CD4+ T cells participate in the nephropathy of canine visceral leishmaniasis

Costa, Francisco Assis Lima; Guerra, José Luiz; Silva, S M M S; Klein, Roseli Pizzigatti; Mendonça, Ivete Lopes de; Goto, Hiro

doi:10.1590/s0100-879x2000001200009

Cited by 32 publications

(38 citation statements)

References 11 publications

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“…According to Costa et al (2000), it may be due to the presence of parasite antigens found in the inflammatory infiltrate. The occurrence of interstitial nephritis in 72.7% of the dogs in this study is similar to the results of a previous study that identified the same alteration in 78% of the dogs (COSTA et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Hypertension and its correlation with renal lesions in dogs with leishmaniosis

Braga

Leite

Rosa

et al. 2015

Rev. Bras. Parasitol. Vet.

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To evaluate the prevalence of hypertension and its correlation with the severity of renal injury and proteinuria in dogs with leishmaniosis, sixty-six dogs were divided into two groups. Group 1 (G1) was composed of 54 dogs included in stage 1 of chronic kidney disease (CKD), and group 2 (G2) of twelve dogs in stages 2 and 3 of CKD. Prevalence of hypertension was 28.8%, comprising 22.2% of the dogs from G1 and 58.3% from G2 (P=0.011). The mean arterial blood pressure (BP) of dogs from G1 (135.7 ± 20.5) was lower than from G2 (170.0 ± 26.3) (P <0.001). Urine proteincreatinine ratio (UP/C) revealed values above 0.5 in 75.7% of the dogs, with 34% presenting hypertension. All dogs with hypertension had histopathological and laboratory evidence of glomerular disease. Although there was no statistically significant correlation between elevated BP and the severity of glomerular lesions (P=0.408), there was a statistically significant correlation between elevated BP and increased UP/C in the studied population (P=0.002). Thus, dogs with leishmaniosis and renal disease must be screened for the presence of hypertension so that treatment may be instituted as early as possible, in countries where treatment is allowed, to prevent the progression of renal damage.Keywords: Histopathology, kidney, Leishmania infantum chagasi, systolic blood pressure. ResumoPara avaliar a prevalência de hipertensão arterial e sua correlação com a severidade da lesão renal e proteinúria em cães com leishmaniose, 66 cães foram divididos em dois grupos. O grupo 1 (G1), composto por 54 cães em estágio 1 de doença renal crônica (DRC), e o grupo 2 (G2) por 12 cães em estágios 2 e 3 de DRC. A prevalência de hipertensão foi de 28,8%, compreendendo 22,2% dos cães de G1 e 58,3% dos cães de G2 (p = 0,011). A pressão arterial média (PA) de G1 (135,7 ± 20,5) foi inferior a de G2 (170,0 ± 26,3) (P <0,001). A relação proteína creatinina urinária (P/C U) foi maior que 0,5 em 75,7% dos cães, dos quais 34% possuíam hipertensão. Todos os cães com hipertensão apresentavam doença glomerular. Embora não tenha sido observada correlação estatisticamente significativa entre elevação da PA e severidade das lesões glomerulares (P =0,408), houve uma correlação significativa entre PA elevada e aumento da UP/C (P = 0,002). Portanto, cães com leishmaniose e doença renal devem ser pesquisados quanto à presença de hipertensão, para que o tratamento possa ser instituído o mais precocemente possível em países onde ele é permitido, para evitar a progressão da lesão renal.Palavras-chave: Histopatologia, rim, Leishmania infantum chagasi, pressão arterial sistólica.

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Section: Discussionmentioning

confidence: 99%

Hypertension and its correlation with renal lesions in dogs with leishmaniosis

Braga

Leite

Rosa

et al. 2015

Rev. Bras. Parasitol. Vet.

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“…The antigen was detected in a cellular pattern in phagocytic cells of the glomeruli, in the interstitial mononuclear cell infiltrate, and seldom in the form of particulate extracellular material as previously seen. 13 The antigen was also detected in tubular epithelial cells, even in apparently normal tubules. The whole parasite was not detected in any case.…”

Section: Detection Of Leishmania Antigenmentioning

confidence: 94%

Histopathologic Patterns of Nephropathy in Naturally Acquired Canine Visceral Leishmaniasis

et al. 2003

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Abstract. Although the nephropathy of visceral leishmaniasis (VL) is known both in humans and dogs, histopathologic alterations have not been thoroughly studied. We examined renal alterations in 55 dogs with naturally acquired VL compared with five noninfected dogs from an endemic area in northeastern Brazil. Glomerulonephritis was found in 55 dogs, interstitial alterations in 53 dogs, and tubular changes in 43 dogs with VL. The glomerular alterations found were minor glomerular abnormalities (n ϭ 8, 14.5%), focal segmental glomerulosclerosis (n ϭ 10, 18.2%), mesangial proliferative glomerulonephritis (n ϭ 17, 32.7%), membranoproliferative glomerulonephritis ,(n ϭ 18, 30.9%), crescentic glomerulonephritis (n ϭ 1, 1.8%), and chronic glomerulonephritis (n ϭ 1, 1.8%). Morphometric and ultrastructural studies complemented the analysis. The five control animals exhibited no glomerular alterations. The glomerular lesions were related to functional alterations. Considering that the alterations of canine and human nephropathy in VL are very similar, the data obtained in this study constitute an important contribution to the understanding of canine and human VL nephropathy.Key words: Dogs; glomerulonephritis; morphometry; renal pathology; ultrastructure; visceral leishmaniasis.Canine visceral leishmaniasis (VL) is a highly prevalent infection encountered throughout the world. In Brazil, VL results from infection by the protozoan Leishmania (Leishmania) chagasi, which occurs in 18 of 27 Brazilian states. 20,22,26 VL is endemic to northeastern Brazil, and in Teresina, in the State of Piaui, some 1,600 dogs presenting naturally acquired VL were known when this study was initiated. At present, VL is also spreading to other urban areas in the southern and southeast regions, where the disease was not previously endemic. 31 In the infectious cycle of VL, the dog is the most important domestic reservoir and exhibits chronic evolution of the disease. 1,8,21 Leishmania is an obligatory intracellular parasite of mononuclear phagocytes. During infection, various host organs are affected including the kidney. Although VL-related nephropathy is known both in humans and dogs, the histopathologic patterns of the lesions present in VL have not been clearly established because most studies are based on very few cases and mainly because well-defined, lesion classification criteria were not used. 3,4,9,10,24,37,38 In human VL, glomerulosclerosis, mesangial cell proliferation, and interstitial nephritis have been reported. 3,9,10,16,18,38 Renal involvement in canine VL is also frequent, and the renal changes are similar to those seen in humans. 2,5,8,23,32 This similarity renders the study of canine VL nephropathy of interest with regard to human pathology. The renal lesion itself does not lead to renal insufficiency. However, when moderate or severe renal lesions are present, VL patients with systemic complications such as secondary infections, sepsis, and hypotension do develop renal insufficiency. 16 Furthermore, glomerular lesions appare...

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“…However, since other studies of glomerulonephritis pathogenesis of other etiologies have revealed the involvement of T cells 65 and adhesion molecules 8 we extended our study to evaluate the participation of other immune elements. We detected CD4 + T cells in the glomeruli of five dogs with naturally acquired visceral leishmaniasis from an area where the disease is endemic 17 . Furthermore, in a parallel study we identified glomerulonephritis in 55 dogs naturally infected with visceral leishmaniasis, characterized their glomerular alterations histopathologically, and classified them into six different patterns (proliferative patterns were most common) 16 .…”

Section: Immunopathogeny In Non-lymphoid Organsmentioning

confidence: 98%

Immunoactivation and immunopathogeny during active visceral leishmaniasis

Goto

Prianti

2009

Rev. Inst. Med. trop. S. Paulo

100

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SUMMARYVisceral leishmaniasis is caused by protozoan parasites of the Leishmania donovani complex. During active disease in humans, high levels of IFN-g and TNF-a detected in blood serum, and high expression of IFN-g mRNA in samples of the lymphoid organs suggest that the immune system is highly activated. However, studies using peripheral blood mononuclear cells have found immunosuppression specific to Leishmania antigens; this poor immune response probably results from Leishmania antigen-engaged lymphocytes being trapped in the lymphoid organs. To allow the parasites to multiply, deactivating cytokines IL-10 and TGF-b may be acting on macrophages as well as anti-Leishmania antibodies that opsonize amastigotes and induce IL-10 production in macrophages. These high activation and deactivation processes are likely to occur mainly in the spleen and liver and can be confirmed through the examination of organ samples. However, an analysis of sequential data from studies of visceral leishmaniasis in hamsters suggests that factors outside of the immune system are responsible for the early inactivation of inducible nitric oxide synthase, which occurs before the expression of deactivating cytokines. In active visceral leishmaniasis, the immune system actively participates in non-lymphoid organ lesioning. While current views only consider immunocomplex deposition, macrophages, T cells, cytokines, and immunoglobulins by diverse mechanism also play important roles in the pathogenesis. KEYWORDS:Visceral leishmaniasis; Human; Immunosuppression; Immunoactivation; Cytokines; Immunopathogenesis.Visceral leishmaniasis is caused by protozoa of the genus Leishmania that are transmitted to mammalian hosts, including humans, by phlebotomine sandflies. The disease is present in 66 countries in tropical and subtropical regions, and 90% of cases occur in India, Sudan, Bangladesh, Nepal, and Brazil. It is estimated that there are 500,000 new cases a year worldwide 68 , and 3,000 new cases occur each year in Brazil 48 . Until recently, the disease was thought to be caused by three species of the Leishmania donovani complex: Leishmania (Leishmania) donovani, L. (L.) infantum, and Leishmania (L.) chagasi (a species present in Brazil). There is now debate, however, over whether L. (L). infantum and Leishmania (L.) chagasi are the same 44 or different 60 species. In this review, the names of the three species will be used as in the original publications. Leishmania (Leishmania) donovani is present in East Africa, India, and parts of the Middle East, while L. (L.) infantum in Europe, North Africa, and South and Central America. Human infections can be asymptomatic or can manifest as oligosymptomatic and progressive diseases; progressive cases can involve hepatosplenomegaly, fever, pancytopenia, hypergammaglobulinemia, and serious weight loss 4 . During active visceral leishmaniasis, the parasite multiplies within the cells of the mononuclear phagocyte system in the spleen, liver, and bone marrow, and the disease is fatal if untreated.Studies...

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CD4+ T cells participate in the nephropathy of canine visceral leishmaniasis

Cited by 32 publications

References 11 publications

Hypertension and its correlation with renal lesions in dogs with leishmaniosis

Hypertension and its correlation with renal lesions in dogs with leishmaniosis

Histopathologic Patterns of Nephropathy in Naturally Acquired Canine Visceral Leishmaniasis

Immunoactivation and immunopathogeny during active visceral leishmaniasis

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