title: Cytokine gene expression in the tissues of dogs infected by Leishmania infantum.
abstract: Canine leishmaniosis (CanL) caused by the protozoan parasite Leishmania infantum is a chronic systemic disease that is endemic in certain parts of the world. The domestic dog is the most important reservoir of L. infantum and is the main source of infection for other animals and for the human population. The aim of this study was to evaluate and compare the level of expression of genes encoding particular cytokines (interleukin [IL]-12, interferon [IFN]-γ, IL-2 and IL-4) in different tissues and organs of 53 adult dogs with or without clinical signs of leishmaniosis and after treatment for the disease. Asymptomatic dogs showed high expression of genes encoding IL-4 in blood leucocytes and of genes encoding IL-12 and IL-2 in lymph nodes. Blood leucocytes from symptomatic dogs had a mixed Th1 and Th2 cytokine gene expression profile, but lymph nodes from these animals had dominant IL-2 and IFN-γ gene expression, while bone marrow appeared to be unresponsive. The predominance of IL-4 gene expression in the blood of asymptomatic dogs may favour parasite replication, while the balance between Th1 and Th2 cytokine gene expression in the blood of symptomatic dogs may be important in reducing parasite replication and delaying the dissemination of Leishmania to other organs. The drugs used to treat CanL do not completely eliminate the parasite, so the high expression of the gene encoding IL-4 in blood leucocytes and the high expression of IL-12 and IL-4 mRNA in lymph nodes may reflect the persistence of residual Leishmania amastigotes. L. infantum appears able to regulate the host immune response in order to ensure its survival, but also to prevent the host from succumbing to infection. This guarantees its transmission and the completion of its life cycle.
authors.affiliation: Universidade Federal Rural de Pernambuco, Departamento de Medicina Veterinária, Recife, Pernambuco, Brazil.
authors.forename: M A G
authors.initials: MA
authors.lastname: Barbosa
authors.forename: G
authors.initials: G
authors.lastname: Alexandre-Pires
authors.forename: M
authors.initials: M
authors.lastname: Soares-Clemente
authors.forename: C
authors.initials: C
authors.lastname: Marques
authors.forename: O Roos
authors.initials: OR
authors.lastname: Rodrigues
authors.forename: T Villa
authors.initials: TV
authors.lastname: De Brito
authors.forename: I Pereira
authors.initials: IP
authors.lastname: Da Fonseca
authors.forename: L C
authors.initials: LC
authors.lastname: Alves
authors.forename: G M
authors.initials: GM
authors.lastname: Santos-Gomes
mesh_terms: D000818:Animals; D001853:Bone Marrow / Q000378:metabolism; D001938:Brazil; D004283:Dog Diseases / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D004285:Dogs; D005260:Female; D005786:Gene Expression Regulation; D006790:Host-Parasite Interactions; D007371:Interferon-gamma / Q000096:biosynthesis* / Q000235:genetics; D018664:Interleukin-12 / Q000096:biosynthesis / Q000235:genetics; D007376:Interleukin-2 / Q000096:biosynthesis / Q000235:genetics; D015847:Interleukin-4 / Q000096:biosynthesis / Q000235:genetics; D007378:Interleukins / Q000096:biosynthesis* / Q000235:genetics; D018314:Leishmania infantum; D007898:Leishmaniasis, Visceral / Q000235:genetics / Q000276:immunology / Q000378:metabolism / Q000662:veterinary*; D008198:Lymph Nodes / Q000378:metabolism; D008297:Male; D011174:Portugal; D012333:RNA, Messenger / Q000096:biosynthesis; D018417:Th1 Cells / Q000378:metabolism; D018418:Th2 Cells / Q000378:metabolism; D014329:Tropical Climate; D014504:Urban Health
chemical_list: D007376:Interleukin-2; D007378:Interleukins; D012333:RNA, Messenger; D018664:Interleukin-12; D015847:Interleukin-4; D007371:Interferon-gamma