Terkild Brink Buus
@TerkildB
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Assistant Professor intrigued by skin immunology and single-cell analyses at @skinUCPH. Move to the other place @terkild.bsky.social
Copenhagen
Joined June 2019
Can bacterial infections make cancer cells resistant to treatment? In Sézary Syndrome (SS), it turns out they can! Want to know more? I will summarize some highlights from our recent study @BloodJournal below.
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RT @theJIDJournal: "Breaking the Vicious Cycle of Staphylococcal aureus Skin Colonization and Progression of Cutaneous T-Cell Lymphoma," a…
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RT @skinucph: New @BloodJournal study by @ChellaKrishnaV and @TerkildB from Niels Ødum’s group @skinucph show bacterial infections can make…
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Our article is accompanied by a great commentary by Prof Jean-Philippe Merlio @CHUBordeaux highlighting the many facets of S. aureus infections in Sézary Syndrome.
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This study was spearheaded by @ChellaKrishnaV and has been a fantastic collaboration between the Ødum group @SkinUCPH @UCPH_Research and our collaborators M.Kamstrup, @EGuenova, M.Wobser, R.Bech @AUHdk, @susanebates, L.Geskin, @SBKoralov , @OsmancevicAmra and their amazing teams!
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Our findings suggest that S. aureus enterotoxins can cause clinical treatment resistance in patients with SS, and that antibacterial measures may improve the outcome of cancer-directed therapy in patients harboring S aureus.
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To determine if SE-induced treatment resistance was dependent on cytokine signaling, we used a clinical JAK-inhibitor (Tofacitinib). Highlighting the heterogeneity of SS, we found that only half the patients were dependent on JAK signaling for their resistance and half were not.
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Indeed, blocking TCR signaling or downstream PKC-θ (upstream of NFkB activation) was sufficient to counteract the treatment resistance. Moreover, only drugs that also inhibited NFkB signaling (Bortezomib & Crystal Violet) were unaffected by SE – implicating the TCR-PKC-NFkB axis.
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The induced resistance was not limited to Romidepsin but made the cancer cells resistant to other HDACi as well as DNA-targeting drugs, Doxorubicin and Etoposide. The S. aureus enterotoxins (SE) did not hamper drug uptake, efflux pumps nor interfered directly with the drugs.
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We pinpointed the effect to a group of toxins called enterotoxins (SE) that have the ability to activate T cells through the T cell receptor (superantigens). Recombinant SE was sufficient to induce HDACi resistance in cells but a mutated SE without superantigenic effect was not.
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@mikhaeldito313 @jlimenitakis Depending on the samples I would argue that there are more batch effects on CITE-seq than GEX as antibody staining is likely done with slightly different concentrations (unless using lyophilized panels), staining different cell numbers and is cell composition dependent.
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