Francesca Tomasi received her B.A. from the University of Chicago and is now a microbiologist.
When it comes to bacterial infectious diseases, often times a prerequisite to being infected by something (contracting an observable pathological condition) is being colonized by it. Colonization simply means that the microbe has set up home somewhere in or on your body, and is quietly living there. Most of the time, this mutual ignorance between you and the bacteria remains blissfully unchanged. You give the bug a home, and it leaves you alone. Sometimes, however – and the exact how’s and why’s of this are currently being studied – bacteria are provoked into turning against you. Such microbes are often termed pathobionts, commensal bacteria that can also be pathogens. Two pathobionts you might have heard of are Staph aureus and Streptococcus pneumoniae. The former is thought to colonize 33% of the world and can cause staph infections with varying degrees of drug resistance (MRSA, methicillin-resistant S. aureus, is a serious public health concern right now and is estimated to colonize 1-2% of the population). The latter is the topic of this article.
Even if you have never heard of Streptococcus pneumoniae itself, you have probably heard of the illnesses it can cause: pneumonia, otitis media, meningitis, or a nasty bout of sinusitis. The World Health Organization estimates over 1 million S. pneumoniae-related deaths every year, predominantly in developing countries and in children under 5 years old. In the US, there are approximately 20,000 deaths per year due to S. pneumoniae infection.
S. pneumoniae often colonizes our throats, and in particular children’s throats. S. pneumoniae comes in over 90 different forms, each of which has a specific adaptation to help it evade our immune systems. Capsules, for instance, enclose the bacteria and prevent phagocytosis, the process by which some of our immune cells can eat up foreign objects such as pathogens and degrade them. As a result, S. pneumoniae infections are taken seriously and can usually be treated with antibiotics. There are some vaccines available too for children that target the most commonly invasive forms of S. pneumoniae. Nonetheless, many children are still colonized by the bacteria, most commonly in their nasal passage, which starts at the nostrils and proceeds through the nasopharynx.
Many harmless bacteria co-colonize the nasal passage right alongside S. pneumoniae. In children, these include microbes spanning four main phyla. Corynebacteria are one such microbe, and are part of a phylum known as Actinobacteria. Corynebacteria are rod-shaped bacteria commonly found on the skin and nasal passage and they are known to be exclusively commensal to humans; that is, unlike their roommate S. pneumoniae, Corynebacteria will not turn against you.
Scientists have observed that Corynebacteria tend to be overrepresented in the nasal passages of children who are not colonized with S. pneumoniae compared with children who are colonized by the pathobiont. Furthermore, studies on certain Corynebacteria species have led researchers to discover that a subset of them require an external source of fatty acids (the building blocks of fat) in order to grow, because they lack the specific physiological machinery to make the fatty acids themselves. Lastly, it is known in the medical community that certain types of fatty acids (known as triacylglycerols) are very prevalent on our skin surfaces.
Is it possible that Corynebacteria that live on our skin are using the fatty acids on our skin to survive? And why are there more Corynebacteria in children who are not colonized by S. pneumoniae? Do the commensal Corynebacteria protect them from the pathobiont S. pneumoniae?
The answer to these questions is yes, according to a recently published study by researchers in Boston. Starting with fatty acid-free minimal growth conditions and adding different fatty acids, the authors were able to identify the physiologically relevant fatty acids that a specific commensal Corynebacteria, C. accolens, could ingest for survival. Among the lipids that C. accolens could metabolize were the same type that are on our skin. Furthermore, growing C. accolens and S. pneumoniae side by side resulted in what is known as a “zone of inhibition,” where S. pneumoniae growth was inhibited. In order to show that this inhibition was caused by C. accolens, and then to explain the mechanism of this inhibition, the authors extracted metabolic products of C. accolens – that is, anything the bacteria produced was collected into tubes – and mixed them with S. pneumoniae. Sure enough, the streptococci stopped growing. It turns out that when C. accolens encounter our skin fatty acids, they use an enzyme called a lipase that cuts the fatty acids up. Some of these cut up products, known as free oleic and linoleic acids, inhibit S. pneumoniae growth.
Bomar and colleagues used a reductionist approach to test the hypothesis that growth of S. pneumoniae is antagonized by C. accolens, a commensal bacterium found in our bodies. Our bodies produce free fatty acids that C. accolens cleaves to produce compounds which inhibit S. pneumoniae growth. The application? C. accolens could be explored as a potential probiotic in children to minimize streptococcus colonization, which in turn reduces the risk of infection.
The interplay between our body and microbes is a very hot topic these days: researchers across the globe are busy characterizing our microbiomes and elucidating relationships between bacteria and our health. The above study by Bomar and colleagues characterizes a definitive link between a commensal microbe, human metabolites, and a pathobiont. This is why, recently, people have been referring to our microbiomes as another organ in our body: its essentiality is proving itself more and more every day.