A microbiota-driven mechanism underlies severity of leishmaniasis infection Leishmaniasis Infection Multiomics Skin medrxivpreprint Penn OhioState ufrb
Study: Multi-omic profiling of cutaneous leishmaniasis infections reveals microbiota-driven mechanisms underlying disease severity. Image Credit: Kateryna Kon / Shutterstock
Studies have reported that the breach in the skin by Leishmania braziliensis results in microbiome dysbiosis, promoting pathological changes and elevated levels of inflammatory cytokines and chemokines such as interleukin-17 and interleukin-1β. However, the clinical relevance of the immunological findings is not clear.
The lesional biopsy tissues were subjected to ribonucleic acid sequencing analysis to determine the host transcriptomic profiles and quantitative polymerase chain reaction was performed to quantify the lesional bacterial burden. Due to greater Staphylococcus aureus abundance in lesions, as determined by differential taxa abundance analysis between the lesional and contralateral unaffected skin swab specimens, a customized Staphylococcus aureus pan-genome was constructed with clinical S.
Results Genetics & Genomics eBook Compilation of the top interviews, articles, and news in the last year. Download a free copy Bacterial burden was more significant in lesional swabs than the unaffected, contralateral skin swabs, and 84% of patients showed skin microbiome alterations in the leishmanial lesions. The lesional microbiome showed Staphylococcus aureus predominance, followed by Streptococcus and Corynebacterium.
Lesions with elevated L. braziliensis counts expressed clinical outcome-associated pro-inflammatory genetic signatures, with elevated cytotoxic T lymphocyte and natural killer lymphocyte counts. S. aureus colonization promoted disease in B6 mice by promoting inflammation, indicating that S. aureus contributed to the leishmaniasis-associated inflammation and disease outcomes.
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