex II supposed to be working ok in ME, but complex V is not? But then complex II wasn't tested in salt AFAIR, so who knows. How long does it take for the nanoneedle to register any changes? The quote below is from a hypothesis paper that speculates about salt issues in ME and the nanoneedle. I don't really understand it but it seems to propose a different mechanism from the one described in the OP. https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-021-02833-2 Discussed here: https://www.s4me.info/threads/patho...ces-in-me-cfs-2021-wirth-scheibenbogen.20256/
I've seen complex two mentioned in the context of ME as well, but I can't remember where. Exposing the immune cells to salt outside the body is not the same as what happens in the body when we eat salt. Giving someone a 6gr supplement of salt seems silly, as a rule of thumb we're told that generally people eat ~10g/salt a day, if that is the case for these participants they would have a total intake of 16g. That's a lot, and probably not something most people would consume. Neither would most people consume six grams in one go. Giving someone pizza and taking their blood afterwards says nothing about the salt in the pizza being the cause for any changes seen in the blood. In the nanoneedle, didn't they just use salt as a general stressor for the cells, not to test a theory that hyperosmotic stress specifically would create a signal?