Reovirus type 2-induced diabetes in mice prevented by immunosuppression and thymic hormone

Onodera, Takashi; Taniguchi, Toshiaki; Shimizu, Shinya; Sato, Mariko; Hayashi, Toshiharu

doi:10.1007/bf00404795

Cited by 23 publications

(39 citation statements)

References 13 publications

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“…In addition, reovirus types 1 and 2 were reported to cause autoimmune-related insulitis in mice (ONODERA et al 1978(ONODERA et al , 1981. Present study revealed that reovirus type 3 was pancreas-trophic.…”

Section: Discussionmentioning

confidence: 51%

Infection of reovirus type 3 in Mongolian gerbils (Meriones unguiculatus) – Lesions in pancreas and brain

Yukawa

Takeuchi

Mochizuki

et al. 1993

J. Basic Microbiol.

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Gerbils were inoculated with reovirus type 3 (Abney strain), and the pancreas, brain and other organs histopathologically evaluated. Male Mongolian gerbils (Meriones unguiculatus) aged 5-10 days (newborn, 9 animals), 4 weeks (juvenile, 5 animals), and 12 weeks (adult, 5 animals) were used. Gerbils inoculated intraperitoneally with the virus were sacrificed 3, 5, 7, or 10 days later. Tissues were observed by light and electron microscopy. The pancreas of newborns showed inflammatory edema with infiltrates of neutrophilis and mononuclear round cells, degranulation of acinar cells and dissociation of lobules and acini with necrosis at 3 days or later after inoculation but not degeneration of pancreatic islets. Brains of newborns had necrosis of neurons and aggregation of microglial cells in the brain stem and cerebral hemisphere. Azurophilic inclusion bodies were seen in the cytoplasm of some neurons. In electron micrographs, virus particles (60-80 nm in diameter) were observed around the nucleus of neurons in the brain stem. No changes were observed in the juvenile and adult gerbils.

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Section: Discussionmentioning

confidence: 51%

Infection of reovirus type 3 in Mongolian gerbils (Meriones unguiculatus) – Lesions in pancreas and brain

Yukawa

Takeuchi

Mochizuki

et al. 1993

J. Basic Microbiol.

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“…However, given that insulitis occurs in NOD mice infected with reovirus, we think it unlikely that passive tolerance alone explains the diabetes delay in these animals. Reovirus also can infect the murine pancreas (20,22,23), and our results suggest that reovirus is capable of infecting pancreatic ␤ cells in NOD mice (Fig. 1B and D).…”

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confidence: 80%

“…After passage in primary cultures of pancreatic ␤ cells, each of the three reovirus serotypes can infect the murine pancreas (20,22,23). Newborn SJL/J mice infected with reovirus develop an acute inflammatory response within pancreatic islets, and viral antigen can be detected by immunofluorescence in ␤ cells (20,23).…”

mentioning

confidence: 99%

Reovirus Delays Diabetes Onset but Does Not Prevent Insulitis in Nonobese Diabetic Mice

Wetzel

Barton

Chappell

et al. 2006

J Virol

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Mice infected with reovirus develop abnormalities in glucose homeostasis. Reovirus strain type 3 Abney (T3A) was capable of systemic infection of nonobese diabetic (NOD) mice, an experimental model of autoimmune diabetes. Reovirus antigen was detected in pancreatic islets of T3A-infected mice, and primary cultures of pancreatic islets from NOD mice supported T3A growth. Significantly fewer T3A-infected animals compared to uninfected controls developed diabetes. However, despite the alteration in diabetes penetrance, insulitis was evident in T3A-infected mice. These results suggest that viral infection of NOD mice alters autoimmune responses to ␤-cell antigens and thereby delays development of diabetes.

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“…1990). Most mice recovered from the disease within three weeks after infection (Onodera et al. 1990; Hayashi et al.…”

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confidence: 99%

“…1998, 2001). This may be due to the fact that a sufficient number of β‐cells were left intact after the destruction, and proliferation accompanied by disappearance of infiltrated cells may occur (Onodera et al. 1990).…”

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confidence: 99%

Reovirus type‐2 infection in newborn DBA/1J mice reduces the development of late allergic asthma

Nakashima¹,

Hayashi²,

Mizuno

2012

Int J Experimental Path

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The aim of the present study was to determine whether or not the development of a helper T (Th) 1 response induced by Reovirus type-2 (Reo-2) infection would protect against the development of Th2-mediated late allergic asthma. This hypothesis was examined by infecting one day old neonatal DB A/1J mice with Reo-2 in an ovalbumin (OVA)-induced late asthma model. Compared with the controls (either infected or uninfected mice with or without OVA sensitization and/or OVA challenge), Reo-2 infection lessened the magnitude of the subsequent allergic Th2-mediated late asthma. In infected mice with allergic late asthma, there was decreased infiltration of interleukin (IL)-4(+), IL-5(+), IL-13(+) and very late antigen (VLA)-4(+) lymphocytes, and eotaxin-2(+) and VLA-4(+) eosinophils, in both bronchial and bronchiolar lesions. Also the expression of vascular cell adhesion molecule (VCAM)-1 and eotaxin-2 on vascular endothelial cells was reduced. Moreover, the systemic production of IL-4, IL-5, tumour necrosis factor-α and OVA-specific IgE was reduced, whereas systemic IFN-γ production was increased. In addition, there was no increase in IFN-α production. Thus the present study suggests that systemic Reo-2 infection at birth may reduce the development of subsequent late allergic asthma by the induction of a Th1 response. Therefore the potential suppressive mechanism(s) that might be induced by Reo-2 infection in newborn mice and their effects on the development of late allergic asthma are discussed.

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Reovirus type 2-induced diabetes in mice prevented by immunosuppression and thymic hormone

Cited by 23 publications

References 13 publications

Infection of reovirus type 3 in Mongolian gerbils (Meriones unguiculatus) – Lesions in pancreas and brain

Infection of reovirus type 3 in Mongolian gerbils (Meriones unguiculatus) – Lesions in pancreas and brain

Reovirus Delays Diabetes Onset but Does Not Prevent Insulitis in Nonobese Diabetic Mice

Reovirus type‐2 infection in newborn DBA/1J mice reduces the development of late allergic asthma

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