Prevention of overt diabetes and insulitis in NOD mice by a single BCG vaccination

Harada, Minoru; Kishimoto, Yoshio; Makino, Susumu

doi:10.1016/0168-8227(90)90017-n

Cited by 111 publications

(71 citation statements)

References 12 publications

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“…Diabetes in animal models can be prevented by a variety of infectious agents, including helminths, bacteria, and viruses. However, the mechanisms of action vary from the induction of regulatory T cells to altered trafficking of diabetogenic T cells (12 Calmette-Guerin (BCG) vaccine protects against diabetes in NOD mice (25,39). Infection of NOD mice with Mycobacterium avium inhibits diabetes in a manner associated with increased production of IFN-␥ and decreased production of IL-4.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Autoimmune Type 1 Diabetes by Gastrointestinal Helminth Infection

et al. 2007

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Gastrointestinal nematode infections are prevalent worldwide and are potent inducers of T helper 2 responses with the capacity to modulate the immune response to heterologous antigens. Parasitic helminth infection has even been shown to modulate the immune response associated with autoimmune diseases. Nonobese diabetic (NOD) mice provide a model for studying human autoimmune diabetes; as in humans, the development of diabetes in NOD mice has been linked to the loss of self-tolerance to beta cell autoantigens. Previous studies with the NOD mouse have shown that helminth and bacterial infection appears to inhibit type 1 diabetes by disrupting the pathways leading to the Th1-mediated destruction of insulin-producing beta cells. The aim of our study was to examine whether infection with the gastrointestinal helminths Trichinella spiralis or Heligmosomoides polygyrus could inhibit the development of autoimmune diabetes in NOD mice and to analyze the mechanisms involved in protection and the role of Th2 responses. Protection from diabetes was afforded by helminth infection, appeared to inhibit autoimmune diabetes by disrupting pathways leading to the destruction of beta cells, and was mediated by seemingly independent mechanisms depending on the parasite but which may be to be related to the capacity of the host to mount a Th2 response.

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Section: Discussionmentioning

confidence: 99%

Inhibition of Autoimmune Type 1 Diabetes by Gastrointestinal Helminth Infection

et al. 2007

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“…NIDDM appears to be caused by (i) a disorder of insulin secretion and (ii) by insulin resistance in target organs [18]. Although it has been reported that an immunopotentiator was effective in the prevention of diabetes in some animal models [19,20], the administration route was limited to injection, i.e., intraperitoneal or intravenously.…”

Section: Discussionmentioning

confidence: 99%

Antidiabetic Effects of an Oral Administration of Lactobacillus casei in a Non-Insulin-Dependent Diabetes Mellitus (NIDDM) Model using KK-Ay Mice.

et al. 1997

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Abstract.The antidiabetic effects of Lactobacillus casei (LC) on a non-insulin-dependent diabetes mellitus (NIDDM) model, KK-AY mice, were investigated. The oral administration of LC to male 4-week-old KK-AY mice, or raising the mice on a 0.05% LC-containing diet significantly decreased the plasma glucose at 8 to 10 weeks of age compared with the control group. The body weights of the LC-treated groups were lower than those of the control group, although the food intake was nearly the same in all groups. Phenotypic analysis of spleen cell surface markers revealed that the increase in CD4+ T cells at 12 weeks was significantly inhibited by the oral treatment with LC. Cytokine production, especially that of interferon-y and interleukin 2, was also inhibited in the oral LC-treated group. The plasma insulin levels of the LC-treated groups were also lower than those of the control group, and the insulin binding potential of red blood cells in the LC-treated mice was augmented more than that in the control group. Taken together, these findings led us to conclude that the oral administration of LC in the NIDDM model mice, KK-AY, was involved in the decrease in the plasma glucose level and modified the host immune responses.

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“…Although the infection is cleared by the mice within 6 wk, the protection from T1D is long lasting. A number of different infectious agents have also been shown to inhibit development of T1D in these mice, including viral (5), bacterial (6), and helminthic (7) pathogens, but we believe that the effects of S. typhimurium infection are particularly interesting, as this infection shows strong protective effects even when exposure to the bacteria occurs well after the establishment of the initial leukocytic pancreatic infiltrates.…”

Section: Salmonella Typhimurium Infection In Nonobese Diabetic Mice Gmentioning

confidence: 99%

Salmonella typhimurium Infection in Nonobese Diabetic Mice Generates Immunomodulatory Dendritic Cells Able to Prevent Type 1 Diabetes

Raine

Zaccone

Mastroeni

et al. 2006

The Journal of Immunology

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Infection, commencing across a wide age range, with a live, attenuated strain of Salmonella typhimurium, will halt the development of type 1 diabetes in the NOD mouse. The protective mechanism appears to involve the regulation of autoreactive T cells in a manner associated with long lasting changes in the innate immune compartment of these mice. We show in this study that autoreactive T cell priming and trafficking are altered in mice that have been infected previously by S. typhimurium. These changes are associated with sustained alterations in patterns of chemokine expression. We find that small numbers of dendritic cells from mice that have been previously infected with, but cleared all trace of a S. typhimurium infection are able to prevent the development of diabetes in the highly synchronized and aggressive cyclophosphamide-induced model. The effects we observe on autoreactive T cell trafficking are recapitulated by the immunomodulatory dendritic cell transfers in the cyclophosphamide model.

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Prevention of overt diabetes and insulitis in NOD mice by a single BCG vaccination

Cited by 111 publications

References 12 publications

Inhibition of Autoimmune Type 1 Diabetes by Gastrointestinal Helminth Infection

Inhibition of Autoimmune Type 1 Diabetes by Gastrointestinal Helminth Infection

Antidiabetic Effects of an Oral Administration of Lactobacillus casei in a Non-Insulin-Dependent Diabetes Mellitus (NIDDM) Model using KK-Ay Mice.

Salmonella typhimurium Infection in Nonobese Diabetic Mice Generates Immunomodulatory Dendritic Cells Able to Prevent Type 1 Diabetes

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