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Plasminogen-deficient (FVB/NPan-plg(tm1Jld), plg(tm1Jld)) mice, which are widely used as a wound-healing model, are prone to spontaneous rectal prolapses. The aims of this study were 1) to evaluate the fecal microbiome of plg(tm1Jld) mice for features that might contribute to the development of rectal prolapses and colonic inflammation and 2) to assess the relevance of the inflammatory phenotype to the variability in wound healing in this model. The (plgtm1Jld) mice exhibited delayed wound healing, and they could be divided into 3 distinct groups that differed according to the time until wound closure. Colonic lesions in plg(tm1Jld) mice, which were characterized by necrotizing ulcerations and cystically dilated glands, were restricted to the intermediate and distal parts of the colon. The cytokine profile was indicative of chronic tissue damage, but the genetic modification did not change the composition of the gut microbiota, and none of the clinical or biochemical parameters correlated with the gut microbiota composition.

OBJECTIVE: Magnesium deficiency has been associated with anxiety in humans, and rodent studies have demonstrated the gut microbiota to impact behaviour.METHODS: We investigated the impact of 6 weeks of dietary magnesium deficiency on gut microbiota composition and anxiety-like behaviour and whether there was a link between the two. A total of 20 C57BL/6 mice, fed either a standard diet or a magnesium-deficient diet for 6 weeks, were tested using the light-dark box anxiety test. Gut microbiota composition was analysed by denaturation gradient gel electrophoresis.RESULTS: We demonstrated that the gut microbiota composition correlated significantly with the behaviour of dietary unchallenged mice. A magnesium-deficient diet altered the gut microbiota, and was associated with altered anxiety-like behaviour, measured by decreased latency to enter the light box.CONCLUSION: Magnesium deficiency altered behavior. The duration of magnesium deficiency is suggested to influence behaviour in the evaluated test.

A high number of Non-responders in induced animal models of depression is a problem in research as it results in a high work load and a waste of animals. The aim of this project is to investigate the possible relationship between diet, gut microbiota (GM), low-grade inflammation in the brain, and behavior in order to generate knowledge enabling researchers to increase the number of responders when inducing these models using environmental modulation. The hypothesis is that a diet-induced change in GM composition can induce a cytokine mediated low-grade neuroinflammation, which is also observed in psychiatric diseases such as depression, thereby affecting the behavior. Furthermore the role of Brain Derived Neutrophic Factor (BDNF) in depressive behavior is investigated. 42 male BALB/c mice were divided in to three groups, and fed either a high-fat/low-sugar diet, a high-sugar/low-fat diet or a control starch-containing diet for 10 weeks. Blood samples were drawn after acclimatization, and fecal samples were taken at relevant time points during the study. Behavioral testing was performed before diet feeding using the Triple test and after the trial by the use of the Sucrose Preference test, the Burrowing test, the Triple test, the Forced Swim test and the Morris Water Maze test. At euthanization blood samples, fecal- and cecal samples and tissue samples were collected. Tissue samples included ileum, abdominal- and subcutaneous fat, hippocampus and prefrontal cortex. Cytokines in blood and brain tissue are still to be analyzed and so is the brain level of BDNF. Fecal- and cecal GM composition are currently being examined. Preliminary results shows that high-fat diet increased terminal weight (p<0.001) even though there was no difference between the groups before the diet feeding. This may lead to a systemic rise in proinflammatory cytokines, thereby inducing neuroinflammation. In the burrowing test the mice on control diet burrowed significantly more bedding out of