Author:
Masoudzadeh Nasrin,Östensson Malin,Persson Josefine,Mashayekhi Goyonlo Vahid,Agbajogu Christopher,Taslimi Yasaman,Erfanian Salim Reza,Zahedifard Farnaz,Mizbani Amir,Malekafzali Ardekani Housein,Gunn Bronwyn M.,Rafati Sima,Harandi Ali M.
Abstract
AbstractAnthroponotic cutaneous leishmaniasis (CL) caused by Leishmania tropica (L. tropica) represents a public health challenge in several resource poor settings. We herein employed a systems analysis approach to study molecular signatures of CL caused by L. tropica in the skin lesions of ulcerative CL (UCL) and non-ulcerative CL (NUCL) patients. Results from RNA-seq analysis determined shared and unique functional transcriptional pathways in the lesions of the UCL and NUCL patients. Several transcriptional pathways involved in inflammatory response were positively enriched in the CL lesions. A multiplexed inflammatory protein analysis showed differential profiles of inflammatory cytokines and chemokines in the UCL and NUCL lesions. Transcriptional pathways for Fcγ receptor dependent phagocytosis were among shared enriched pathways. Using L. tropica specific antibody (Ab)-mediated phagocytosis assays, we could substantiate Ab-dependent cellular phagocytosis (ADCP) and Ab-dependent neutrophil phagocytosis (ADNP) activities in the lesions of the UCL and NUCL patients, which correlated with L. tropica specific IgG Abs. Interestingly, a negative correlation was observed between parasite load and L. tropica specific IgG/ADCP/ADNP in the skin lesions of CL patients. These results enhance our understanding of human skin response to CL caused by L. tropica.
Funder
Iran National Science Foundation
Iran’s National Elites Foundation
Pasteur Institute of Iran
H2020 Marie Skłodowska-Curie Actions
European Commission
Gothenburg University Library
Publisher
Springer Science and Business Media LLC
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