Inflammation, cancer and stem cells in autoimmune diseases

Three of the principal theories of aging articulated in my are treatise ANTI-AGING FIREWALLS – THE SCIENCE AND TECHNOLOGY OF LONGEVITY are Chronic or Excess Inflammation, Susceptibilities to Cancers, and Decline In Adult Stem Cell Differentiation. Recent research suggests an underlying mechanism that links inflammation, cancer and the role of adult stem cells, at least in the case of autoimmune diseases such as rheumatoid arthritis, Lupus erythematosus, scleroderma and Sjögren’s syndrome.   For some time, it has been noted that these inflammation-promoting autoimmune diseases are associated with elevated probabilities for incidences of cancer, lung cancer in the case of rheumatoid arthritis and lymphoma in the case of lupus for example(ref)(ref)(ref).  However, the reason for this association remained unclear.  Recent research suggests that what might be happening is a) adult stem cells are attracted to the sites of inflammation associated with the disease, basically on a repair mission b) in the abnormal signaling environment of the inflammation  sites, other things are going on possibly leading some of these stem cells to mutate and become cancerous.  “Recent studies have underscored a striking connection between tissue injury, repair and malignancy that may be of significant importance to the pathogenesis of systemic rheumatic diseases.  At the center of this connection lies the stem cell, the effector of tissue repair and regeneration that can arise from the tissue itself or be recruited from immigrant precursors(ref).”

For example, it is well known that lupus can lead to lung inflammation associated with interstitial lung disease and idiopathic pulmonary fibrosis (ref).  Tissue damage ensues which recruits stem cells to the sites of injury, endothelial progenitor cells being among them(ref).  However, the inflammation may also promote the recruitment of circulating tumor cells to the same sites(ref).  What exactly can happens next is unclear, but one theory gaining traction is that the environment is mutantogenic for the stem cells.  The title of one research publication telegraphs the message:

Stem Cells in Inflammatory Disease: Chronic Inflammation and Tissue Damage Recruits Stem Cells, Which Accumulate Mutations and May Become Transformed.

“A recent study by Houghton and colleagues using a mouse model demonstrates a very striking connection between chronic inflammation, hematopoietic stem-cell recruitment and mutation, and cancer formation in the inflamed target tissue. These authors showed that chronic Helicobacter pylori infection stimulates the recruitment of bone marrow derived stem cells (BMDC) into the gastric mucosa, which engraft permanently into the tissue stem-cell niche, assuming functions of the former. In the inflammatory microenvironment generated by H. pylori, the engrafted BMDCs accumulate mutations, and appear to be the cells that give rise to the gastric tumors arising in these animals(ref).”  Another publication reports “Data from emerging studies provide a growing body of evidence that stem cells play critical roles at the injury-repair interface. While performing the function of regeneration so critical for life, they may also be inadvertent partners in pathology, through their ability to self-renew and express various autoantigens also expressed in tumors.”

There is much current research activity in the associated fields of autoimmune diseases, stem cell activities, oncogenesis and inflammation.  So, I expect there will be further clarification of the phenomena described here as time progresses.  Meanwhile, a general message for both healthy people and ones with autoimmune diseases appears to be “keep the inflammation down as much as possible.”  For someone in the midst of a roaring lupus flare, this could require a medical intervention such as prescribing a strong corticosteroid like prednisone.  For healthy people, there is my suggested anti-aging Firewall against Chronic or Excess Inflammation.