Advances in hidradenitis suppurativa
Transcript: Cells, mediators and bacteria
Dr Philippe Guillem
Interview recorded Feb 2024, EHSF 2024. All transcripts are created from interview footage and directly reflect the content of the interview at the time. The content is that of the speaker and is not adjusted by Medthority.
All the communications that have been presented during the pathophysiology session of the EHSF conference, were around the well known, well accepted now theory of dysbiosis, that is, a bad interaction between skin bacteria and the immune system. And all the presentations were about these two actors of the duo. We had some presentations about immune cells. For example, a study from Lyon, about mucosal mucosal T-cells that are involved in both innate, and acquired immunity, and could be very specific immune cell type involved in HS pathophysiology.
We also had an important communication about stromal cells. We always think about immune cells, but stromal cells that are associated with immune cells are very important. And for example, a study from Ireland showed that fibroblasts could be involved in the fibrotic scarring, that occurs in HS. Of course the immune meditals are also important, and for example, we had a very nice communication from Pisa, about the interleukin-1 family. There is no agreed, or open label treatment, using interleukin-1, using biologics, against interleukin-1 family. But we probably will have this kind of treatment in the near future, probably because of this family, as demonstrated by the Italian team, is very important in this HS pathophysiology. The other part of interaction, the bad interaction, is bacteria of course. And we have, we had many, many communications about the involvement of the skin microbiota.
For example, using metagenomics, such as presented by Spanish team from Barcelona. And it's interesting to see these kinds of very precise studies, that could identify known bacteria such as anaerobic, but also perhaps new ones of such as mycoplasma. So very interesting to see that. But pathophysiology, our last communication explored endotype, it was from Lyon. I participated in the study. And it's an example of where we are going to go with this kind of study. It is a characterisation of molecular endotypes. That is to say that some patients are specific molecular endotype. And using these endotypes to tailor specifically new treatment, is probably an important care with future treatments.
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