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1.
Front Cell Infect Microbiol ; 11: 687499, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34336715

RESUMO

Leishmania (Viannia) braziliensis is one of the main causes of cutaneous leishmaniasis in the Americas. This species presents genetic polymorphism that can cause destructive lesions in oral, nasal, and oropharyngeal tracts. In a previous study, the parasite caused several histopathological changes to hamster ileums. Our study evaluates immune response components, morphological changes, and effects on neurons in the ileums of hamsters infected by three different strains of L. (V.) braziliensis in two infection periods. For the experiment, we separated hamsters into four groups: a control group and three infected groups. Infected hamsters were euthanized 90- or 120-days post infection. We used three strains of L. (V.) braziliensis: the reference MHOM/BR/1975/M2903 and two strains isolated from patients who had different responses to Glucantime® treatment (MHOM/BR/2003/2314 and MHOM/BR/2000/1655). After laparotomy, ileums were collected for histological processing, biochemical analysis, and evaluation of neurons in the myenteric and submucosal plexuses of the enteric nervous system (ENS). The results demonstrated the increase of blood leukocytes after the infection. Optical microscopy analysis showed histopathological changes with inflammatory infiltrates, edemas, ganglionitis, and Leishmania amastigotes in the ileums of infected hamsters. We observed changes in the organ histoarchitecture of infected hamsters when compared to control groups, such as thicker muscular and submucosa layers, deeper and wider crypts, and taller and broader villi. The number of intraepithelial lymphocytes and TGF-ß-immunoreactive cells increased in all infected groups when compared to the control groups. Mast cells increased with longer infection periods. The infection also caused remodeling of intestinal collagen and morphometry of myenteric and submucosal plexus neurons; but this effect was dependent on infection duration. Our results show that L. (V.) braziliensis infection caused time-dependent alterations in hamster ileums. This was demonstrated by the reduction of inflammatory cells and the increase of tissue regeneration factors at 120 days of infection. The infected groups demonstrated different profiles in organ histoarchitecture, migration of immune cells, and morphometry of ENS neurons. These findings suggest that the small intestine (or at least the ileum) is a target organ for L. (V.) braziliensis infection, as the infection caused changes that were dependent on duration and strain.


Assuntos
Íleo/parasitologia , Leishmania braziliensis , Leishmaniose/patologia , Animais , Cricetinae , Humanos
2.
J Helminthol ; 94: e166, 2020 Jun 23.
Artigo em Inglês | MEDLINE | ID: mdl-32571437

RESUMO

Pseudocorynosoma constrictum (Van Cleave, 1918) is a polymorphid acanthocephalan that attaches to the digestive tract of waterfowl to complete its life cycle, causing severe histological damage to its definitive avian hosts. In the present study, we present a histopathological analysis of the lesions that P. constrictum induced in the layers of the ileum of the blue-winged teal Anas discors. The results revealed that worms insert the attachment structures into the inner gut muscular layer, which causes substantial swelling, haemorrhaging and necrosis in the tissue near the parasite's proboscis. We also observed that the number of parasites attached to the tissue can obstruct the intestinal lumen; in the most serious case, we observed more than 30 parasites penetrating completely the walls of the bird intestine.


Assuntos
Acantocéfalos/patogenicidade , Aves/parasitologia , Íleo/patologia , Íleo/parasitologia , Acantocéfalos/anatomia & histologia , Animais , México , Mucosa/parasitologia , Necrose
3.
Rev Soc Bras Med Trop ; 51(4): 537-541, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30133641

RESUMO

INTRODUCTION: Leishmania species cause skin, mucosal, and disseminated lesions. We studied the effects of three Leishmania species on ileal morphology in mice. METHODS: BALB/c mice were intraperitoneally inoculated with Leishmania (Leishmania) amazonensis, Leishmania (Viannia) braziliensis, and Leishmania (Leishmania) major (4 animals/group). After 72h, the ilea were collected and histologically processed. RESULTS: Following inoculation, the goblet cell and intraepithelial lymphocyte populations increased, while Paneth cell number and crypt width decreased. In addition, enterocyte size, villi height, and mucosa, submucosa, and muscular tunic thickness increased. CONCLUSIONS: Leishmania modified the quantity of cells in and morphology of mice ilea.


Assuntos
Íleo/patologia , Íleo/parasitologia , Leishmania/patogenicidade , Leishmaniose/patologia , Leishmaniose/parasitologia , Animais , Modelos Animais de Doenças , Feminino , Leishmania/classificação , Camundongos , Camundongos Endogâmicos BALB C , Especificidade da Espécie
4.
Biomed Pharmacother ; 106: 1624-1632, 2018 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-30119238

RESUMO

AIM: The present study compared and evaluated morphological and quantitative alterations in the ileum of hamsters infected by two L. (V.) braziliensis strains isolated from patients with different lesion aspects and treatment responses. MAIN METHODS: Hamsters were infected in the left hindpaw with a suspension of promastigotes (2 × 107/100 µl) of two different strains of L. (V.) braziliensis. After 90 or 120 days, the animals were euthanized. Samples of the ileum and mesenteric lymph node were collected for histological examination and quantitative polymerase chain reaction. KEY FINDINGS: All infected animals developed similar profile of paw lesions. In peripheral blood there was an increase in the number of mononuclear cells which contributed to elevated global leukocytes count. Increases in the width and height of villi and width and depth of crypts were observed. The thickness of the muscular layers, submucosa, and intestinal wall also increased. Histopathological alterations were observed, including inflammatory infiltrate in crypts and a large number of immune cells in the lamina propria, submucosa, and muscular layer. Immune cells were found inside myenteric ganglia, with an increase in the number of intraepithelial lymphocytes. Leishmania DNA was detected in the ileum and mesenteric lymph node at both times of infection. The presence of amastigotes in the ileum was revealed by immunohistochemistry. SIGNIFICANCE: The infection with different strains of L. (V.) braziliensis causes morphological and quantitative alterations in the ileum of hamsters and the parasite can migrate to the mesenteric lymph node and intestine.


Assuntos
Íleo/parasitologia , Leishmania braziliensis/patogenicidade , Leishmaniose Cutânea/parasitologia , Animais , DNA de Protozoário/genética , Modelos Animais de Doenças , Feminino , Interações Hospedeiro-Parasita , Íleo/imunologia , Íleo/patologia , Leishmania braziliensis/genética , Leishmania braziliensis/imunologia , Leishmaniose Cutânea/imunologia , Leishmaniose Cutânea/patologia , Linfonodos/parasitologia , Mesocricetus , Carga Parasitária , Fatores de Tempo
5.
Rev. Soc. Bras. Med. Trop ; 51(4): 537-541, July-Aug. 2018. tab, graf
Artigo em Inglês | LILACS | ID: biblio-1041471

RESUMO

Abstract INTRODUCTION: Leishmania species cause skin, mucosal, and disseminated lesions. We studied the effects of three Leishmania species on ileal morphology in mice. METHODS: BALB/c mice were intraperitoneally inoculated with Leishmania (Leishmania) amazonensis, Leishmania (Viannia) braziliensis, and Leishmania (Leishmania) major (4 animals/group). After 72h, the ilea were collected and histologically processed. RESULTS: Following inoculation, the goblet cell and intraepithelial lymphocyte populations increased, while Paneth cell number and crypt width decreased. In addition, enterocyte size, villi height, and mucosa, submucosa, and muscular tunic thickness increased. CONCLUSIONS: Leishmania modified the quantity of cells in and morphology of mice ilea.


Assuntos
Animais , Feminino , Leishmaniose/parasitologia , Leishmaniose/patologia , Íleo/parasitologia , Íleo/patologia , Leishmania/patogenicidade , Camundongos , Especificidade da Espécie , Modelos Animais de Doenças , Leishmania/classificação , Camundongos Endogâmicos BALB C
6.
Parasite ; 25: 22, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29633710

RESUMO

Human abdominal angiostrongyliasis (HAA) is a parasitic disease caused by the accidental ingestion of the nematode Angiostrongylus costaricensis in its larval form. Human infection can lead to severe ischemic and inflammatory intestinal lesions, sometimes complicated by life-threatening ileal perforations. Only one case had been reported in Martinique, an Island in the French Antilles, in 1988. We retrospectively reviewed the medical charts of patients diagnosed with abdominal angiostrongyliasis at the University Hospital of Martinique between 2000 and 2017. The objectives of this study were to evaluate the incidence and perform a descriptive analysis of the clinical, biological, radiological, and histopathological features of HAA in Martinique. Two confirmed cases and two probable cases were identified in patients aged from 1 to 21 years during the 18-year period, with an estimated incidence of 0.2 cases per year (0.003 case/year/100.000 inhabitants (IC95% = 0.00-0.05)). All patients presented with abdominal pain associated with high blood eosinophilia (median: 7.24 G/L [min 4.25; max 52.28 G/L]). Two developed ileal perforation and were managed by surgery, with diagnostic confirmation based on histopathological findings on surgical specimens. The other two cases were probable, with serum specimens reactive to Angiostrongylus sp. antigen in the absence of surgery. All cases improved without sequelae. The description of this case series highlights the need to increase awareness of this life-threatening disease in the medical community and to facilitate access to specific diagnostic tools in Martinique. Environmental and epidemiological studies are needed to broaden our knowledge of the burden of this disease.


TITLE: Infections par Angiostrongylus costaricensis à la Martinique, Antilles, de 2000 à 2017. ABSTRACT: L'angiostrongylose abdominale humaine (AAH) est une maladie parasitaire causée par l'ingestion accidentelle du nématode Angiostrongylus costaricensis sous sa forme larvaire. L'infection humaine peut conduire à des lésions intestinales ischémiques et inflammatoires sévères, parfois compliquées par des perforations iléales menaçant le pronostic vital. Un seul cas avait été signalé en Martinique, une île des Antilles françaises, en 1988. Nous avons revu rétrospectivement les dossiers médicaux des patients ayant reçu un diagnostic d'angiostrongylose abdominale au CHU de la Martinique entre 2000 et 2017. Les objectifs de cette étude étaient d'évaluer l'incidence et effectuer une analyse descriptive des caractéristiques cliniques, biologiques, radiologiques et histopathologiques de l'AAH en Martinique. Deux cas confirmés et deux cas probables ont été identifiés chez des patients âgés de 1 à 21 ans au cours de la période de 18 ans, avec une incidence estimée à 0,2 cas par an (0,003 cas / an / 100 000 habitants (IC95% = 0,00 − 0,05)). Tous les patients présentaient une douleur abdominale associée à une éosinophilie sanguine élevée (médiane: 7,24 G/L [min 4,25; max 52,28 G / L]). Deux ont développé une perforation iléale et ont été traités par chirurgie, avec une confirmation diagnostique basée sur les résultats histopathologiques sur des échantillons chirurgicaux. Les deux autres cas étaient probables, avec des échantillons sériques réagissant aux antigènes d'Angiostrongylus sp. en l'absence de chirurgie. Tous les cas se sont améliorés sans séquelles. La description de cette série de cas souligne la nécessité de sensibiliser davantage la communauté médicale à cette maladie potentiellement mortelle et de faciliter l'accès à des outils diagnostiques spécifiques en Martinique. Des études environnementales et épidémiologiques sont nécessaires pour élargir nos connaissances sur cette parasitose.


Assuntos
Infecções por Strongylida/epidemiologia , Dor Abdominal/parasitologia , Adolescente , Angiostrongylus/imunologia , Animais , Anticorpos Anti-Helmínticos/sangue , Criança , Pré-Escolar , Colo/diagnóstico por imagem , Colo/parasitologia , Colo/patologia , Eosinofilia/parasitologia , Feminino , Humanos , Íleo/parasitologia , Íleo/patologia , Incidência , Lactente , Masculino , Martinica/epidemiologia , Artérias Mesentéricas/parasitologia , Artérias Mesentéricas/patologia , Radiologia , Chuva , Estudos Retrospectivos , Estações do Ano , Infecções por Strongylida/sangue , Infecções por Strongylida/diagnóstico por imagem , Infecções por Strongylida/patologia , Adulto Jovem
7.
Exp Parasitol ; 184: 22-30, 2018 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-29146488

RESUMO

Recent data shows that prior infection by Toxoplasma gondii does not protect the host from subsequent reinfection even after the development of immunological memory. Although animal models for T. gondii reinfection were proposed after cases of natural human reinfection were described, little is known about the events that occur immediately after challenge. To further understand these events, BALB/c mice were chronically infected with D8 non-virulent strain (genotype ToxoDB#8 BrIII) and challenged with two different virulent strains: EGS (genotype ToxoDB #229) or CH3 strain (genotype ToxoDB #19). Primary infection protected animals from lethal challenge and morbidity was reduced. Reinfection was confirmed by PCR-RFLP, showing differences in the way the parasites spread in challenged animals. Parasites reached the lungs during early infection and a parasitism delay in the intestine was observed in D8+CH3 group. Parasites from challenge strains were not detected in the brain of D8+CH3 and in the intestine and brain of D8+EGS group. Previous infection with D8 strain of T. gondii protected against lethal challenges, but it did not prevent parasite spread to some organs.


Assuntos
Toxoplasma/fisiologia , Toxoplasmose Animal/parasitologia , Animais , Encéfalo/parasitologia , Encéfalo/patologia , Galinhas , DNA de Protozoário/isolamento & purificação , Modelos Animais de Doenças , Cães , Feminino , Marcadores Genéticos , Humanos , Íleo/parasitologia , Íleo/patologia , Pulmão/parasitologia , Pulmão/patologia , Camundongos , Camundongos Endogâmicos BALB C , Recidiva , Toxoplasma/classificação , Toxoplasma/genética , Toxoplasma/imunologia , Toxoplasmose Animal/imunologia
8.
PLoS One ; 6(9): e25259, 2011.
Artigo em Inglês | MEDLINE | ID: mdl-21977228

RESUMO

BACKGROUND: Macrophage migration inhibitory factor (MIF) is essential for controlling parasite burden and survival in a model of systemic Toxoplasma gondii infection. Peroral T. gondii infection induces small intestine necrosis and death in susceptible hosts, and in many aspects resembles inflammatory bowel disease (IBD). Considering the critical role of MIF in the pathogenesis of IBD, we hypothesized that MIF participates in the inflammatory response induced by oral infection with T. gondii. METHODOLOGY/PRINCIPAL FINDINGS: Mif deficient (Mif(-/-)) and wild-type mice in the C57Bl/6 background were orally infected with T. gondii strain ME49. Mif(-/-) mice had reduced lethality, ileal inflammation and tissue damage despite of an increased intestinal parasite load compared to wt mice. Lack of MIF caused a reduction of TNF-α, IL-12, IFN-γ and IL-23 and an increased expression of IL-22 in ileal mucosa. Moreover, suppressed pro-inflammatory responses at the ileal mucosa observed in Mif(-/-) mice was not due to upregulation of IL-4, IL-10 or TGF-ß. MIF also affected the expression of matrix metalloproteinase-9 (MMP-9) but not MMP-2 in the intestine of infected mice. Signs of systemic inflammation including the increased concentrations of inflammatory cytokines in the plasma and liver damage were less pronounced in Mif(-/-) mice compared to wild-type mice. CONCLUSION/SIGNIFICANCE: In conclusion, our data suggested that in susceptible hosts MIF controls T. gondii infection with the cost of increasing local and systemic inflammation, tissue damage and death.


Assuntos
Fatores Inibidores da Migração de Macrófagos/metabolismo , Boca/parasitologia , Toxoplasma/fisiologia , Toxoplasmose/patologia , Toxoplasmose/parasitologia , Animais , Citocinas/metabolismo , Ileíte/complicações , Ileíte/parasitologia , Ileíte/patologia , Íleo/parasitologia , Íleo/patologia , Mediadores da Inflamação/metabolismo , Mucosa Intestinal/enzimologia , Mucosa Intestinal/parasitologia , Mucosa Intestinal/patologia , Fatores Inibidores da Migração de Macrófagos/deficiência , Metaloproteinase 2 da Matriz/metabolismo , Metaloproteinase 9 da Matriz/metabolismo , Camundongos , Camundongos Endogâmicos C57BL , Carga Parasitária , Sepse/complicações , Sepse/parasitologia , Sepse/patologia , Análise de Sobrevida , Toxoplasmose/complicações
10.
Parasite Immunol ; 32(6): 420-9, 2010 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-20500673

RESUMO

Nematode infections induce the upregulation of mucin- and glycosylation-related genes in intestinal epithelial cells in vivo. However, the factor(s) that induce these changes in epithelial cells have not been fully elucidated. In the present study, we analysed the effects of the Th2 cytokines IL-4 and IL-13 and the excretory-secretory (ES) product of the nematode Nippostrongylus brasiliensis on the gene expression of the major mucin core peptide MUC2, the sialyltransferase ST3GalIV (Siat4c) and the sulphotransferase HS3ST1 in intestinal epithelium-derived IEC-6 cells by quantitative reverse transcription (RT)-PCR. The administration of IL-4 and IL-13 resulted in a significant upregulation of ST3GalIV and HS3ST1 gene transcription, but had no effect on MUC2, in IEC-6 cells. RT-PCR studies also demonstrated the constitutive expression of IL-13Ralpha1 and IL-4R in IEC-6 cells. On the other hand, the ES product induced upregulation of ST3GalIV, but not HS3ST1 or MUC2, while coadministration of IL-13 and the ES product induced a slight but significant upregulation of MUC2. Co-incubation of live N. brasiliensis adult worms with IEC-6 cells resulted in the upregulation of ST3GalIV and MUC2. These results suggested that HS3ST1 gene expression is strictly regulated by IL-4/IL-13, while ST3GalIV and MUC2 gene expressions are regulated by redundant mechanisms.


Assuntos
Íleo/parasitologia , Interleucina-13/fisiologia , Interleucina-4/fisiologia , Mucina-2/biossíntese , Nippostrongylus/patogenicidade , Sialiltransferases/biossíntese , Sulfotransferases/biossíntese , Animais , Antígenos de Helmintos/fisiologia , Células Epiteliais/imunologia , Células Epiteliais/parasitologia , Perfilação da Expressão Gênica , Íleo/imunologia , Masculino , Ratos , Reação em Cadeia da Polimerase Via Transcriptase Reversa , beta-Galactosídeo alfa-2,3-Sialiltransferase
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