In ecology, there is the concept of generalist vs. specialist species. The former describes organisms that can live in a wide range of environments and utilize a broad spectrum of resources (e.g., raccoons adapting to live in urban environments), whereas the latter refers to organisms that can only survive in particular environments and use a restricted set of resources. Shifts in these environments tend to affect specialists more profoundly, and can even lead to their distinction. However, these species tend to occupy narrow ecological niches, which makes them better equipped to compete against other organisms.
I think that there are some parallels between generalism/specialism/niches and scientists. Researchers are pictured by the public as being hyper-specialized in terms of their areas of interest. This is true for many scientists, but some of us work in fundamental disciplines with far-reaching implications. For instance, researchers focused on understanding RNA biology could be considered scientific “generalists” because their work has broad ramifications.
On the surface, our lab, the Bladder Immunology Group, appears to be a bunch of specialists.
We study a particular organ, the bladder, and how it is affected by specific stimuli, namely bacterial uropathogens, the parasitic Schistosoma haematobium worm, and nitrosamine carcinogens.
Our research group came to study these particular organs, organisms, and chemicals somewhat serendipitously. As a graduate student in immunology I often had discussions with De’Broski Herbert, my classmate (and now faculty member at Penn), regarding the lack of a good mouse model for urogenital schistosomiasis (infection with S. haematobium worms). After I completed my clinical training as a urologist, I decided to combine my immunologic and urologic backgrounds. Focusing on the bladder and urinary tract infections was a natural choice. I wanted to work on an important yet under-studied (e.g., urogenital schistosomiasis) area. I was seeking my scientific niche in order to stand out and reduce competition.
One of the first projects I embarked upon as a junior faculty member was to develop a tractable mouse model of urogenital schistosomiasis. Although it’s certainly true that we focus on the bladder and its noxious stimuli for their own sake, our work has broader implications than may be immediately apparent. We are interested in epithelial biology, host-pathogen interactions, and cancer biology in general, and we hope to delineate important principles relevant to these areas of study through our work.
We have made some headway in this regard. For example, we recently published a paper demonstrating that H-IPSE, an S. haematobium ortholog of a Schistosoma mansoni immunomodulatory protein, can infiltrate into host urothelial cell nuclei (i.e., an infiltrin). In published and unpublished data, we and others have shown that the S. mansoni and Fasciola hepatica orthologs of this infiltrin can enter the nuclei of many other host cell types. Once in host cell nuclei, these infiltrins may alter transcription of a large number of genes. Thus, our work illustrates that multiple worm species can secrete infiltrins which infiltrate a range of host cells and may modify transcription to suit their parasitic needs.
I have long-argued that studying schistosomiasis can help us highlight the underpinnings of seemingly unrelated biological disciplines. Thus, we aren’t specialists, but rather, generalists in specialists’ clothing.