A Comparison of Radiation-Induced Bone Marrow Degeneration in Germfree and Conventional Mice

Heit, H.; Tm, Fliedner; Fache, I.; Schnell, Guillaume

doi:10.2307/3572904

Cited by 13 publications

(8 citation statements)

References 5 publications

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“…At low levels (500 to 1000 R) haematological failure occurs due to destruction of bone marrow cells. In the experiments of Heit, Fliedner, Fache & Schnell (1970) there was no evidence of difference in bone-marrow response between germ-free and conventional mice, and the authors concluded that bacterial infection and consequent toxaemia was the likely cause of earlier death in the conventional animals. At higher doses (1000 to 10000 R) there is gastrointestinal injury.…”

Section: The Microbiologicalmentioning

confidence: 95%

Gnotobiotic animals in research: their uses and limitations

Coates¹

1975

Lab Anim

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Section: The Microbiologicalmentioning

confidence: 95%

Gnotobiotic animals in research: their uses and limitations

Coates¹

1975

Lab Anim

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“…Third, the minimum TBI dose that produces histological evidence of radiation enteritis (mucosal atrophy, mesenchymal inflammation, and fibrosis) is higher in GF mice, compared with animals with a microbiota (21). In contrast, the dose threshold and extent of TBI-induced damage to bone marrow are equivalent in GF and CONV-R mice (23,24).…”

mentioning

confidence: 99%

Microbial regulation of intestinal radiosensitivity

Crawford

Gordon

2005

Proc. Natl. Acad. Sci. U.S.A.

208

166

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We describe a method for treating germ-free (GF) mice with ␥-irradiation and transplanting them with normal or genetically manipulated bone marrow while maintaining their GF status. This approach revealed that GF mice are markedly resistant to lethal radiation enteritis. Furthermore, administering lethal doses of total body irradiation to GF mice produces markedly fewer apoptotic endothelial cells and lymphocytes in the mesenchymal cores of their small intestinal villi, compared with conventionally raised animals that have acquired a microbiota from birth. Analysis of GF and conventionally raised Rag1 ؊/؊ mice disclosed that mature lymphocytes are not required for the development of lethal radiation enteritis or the microbiota-associated enhancement of endothelial radiosensitivity. Studies of gnotobiotic knockout mice that lack fasting-induced adipose factor (Fiaf), a fibrinogen͞angio-poietin-like protein normally secreted from the small intestinal villus epithelium and suppressed by the microbiota, showed that Fiaf deficiency results in loss of resistance of villus endothelial and lymphocyte populations to radiation-induced apoptosis. Together, these findings provide insights about the cellular and molecular targets involved in microbial regulation of intestinal radiosensitivity.endothelial cell apoptosis ͉ fasting-induced adipose factor ͉ gnotobiotic knockout and radiation chimeric mice ͉ gut microbiota ͉ radiation enteritis

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“…This could be due to absorption or inactivation of CSF by bone marrow cells (14) , or to the restoration of immunocompetence which would reduce the extent of endotoxinemia. The decrease in bone marrow cell populations has been found to be similar in both germfree and conventional animals: by Day 4 after exposure to 700 R, the bone marrow was almost aplastic (11). If the absorption of CSF by bone marrow cells could explain the reduction of CSF in the group which was transplanted with bone marrow cells, then irradiated germfree mice should have elevated levels of CSF in their serums.…”

Section: Methodsmentioning

confidence: 92%

“…These two possifbilities are not mutually exclusive. However, they could not detect increased CSF level in irradiated germfree mice (4) and germfree mice like conventional animals, developed postirradiation neutropenia ( 11). This suggested that the bacterial flora of the gut would have a role in the level of serum CSF following X-irradiation.…”

Section: Methodsmentioning

confidence: 96%