What I did:
We found and processed data from an existing database to learn more about the effects of microbiome on psoriasis patients. Through many tools available on Galaxy, we were not only able to confirm the current consensus on the gut-skin axis but also find an interesting genus that could be further explored later. What I found most interesting was how we were able to somewhat connect two different microbiomes based on the evidence we collected, which show inter-talk in the two environments.
How You Can Help:
If you’d like to dive deeper into what we started so far, it could be interesting to investigate the probiotics and see if there are any effects to the microbiome to these patients that could provide relief. It might also be interesting to also inquire about fecal microbiota transplantation (FMT) with respect to psoriatic gut. There’s a lot more interplay between the gut and the skin, which means that our inflammatory approach may be too narrow. There might be a possibility to look at if there’s other gut-skin axis communication that play a role in psoriasis pathogenesis such as having the CNS as a middleman.
What I Did
An overview of what I did was that I analyzed two fecal samples: one from a healthy patient and one from a patient with psoriasis. Using the Galaxy platform and its metagenomic tools, I explored and compared the taxonomic composition of the core human gut genera. Based on prior literature identifying the Clostridium genus as a potential contributor to skin inflammation, I focused on its relative abundance across both samples. My analysis revealed that Clostridium showed the greatest percent increase among core genera, with a 189% rise in the psoriasis sample. I then narrowed the focus to specific pro-inflammatory species within Clostridium, particularly C. perfringens and C. tetani. The psoriasis sample showed a nearly threefold increase in both species that were linked to Th17/Treg imbalance and inflammatory skin responses. What I found most interesting was how clearly this microbial shift aligned with inflammation-associated pathways, highlighting the potential of gut-skin axis research in understanding psoriasis.
How You Can Help
Others can build on this analysis by expanding the sample size to include more healthy and psoriasis-affected individuals, which would strengthen the statistical power of the findings. Future work could focus on longitudinal sampling to see how Clostridium abundance changes over time or in response to treatment. If I were to continue this project, I would perform functional profiling of the microbiome to identify specific genes or pathways, such as those involved in short-chain fatty acid metabolism or toxin production, that may be contributing to inflammation.
What I did:
I explored all the possible long-read datasets that could possibly work as a long-read control sample for a healthy gut to compare with our sample gut and skin samples for psoriasis and healthy patients. Then, we used a streamlined process on Galaxy to normalize all of our data collection and processing methods. Then, by using the tools on Galaxy, we were able to draw conclusions on the gut, skin, and gut-skin axis between healthy and affected samples of patients with psoriasis. Specifically interesting significance increases in the gut in inflammatory bacteria like Clostridium Perfringens and Clostridium Tetani and that the long read controls and short read controls for healthy gut samples showed no statistically significant differences between species, which was essential in proving that the short read samples were not heavily skewed and comparable to a more complete long read WGS. These specific bacteria were associated with balancing inflammatory skin responses within the Th17/Treg Axis, according to a referenced piece of literature on the subject. It was really interesting how, within our short and limited time we found significant differences between the skin and gu,t which shows that there may be interesting research to be done on the gut-skin axis with experiments on relevant samples to more clearly understand how this microbial shift affects inflammatory pathways in relation to the gut-skin axis.
How You Can Help
Building on my last point, future researchers can expand upon our work by first expanding the sample sizes, as we had a limited amount of publicly available samples. By increasing the sample size of this research, you could determine the validity of our findings and whether or not these significant differences were actually statistically significant and not a one of thing. Additionally, we were limited by the fact that our samples were not organized to find the relationship between the gut and skin axis in relation to psoriasis, which meant that some items, such as the control parameters, were not normalized across samples. Finally, to continue this work, I would recommend a better planned out study that identifies shifts in the microbiome to potentially find specific genes or pathways like the short-chain fatty acid metabolism that was found in recent literature to better discover what is contributing to inflammation and whether or not there is a significant relationship between the gut and skin.