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AIM 2 inflammasome is associated with disease severity in tegumentary leishmaniasis caused by Leishmania (V.) braziliensis
Author(s) -
Moreira R. B.,
Pirmez C.,
OliveiraNeto M. P.,
Aguiar L. S.,
Gonçalves A. J. S.,
Pereira L. O. R.,
Abreu L.,
De Oliveira M. P.
Publication year - 2017
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/pim.12435
Subject(s) - inflammasome , aim2 , pathogenesis , leishmania braziliensis , biology , cutaneous leishmaniasis , immunology , leishmaniasis , leishmania , pathology , inflammation , medicine , parasite hosting , world wide web , computer science
Summary The inflammasome is a multiprotein signalling platform involved in the pathogenesis of various inflammatory skin diseases. Herein, we investigated gene and protein expression of the inflammasome molecules AIM 2 and NLRP 3 in active lesions from patients with L. (V.) braziliensis ‐associated tegumentary leishmaniasis ( TL ) and correlated these findings with the clinical presentations and responses to therapy. Real‐time PCR assays showed a significantly higher AIM 2 gene expression in mucosal leishmaniasis ( ML ) compared with that in cutaneous leishmaniasis ( CL ). Additionally, AIM 2 mRNA expression was significantly higher in lesions from poor responders than in lesions from good responders. In situ protein quantification analyses revealed greater AIM 2 expression in ML lesions than in CL lesions. The percentage of AIM 2‐producing cells was higher in poor responders than in good responders. Although not quite significant, IL ‐1β+ cells were slightly more prominent in poor responders than in good responders. Similar results were observed when patients were evaluated according to clinical form. GP 63 immunostaining was identified in all samples, but no significant variation between mucosal and cutaneous lesions was observed. GP 63 could be associated with reduced NLRP 3 inflammasome expression in CL and ML patients. Taken together, these data demonstrate that AIM 2 is an important component of the inflammasome in TL patients and is directly associated with the severity of lesions.