Pandora didn’t unleash evils on the world by opening her box. Rather, the evils existed; the world didn’t have a name for them or understood what they were. So the ancients made up stories about gods fighting and striking a stone with a staff and constellations and planetary motion. Maybe there’s some truth in some of those stories? Who knows. Coincidences happen.
We have a new study led by Dr. Katherine King of the Baylor College of Medicine and Texas Children’s Hospital that may tell us more than we have ever known about what ails us. And if you have a paranoid streak, put on your seatbelt.
Current theory holds that the root of our immune system is in gut bacteria. However, the mechanism for resisting injury and disease is via white blood cells that are generated in bone morrow. In those two sentences, there is a massive complexity that we still don’t fully understand. We’re learning.
In simple terms, Dr. King’s research shows that long term infections can cause mutations in the production of white blood cells that make us more vulnerable to
- Blood cancers
- Cardiovascular disease
- Death from all causes.
Humans are born with tens of thousands of hematopoietic stem cells (HSCs) that collectively ensure lifelong production of blood and immune cells that protect us from infections. HSCs can either duplicate to produce more stem cell progeny or differentiate to produce distinct immune cell lineages, an extremely critical decision that ensures that the body achieves the fine balance between having enough immune cells to fight invaders while still retaining enough HSCs to maintain future blood production.https://medicalxpress.com/news/2021-03-reveals-long-term-infection-inflammation-impairs.html
The mutations may be necessary to fight specific infections, but they subtract resources from the core mission of HSCs, and may increase vulnerabilities to new infections. The accumulations of mutations is a process called clonal hematopoiesis, and creates distinct subpopulations that may have little value in production of new general immune cells. Clonal hematopoiesis seems to pick up just after age 50. Current thinking is focusing on mutations in a DNMT3A gene.
Basically, specialization of cells to fight one disease decreases the body’s ability to produce cells to fight other diseases. This dissipation of the body’s defenses may explain some of the ways in which we die.
What we don’t know from this research is the potential impact of COVID-19 on these immune cells or if there is a relationship between PASC and clonal hematopoiesis.
Interestingly, some viral and bacterial infections prompt the release of “interferon gamma (IFNγ) by the immune system, which in turn, initiates a cascade of protective immune responses.” These responses promote the creation of original immune cells, sacrificing effectiveness in fighting the specific infection prompting the IFNy release. IFNy may provide a path for rebuilding immune systems.
This is a very exciting article providing insight into the mechanics of death and how we might be able to prolong quality of life.
- Daniel Hormaechea-Agulla et al, Chronic infection drives Dnmt3a-loss-of-function clonal hematopoiesis via IFNγ signaling, Cell Stem Cell (2021). DOI: 10.1016/j.stem.2021.03.002