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Profiling inflammatory response in lesions of cutaneous leishmaniasis patients using a non-invasive sampling method combined with a high-throughput protein detection assay

Artikel i vetenskaplig tidskrift
Författare Y. Taslimi
Christopher Agbajogu
S. F. Brynjolfsson
N. Masoudzadeh
V. Mashayekhi
S. Gharibzadeh
Malin Östensson
Sravya Sowdamini Nakka
A. Mizbani
S. Rafati
Ali M Harandi
Publicerad i Cytokine
Volym 130
Nummer/häfte June
Sidor 8
ISSN 1043-4666
Publiceringsår 2020
Publicerad vid Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi
Sidor 8
Språk en
Länkar dx.doi.org/10.1016/j.cyto.2020.1550...
Ämnesord Cutaneous leishmaniasis, Non-invasive sampling, Proximity extension, assay, Inflammation biomarkers, major infection, parasite survival, immune-responses, activation, expression, mice, Biochemistry & Molecular Biology, Cell Biology, Immunology
Ämneskategorier Reumatologi och inflammation

Sammanfattning

Background: Cutaneous leishmaniasis (CL) is an infection caused by Leishmania (L.) protozoa transmitted through the bite of infected sand fly. Previously, invasive sampling of blood and skin along with low throughput methods were used for determination of inflammatory response in CL patients. Aims/Methodology: We established a novel approach based on a non-invasive adhesive tape-disc sampling combined with a powerful multiplexing technique called proximity extension assay for profiling 92 inflammatory cytokines, chemokines and surface molecules in the lesions of CL patients infected with L. tropica. Sample collection was done non-invasively by using adhesive tape-discs from lesion and normal skin of 33 L. tropica positive patients. Results: Out of 92 inflammatory proteins, the level of 34 proteins was significantly increased in the lesions of CL patients compared to their normal skin. This includes the chemokines CCL2, CCL3, CCL4, CXCL1, CXCL5, CXCL9, CXCL10 and CXCL11, together with the interleukins IL-6, IL-8, IL-18, LIF and OSM. The remaining significantly changed inflammatory proteins include 7 surface molecules and receptors: CD5, CD40, CDCP1, 4E-BP1, TNFRSF9, IL-18R1 and OPG as well as 16 other cytokines and proteins: MMP-1, CSF-1, VEGFA, uPA, EN-RAGE, LAP TGF-beta 1, HGF, MMP-10, CASP-8, TNFSF14, STAMPB, ADA, TRAIL and ST1A1. Further, 13 proteins showed an increasing trend, albeit not statistically significant, in the CL lesions, including TGF-alpha, CCL23, MCP-2, IL-12B, CXCL6, IL-24, FGF-19, TNF beta, CD6, TRANCE, IL10, SIR2 and CCL20. Conclusion: We herein report a novel approach based on a non-invasive sampling method combined with the high-throughput protein assay for profiling inflammatory proteins in CL lesions. Using this approach, we could profile inflammatory proteins in the lesions from CL patients. This new non-invasive approach may have implications for studying skin inflammatory mediators in CL and other skin disorders.

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