Transcriptomic and Immunopathological Profiles of Inflammasomes in Different Clinical Forms of American Cutaneous Leishmaniasis

Transcriptomic and Immunopathological Profiles of Inflammasomes in Different Clinical Forms of American Cutaneous Leishmaniasis

American cutaneous leishmaniasis (ACL), caused by <i>Leishmania (Leishmania) amazonensis</i> and <i>L. (Viannia) braziliensis</i>, presents a wide spectrum of clinical and immunopathological manifestations, ranging from localized cutaneous leishmaniasis (LCL) to severe forms...

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Main Authors: Larissa dos Santos Alcântara, Marliane Batista Campos, Ana Carolina Stocco Lima, Alessandra Pontillo, Kamilla Batista da Silva Souza, Aurea Favero Ferreira, Cristina Pires Camargo, Sueli Mieko Oba-Shinjo, Márcia Dalastra Laurenti, Carlos Eduardo Pereira Corbett, Vania L. R. da Matta, Helder Nakaya, Fernando T. Silveira, Claudia Maria de Castro Gomes
Format: Article
Language:English
Published: MDPI AG 2025-04-01
Series:Microorganisms
Subjects:
american cutaneous leishmaniasis
inflammasomes
transcriptomic
immunopathological profiles
<i>Leishmania (Leishmania) amazonensis</i>
<i>Leishmania (Viannia) braziliensis</i>
Online Access:https://www.mdpi.com/2076-2607/13/5/980
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Summary:American cutaneous leishmaniasis (ACL), caused by <i>Leishmania (Leishmania) amazonensis</i> and <i>L. (Viannia) braziliensis</i>, presents a wide spectrum of clinical and immunopathological manifestations, ranging from localized cutaneous leishmaniasis (LCL) to severe forms like anergic diffuse cutaneous (ADCL) and mucocutaneous leishmaniasis (MCL). Despite evidence of the immune response’s complexity, the role of inflammasomes in disease severity and parasite persistence remains unclear. We investigated the transcriptomic and immunopathological profiles of inflammasome components in patient lesions across the clinical spectrum. Genes such as <i>NLRP3</i>, <i>AIM2</i>, <i>NLRP12</i>, <i>NLRC4</i>, <i>CASP1</i>, <i>CASP5</i>, <i>GSDMD</i>, and <i>IL1B</i> and all evaluated proteins, showed higher expression in ACL compared to healthy controls. Distinct inflammasome activation patterns were observed: MCL, the hyperreactive form, showed elevated <i>NLRP3</i>, <i>AIM2</i>, and <i>IL-1β</i>, indicating an intensified inflammatory environment. ADCL, the hyporeactive form, displayed increased <i>NLRP12</i> and <i>NLRC4</i> expression with reduced <i>GSDMD</i>. Localized forms showed transitional profiles, highlighting ACL’s multifactorial pathogenesis. These findings advance our understanding of inflammasome mechanisms in ACL, identifying potential therapeutic targets to modulate inflammation and improve management.
ISSN:2076-2607

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