Inflammation and structural changes of splenic lymphoid tissue in visceral leishmaniasis: A study on naturally infected dogs

Santana, César Costapinto; Vassallo, José; Freitas, Luiz Antônio Rodrigues de; Oliveira, Geraldo G. S.; Pontes-de-Carvalho, Lain Carlos; dosSantos, Washington Luis Conrado

doi:10.1111/j.1365-3024.2008.01051.x

Cited by 68 publications

(118 citation statements)

References 42 publications

(52 reference statements)

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“…Our results coincided with others studies (GIUNCHETTI et al, 2008;LIMA et al, 2007;TAFURI et al, 1996), who observed well-organized intralobular granulomas in the livers of infected dogs. The disorganized tissue architecture in the spleen relating to predominance of parasitized macrophages was observed in our study and others researches (SANTANA et al, 2008;TASCA et al, 2009).…”

Section: Discussionsupporting

confidence: 84%

Influence of apoptosis on liver and spleen resistance in dogs with visceral leishmaniosis

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Rossit

et al. 2016

Rev. Bras. Parasitol. Vet.

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The aim of this study was to evaluate apoptosis and parasite load in the liver and spleen of dogs with visceral leishmaniosis (VL), using immunohistochemistry. Liver and spleen samples from 71 dogs with VL were used. The parasite load in the spleen and liver showed significant difference between organs in infected group (P=0.0219). The density of the parasite load in the spleen (median=2.4) was higher than liver (median=0.8). Immunodetection of apoptotic cells was predominant in lymphocytes and differ between the infected and control group in spleen (P=0.0307) and liver (P=0.0346). There was a significant correlation between apoptosis and parasite load (P = 0.0084; r=0.3104) only in the spleen of the infected group, where it was observed that, when increasing the number of apoptotic cells increases the parasitic load. It was concluded that the liver and spleen of infected dogs presented greater numbers of cells undergoing apoptosis (lymphocytes) than the control group, thus suggesting that this process may be contributing towards the survival of Leishmania in these organs, because lymphocyte in apoptosis did not have the ability to present and recognize the antigen, allowing the survival of the parasite.Keywords: Leishmania infantum, immune escape, apoptosis, dogs. ResumoO objetivo deste estudo foi avaliar a apoptose e a carga parasitária no fígado e baço de cães com leishmaniose visceral (LV), pela técnica de imuno-histoquímica. Foram utilizadas amostras de fígado e baço de 71 cães com LV. A carga parasitária no baço e fígado mostrou diferença significativa entre os órgãos no grupo infectado (P=0,0219). A densidade da carga de parasita no baço (média=2,4) foi maior do que no fígado (média=0,8). A imunodetecção de células em apoptose foi predominante nos linfócitos, com diferenças entre o grupo infectado e controle no baço (P=0,0307) e fígado (P=0,0346). Houve uma correlação positiva fraca entre apoptose e carga parasitária (P=0,0084; r=0,3104) apenas no baço do grupo infectado, onde observou-se que quando aumentava o número de células em apoptose aumentava a carga parasitária. Concluiu-se que o fígado e o baço de cães infectados apresentam um maior número de células que sofrem apoptose (linfócitos) do que o grupo controle, sugerindo que este processo possa contribuir para a sobrevivência de Leishmania nestes órgãos, pois os linfócitos em apoptose não tiveram a capacidade de apresentar e reconhecer o antígeno, permitindo a sobrevivência do parasita.Palavras-chave: Leishmania infantum, evasão da resposta imune, apoptose, cães.

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Section: Discussionsupporting

confidence: 84%

Influence of apoptosis on liver and spleen resistance in dogs with visceral leishmaniosis

Moreira

Franciscato

Rossit

et al. 2016

Rev. Bras. Parasitol. Vet.

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“…27 Lesions of the spleen of dogs with leishmaniasis are characterized by thickening of trabecular regions, granulomatous reaction and hemorrhagic areas, atrophy of lymphoid follicles and marginal zone, abundant macrophages with amastigotes in the cytoplasm, and perisplenitis. 36,39,50 Considering bacterial splenitis, dogs with Staphylococcus spp., 1 Mycobacterium avium Mycobacterium tuberculosis, 6,17,26,31 Listeria monocytogenes, 42 Bartonella henselae, and Bartonella vinsonii, 40 Clostridium spp., 2 Bacillus anthracis, 28 Burkholderia pseudomallei, 48 and multiple bacterial infection 11 have been described; in these cases, histologic lesions of the spleen are generally pyogranulomatous 6,40 or neutrophilic. 2 Splenic abscesses, likely due to bacterial infection, have been described in some dogs.…”

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confidence: 99%

Splenitis in 33 Dogs

et al. 2016

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Splenitis is uncommonly reported in dogs. Herein, the authors describe its prevalence, clinical findings and outcomes, histologic patterns, and causes. Splenic samples of dogs diagnosed with splenitis between 2005 and 2013 were collected and stained with hematoxylin and eosin, Gram, green-Gram, Giemsa, periodic acid-Schiff, and Ziehl-Neelsen. Samples were processed for polymerase chain reaction (PCR) to detect bacteria, fungi, and protozoa ( Leishmania infantum, Hepatozoon canis). Thirty-three of 660 splenic samples (5%) had splenitis. Clinical findings and outcomes were available in 19 dogs (58%); 49% had weakness, 33% had fever, and 84% survived. The most frequent inflammatory patterns included purulent splenitis (27%), pyogranulomatous splenitis (24%), and neutrophilic perisplenitis (15%). One dog had a putative diagnosis of primary splenitis; in 8 dogs, microorganisms were identified histologically or by PCR in the spleen without obvious comorbidities. Twenty-four dogs (73%) had concurrent diseases; a permissive role in the development of splenitis was suspected in 21 of these cases. Histologic examination identified the cause of splenitis in 10 dogs. Bacteria were identified by PCR in 23 cases, but the bacteria were confirmed histologically in only 6 of these. Leishmania was detected with PCR in 6 dogs. Leishmania was identified in 1 dog and H. canis in another histologically, but both were PCR negative. Fungi were identified in 8 spleens by PCR and in 1 by histology. This study suggests that splenitis is uncommon in dogs and is frequently associated with systemic diseases. Prognosis is favorable in most cases. Identification of bacteria, fungi, and protozoa in the spleens of affected dogs with PCR should be interpreted cautiously, because the findings are not confirmed histologically in many cases.

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“…is observed in vivo with a negative Montenegro test . Dogs infected with Leishmania infantum have a reduced number of T lymphocytes (Bourdoiseau et al, 1997) and a disruption of the splenic white pulp (Santana et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

PD-1 function in apoptosis of T lymphocytes in canine visceral leishmaniasis

et al. 2016

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Dogs infected with Leishmania infantum have a reduced number of T lymphocytes. PD-1 (Programmed cell death 1) a new member of the B7-CD28 family that is expressed by immune cells, and its binding to PD-L1 (CD274) or PD-L2 (CD273) induces the deactivation or apoptosis of T cells. This study aimed to evaluate the expression of PD-1 and its ligands, as well as blocking in the induction of apoptosis in T lymphocytes, TNF-α, IL-4 and nitric oxide production by leucokocytes from PBMC and spleen and the parasite load in dogs with visceral leishmaniasis (VL). Our results showed that the expression of PD1 and its ligands was increased in CD3(+) T cells and CD21(+) B lymphocytes within the peripheral blood and splenic mononuclear cells of dogs with VL. In peripheral blood monocytes, only PD-1 ligands exhibited increased expression; however, in spleen macrophages, increased expression of both PD-1 and its ligands was observed. Levels of apoptosis in peripheral blood and splenic T lymphocytes were higher in dogs with VL compared to healthy dogs. Blocking monoclonal antibodies to PD-1 and its ligands in the culture of mononuclear cells from the peripheral blood and spleen decreased the amount of CD3(+) T lymphocyte apoptosis. The concentration of nitric oxide, TNF-α and IL-4 increased in the culture supernatants of peripheral blood mononuclear cells treated with a blocking monoclonal antibody against PD-1. The TNF-α concentration increased in the culture supernatants of splenic cells following all treatments with antibodies blocking PD-1 and its ligands; however, the amount of IL-4 increased only in the presence of a PD-1 blocking agent. Treatment with a PD-1 blocking monoclonal antibody in the mononuclear peripheral blood of dogs with VL reduced the parasite burden while increased TNF-α. We conclude that in canine visceral leishmaniasis, PD-1 and its ligands are involved in the induction of T lymphocyte apoptosis and in regulating the production of nitric oxide, TNF-α, and IL-4, as well as the parasitic load.

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Inflammation and structural changes of splenic lymphoid tissue in visceral leishmaniasis: A study on naturally infected dogs

Cited by 68 publications

References 42 publications

Influence of apoptosis on liver and spleen resistance in dogs with visceral leishmaniosis

Influence of apoptosis on liver and spleen resistance in dogs with visceral leishmaniosis

Splenitis in 33 Dogs

PD-1 function in apoptosis of T lymphocytes in canine visceral leishmaniasis

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