If you have nothing better to do on a cold Winter’s day, try researching the links between bacteria and cancer. Want more? Try researching the links between bacteria and a host of other diseases.
Rabbit hole, indeed.
The link between bacteria and cancer was first proposed in 1890. In a lecture published in the British Medical Journal, Dr. William Russell proposed this link based on a series of staining observations.
The evidence was rather circumstantial. In the 1930s, additional circumstantial links between bacteria and cancer were established. But uncertainty remained.
Were the bacteria triggering the formation of cancerous cells and tumors? Did their presence merely facilitate the process? Perhaps a bacterial metabolite or surface protein is involved? Are viruses the actual culprits in this process? Or, was it simply a coincidence?
Links between bacteria and gastrointestinal cancer have been widely studied. For example, it is believed that H. pylori is a critical factor in the development of gastric cancer and mucosa-associated lymphoid tissue cancers (Mager, 2006).
And it has been suspected since the 1950s that certain species of Streptococcus may be associated with colon cancer (Sobhani, et al., 2013).
What about lung cancer?
A number of bacteria and fungi are associated with cancerous lung tissue.
Whether or not they play a major role in local inflammation and carcinogeneisis remains an open question (Apostolou et al., 2011).
Breast cancer is an interesting one, since it was long believed that breast tissue was privilidged and did not harbor microbes. Not only is this not true, there are casual links between cancer and the presence of bacteria in this tissue.
A recent study found that different bacterial profiles exist between healthy women and those with breast cancer (Urbaniak, et al., 2016).
So what’s going on here?
The prevailing hypothesis is that bacteria may contribute to carcinogenesis via two mechanisms.
First, bacteria could trigger local inflammation, which induces cell proliferation and the production of mutagenic free radicals. This is exactly the mechanism by which Helicobacter pylori infection triggers adenocarcinoma of the stomach.
Second, bacterial metabolites, such as secondary bile acids, can be potent mutagens (Louis, et al., 2014).
Pick nearly any disease outside of those with a clear genetic origin, and you may find at least some casual link between bacteria and that disease.
How about rheumatoid arthritis?
Intestinal colonization by Prevotella copri is casually associated with rheumatoid arthritis. The hypothesis is that the presence of this bacterium triggers an immune response, which in turn also recognizes joint bone and cartilage as antigenic.
In other words, bacteria are triggering an immune response, as they should. But, in an unfortunate coincidence, this same immune response is also marking otherwise heathy tissue as foreign.
It is a very sensible hypothesis. And it raises many interesting questions.
In the case of rheumatoid arthritis, for example, is it possible to treat Prevotella infection with antibiotics? Would eliminating the antigen also reduce symptoms? Or is it too late at this point?
Are there genetic predispositions to Prevotella infection? Geographic considerations? Diet? Can rheumatoid arthritis be prevented?
We suspect that nearly every autoimmune disease has some casual link with bacterial infection?
Not convinced? Be our guest.
While some of the recent hype surrounding the gut microbiome has died down a little, it is unquestionably a critical area of research. Indeed, with healthy individuals hosting thousands of bacterial species, it is perhaps unsurprising that there is at least some casual link between bacteria and disease (Shreiner, et al., 2015).
Whether or not this will lead to new therapeutics is an open question. But from a prevention perspective, it’s clear that we all need to pay far more attention to our microbiome as a way to prevent future disease.
This is a fascinating subject. And we hope others more knowledgeable than ourselves will continue to research and report on this topic.