SALO, a novel classical pathway complement inhibitor from saliva of the sand fly Lutzomyia longipalpis.

Détails

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Etat: Public
Version: de l'auteur
ID Serval
serval:BIB_278D88796FDF
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
SALO, a novel classical pathway complement inhibitor from saliva of the sand fly Lutzomyia longipalpis.
Périodique
Scientific Reports
Auteur(s)
Ferreira V.P., Fazito Vale V., Pangburn M.K., Abdeladhim M., Ferreira Mendes-Sousa A., Coutinho-Abreu I.V., Rasouli M., Brandt E.A., Meneses C., Lima K.F., Nascimento Araújo R., Horácio Pereira M., Kotsyfakis M., Oliveira F., Kamhawi S., Ribeiro J.M., Gontijo N.F., Collin N., Valenzuela J.G.
ISSN
2045-2322 (Electronic)
ISSN-L
2045-2322
Statut éditorial
Publié
Date de publication
2016
Peer-reviewed
Oui
Volume
6
Pages
19300
Langue
anglais
Résumé
Blood-feeding insects inject potent salivary components including complement inhibitors into their host's skin to acquire a blood meal. Sand fly saliva was shown to inhibit the classical pathway of complement; however, the molecular identity of the inhibitor remains unknown. Here, we identified SALO as the classical pathway complement inhibitor. SALO, an 11 kDa protein, has no homology to proteins of any other organism apart from New World sand flies. rSALO anti-complement activity has the same chromatographic properties as the Lu. longipalpis salivary gland homogenate (SGH)counterparts and anti-rSALO antibodies blocked the classical pathway complement activity of rSALO and SGH. Both rSALO and SGH inhibited C4b deposition and cleavage of C4. rSALO, however, did not inhibit the protease activity of C1s nor the enzymatic activity of factor Xa, uPA, thrombin, kallikrein, trypsin and plasmin. Importantly, rSALO did not inhibit the alternative or the lectin pathway of complement. In conclusion our data shows that SALO is a specific classical pathway complement inhibitor present in the saliva of Lu. longipalpis. Importantly, due to its small size and specificity, SALO may offer a therapeutic alternative for complement classical pathway-mediated pathogenic effects in human diseases.
Pubmed
Open Access
Oui
Création de la notice
19/02/2016 8:21
Dernière modification de la notice
20/08/2019 14:06
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