Ultrastructural aspects of experimental cryptosporidiosis in pigs Aspectos ultraestruturais da criptosporidiose experimental em suínos

The aim of this work was to determine ultrastructural changes on the intestinal mucosa and associated lymphoid tissues after an experimental infection with Cryptosporidium sp. Twelve piglets dosed orally with 1×10(6) oocysts were slaughtered on days 3, 6, 9 and 12 after inoculation. The ultrastructural lesions in the intestinal cells were irregular with thickened microvilli, cytoplasmic protrusions and vacuolation, swollen mitochondria, hypertrophic organelles and nuclei. The lymphocytes of the Peyer’s patches occasionally were mitotic with a larger number of lymphoblasts in the inoculated animals.<br>O presente estudo teve por objetivo investigar as alterações ultraestruturais da mucosa intestinal e do tecido linfóide associado na inoculação experimental de Cryptosporidium sp. Doze leitões foram inoculados experimentalmente por via oral com 1×10(6) oocistos e sacrificados 3, 6, 9 e 12 dias depois. Ao exame ultraestrutural de células intestinais observou-se espessamento e irregularidade de microvilosidades, citoplasma vacuolizado e com protrusões, edema mitocondrial, hipertrofia de organelas citoplasmáticas e do núcleo. Nas placas de Peyer observou-se ocasionalmente mitose de células linfóides, verificando-se maior número de células blásticas

Delayed Schwann cell and oligodendrocyte remyelination after ethidium bromide injection in the brainstem of Wistar rats submitted to streptozotocin diabetogenic treatment

Schwann cell disturbance followed by segmental demyelination in the peripheral nervous system occurs in diabetic patients. Since Schwann cell and oligodendrocyte remyelination in the central nervous system is a well-known event in the ethidium bromide (EB) demyelinating model, the aim of this investigation was to determine the behavior of both cell types after local EB injection into the brainstem of streptozotocin diabetic rats. Adult male Wistar rats received a single intravenous injection of streptozotocin (50 mg/kg) and were submitted 10 days later to a single injection of 10 µL 0.1% (w/v) EB or 0.9% saline solution into the cisterna pontis. Ten microliters of 0.1% EB was also injected into non-diabetic rats. The animals were anesthetized and perfused through the heart 7 to 31 days after EB or saline injection and brainstem sections were collected and processed for light and transmission electron microscopy. The final balance of myelin repair in diabetic and non-diabetic rats at 31 days was compared using a semi-quantitative method. Diabetic rats presented delayed macrophage activity and lesser remyelination compared to non-diabetic rats. Although oligodendrocytes were the major remyelinating cells in the brainstem, Schwann cells invaded EB-induced lesions, first appearing at 11 days in non-diabetic rats and by 15 days in diabetic rats. Results indicate that short-term streptozotocin-induced diabetes hindered both oligodendrocyte and Schwann cell remyelination (mean remyelination scores of 2.57 ± 0.77 for oligodendrocytes and 0.67 ± 0.5 for Schwann cells) compared to non-diabetic rats (3.27 ± 0.85 and 1.38 ± 0.81, respectively)

Delayed Schwann cell and oligodendrocyte remyelination after ethidium bromide injection in the brainstem of Wistar rats submitted to streptozotocin diabetogenic treatment

Schwann cell disturbance followed by segmental demyelination in the peripheral nervous system occurs in diabetic patients. Since Schwann cell and oligodendrocyte remyelination in the central nervous system is a well-known event in the ethidium bromide (EB) demyelinating model, the aim of this investigation was to determine the behavior of both cell types after local EB injection into the brainstem of streptozotocin diabetic rats. Adult male Wistar rats received a single intravenous injection of streptozotocin (50 mg/kg) and were submitted 10 days later to a single injection of 10 µL 0.1% (w/v) EB or 0.9% saline solution into the cisterna pontis. Ten microliters of 0.1% EB was also injected into non-diabetic rats. The animals were anesthetized and perfused through the heart 7 to 31 days after EB or saline injection and brainstem sections were collected and processed for light and transmission electron microscopy. The final balance of myelin repair in diabetic and non-diabetic rats at 31 days was compared using a semi-quantitative method. Diabetic rats presented delayed macrophage activity and lesser remyelination compared to non-diabetic rats. Although oligodendrocytes were the major remyelinating cells in the brainstem, Schwann cells invaded EB-induced lesions, first appearing at 11 days in non-diabetic rats and by 15 days in diabetic rats. Results indicate that short-term streptozotocin-induced diabetes hindered both oligodendrocyte and Schwann cell remyelination (mean remyelination scores of 2.57 ± 0.77 for oligodendrocytes and 0.67 ± 0.5 for Schwann cells) compared to non-diabetic rats (3.27 ± 0.85 and 1.38 ± 0.81, respectively)

Immunohistochemical Staining Of The Macrophagic And Astrocytic Response In The Brainstem Of Wistar Rats Submitted To The Ethidium Bromide Gliotoxic Model And Treated With Cyclophosphamide [marcação Imuno-histoquímica Da Resposta Macrofágica E Astrocitária No Tronco Encefálico De Ratos Wistar Submetidos Ao Modelo Gliotóxico Do Brometo De Etídio E Tratados Com Ciclofosfamida]

The gliotoxic ethidium bromide (EB) was used to study morphologically the macrophagic and astrocytic response under immunosuppression by cyclophosphamide (CY). Astrocyte immunoreactivity to glial fibrillary acidic protein (GFAP) and vimentin (VIM) and macrophagic immunoreactivity to ED1 were investigated after EB injection. Male Wistar rats were injected with 0.9% saline solution (group I), 0.1% BE (group II) and 0.1% EB associated with CY treatment (group III). Brainstem samples were collected from the 1st to the 21st day post-injection for GFAP, VIM and ED1 immunostaining. In groups II and III, it was observed increased immunoreactivity to GFAP and reexpression of VIM. In group II, ED1-positive cells were noted after the 2nd day and in group III, after the 3rd day. On the 14th day post-injection, it was observed a greater quantity of ED1- positive cells in group III than in group II. 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