02970nas a2200457   4500000000100000008004100001260005300042653002800095653003800123653002900161653001700190653002800207653002600235100001600261700002400277700001600301700001400317700002200331700002200353700001700375700002200392700001800414700001700432700001600449700001600465700002300481700001700504700002100521700002400542700002200566700002300588700002400611700001600635700002600651245014800677856007300825300001100898490000600909520158300915022001402498       2026                            d  c03/2026bSpringer Science and Business Media LLC10aCutaneous leishmaniasis10aLocalized cutaneous leishmaniasis10aSoluble immune mediators10aCirculation 10aLesion microenvironment10aTime evolution lesion1 ade Souza JP1 aFerreira-Gontijo CM1 aPereira FRV1 aEller MTC1 aOttoni-Vieira MFG1 aPereira-Martins J1 aRodrigues MP1 aBrito-de-Sousa JP1 aNascimento AS1 ade Brito MNP1 ae Silva BOS1 ada Silva TR1 ade Figueiredo MCCM1 aMonteiro ÉM1 aMartins-Filho OA1 aCoelho-dos-Reis JGA1 aPascoal-Xavier MA1 aSampaio-Pereira AA1 aTeixeira-Carvalho A1 aMiranda VHS1 aPeruhype-Magalhães V00aImmune Mediator Profile in the Inflammatory Microenvironment Reveals Potential Biomarkers of Wound Healing in Localized Cutaneous Leishmaniasis  uhttps://link.springer.com/content/pdf/10.1007/s43152-026-00065-4.pdf  a1 - 170 v73 a<p>Localized cutaneous leishmaniasis (LCL) is the most prevalent form of leishmaniasis, with infection control primarily dependent on cell-mediated immunity. Lesion healing results from a complex interplay among immune cells and soluble mediators. Using Luminex technology, we evaluated circulating and lesion microenvironment immune mediators, including chemokines, cytokines, and growth factors, in patients with LCL and nonspecific dermatitis. A robust proinflammatory response was observed in the lesion microenvironment of LCL patients, characterized by elevated levels of growth factors, important immune mediators potentially involved in tissue repair. Predictive modeling identified FGF, G-CSF, GM-CSF, IL-2, and IL-9 as key immune mediators distinguishing LCL from nonspecific dermatitis. Our results reveal that LCL presents a distinct soluble immune mediator signature from nonspecific dermatitis, exhibiting a set of biomarkers that not only define its immune mediator signature but also signal a possible role in the tissue repair process. Furthermore, we characterized the profile of soluble immune mediators of LCL patients, categorized according to the time evolution lesion. Our analysis revealed a predominance of biomarkers within the lesion microenvironment in patients with recent lesions (2 months of evolution), our data showed a predominance of biomarkers in the systemic circulation. Collectively, these findings provide novel insights into the immunopathogenesis of LCL and highlight candidate immune mediators for targeted prognostic evaluation.</p>
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