The microbiome and rodent models of immune mediated diseases

Hansen, Axel Kornerup; Hansen, Camilla Hartmann Friis

doi:10.1007/s00335-021-09866-4

Cited by 12 publications

(8 citation statements)

References 132 publications

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“…Among the different compartments of the host microbiome, the gastrointestinal tract deserves special attention, as it harbours the largest microbial abundance and diversity ( 4 , 5 ). To date, most studies exploring the influence of the gut microbiota on the immune system have focused on rodents and humans ( 6 , 7 ). It is, therefore, important to consider the impact of the microbiota on immune processes in other species to evaluate if findings from these systems apply more generally.…”

Section: Introductionmentioning

confidence: 99%

The influences of microbial colonisation and germ-free status on the chicken TCRβ repertoire

Dascalu

Preston²,

Dixon³

et al. 2023

Front. Immunol.

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Microbial colonisation is paramount to the normal development of the immune system, particularly at mucosal sites. However, the relationships between the microbiome and the adaptive immune repertoire have mostly been explored in rodents and humans. Here, we report a high-throughput sequencing analysis of the chicken TCRβ repertoire and the influences of microbial colonisation on tissue-resident TCRβ+ cells. The results reveal that the microbiome is an important driver of TCRβ diversity in both intestinal tissues and the bursa of Fabricius, but not in the spleen. Of note, public TCRβ sequences (shared across individuals) make a substantial contribution to the repertoire. Additionally, different tissues exhibit biases in terms of their V family and J gene usage, and these effects were influenced by the gut-associated microbiome. TCRβ clonal expansions were identified in both colonised and germ-free birds, but differences between the groups were indicative of an influence of the microbiota. Together, these findings provide an insight into the avian adaptive immune system and the influence of the microbiota on the TCRβ repertoire.

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Section: Introductionmentioning

confidence: 99%

The influences of microbial colonisation and germ-free status on the chicken TCRβ repertoire

Dascalu

Preston²,

Dixon³

et al. 2023

Front. Immunol.

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“…Strong microbiota impact has also been described for a number of animal models within a broad spectrum of other biomedical disciplines 41 , 42 , such as brain-related 43 , 44 , autoimmune 45 , and allergic 46 diseases, as well as solid organ transplant outcomes 47 , blood pressure 48 , acute pancreatitis 49 , colorectal cancer 50 and others. Therefore, it seems as if the microbiome composition also influences results of mouse studies not previously thought to be influenced by it.…”

Section: Discussionmentioning

confidence: 95%

Controlling the uncontrolled variation in the diet induced obese mouse by microbiomic characterization

Bondarenko¹,

Løkke²,

Dobrowolski³

et al. 2022

Sci Rep

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Group sizes in an animal study are calculated from estimates on variation, effect, power and significance level. Much of the variation in glucose related parameters of the diet-induced obese (DIO) mouse model is due to inter-individual variation in gut microbiota composition. In addition, standard tandem repeats (STRs) in the non-coding DNA shows that inbred mice are not always homogenic. C57BL/6NTac (B6NTac) mice from Taconic and C57BL/6NRj (B6NRj) mice from Janvier Labs were fed a high calorie diet and treated with liraglutide. The fecal microbiota was sequenced before high-calorie feeding (time 1) and after diet-induced obesity instantly before liraglutide treatment (time 2) and mice were divided into clusters on the basis of their microbiota. Although liraglutide in both sub-strains alleviated glucose intolerance and reduced body weight, in a one-way ANOVA a borderline reduction in glycosylated hemoglobin (HbA1c) could only be shown in B6NTac mice. However, if the microbiota clusters from time 1 or time 2 were incorporated in a two-way ANOVA, the HbA1c effect was significant in B6NTac mice in both analyses, while this did not change anything in B6NRj mice. In a one-way ANOVA the estimated group size needed for a significant HbA1c effect in B6NTac mice was 42, but in two-way ANOVAs based upon microbiota clusters of time 1 or time 2 it was reduced to 21 or 12, respectively. The lowering impact on glucose tolerance was also powered by incorporation of microbiota clusters of both times in both sub-strains. B6NRj had up to six, while B6NTac had maximum three alleles in some of their STRs. In B6NRj mice in 28.8% of the STRs the most prevalent allele had a gene frequency less than 90%, while this was only 6.6% in the B6NTac mice. However, incorporation of the STRs with the highest number of alleles or the most even distribution of frequencies in two-way ANOVAs only had little impact on the outcome of data evaluation. It is concluded that the inclusion of microbiota clusters in a two-way ANOVA in the evaluation of the glucose related effects of an intervention in the DIO mouse model might be an efficient tool for increasing power and reducing group sizes in mouse sub-strains, if these have a microbiota, which influences these parameters.

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“…It can be simplified by using fewer pathogens or tailored by including specific pathogens to target particular immunological responses. Future studies should encompass the examination of other inflammatory disease models such as inflammatory bowel disease, type 1 diabetes, and rheumatic arthritis, as well as vaccination studies and investigations on immunological receptor agonists/antagonists, 31 and it should include both sexes. It would also have been more optimal to allow the pet shop mice an acclimatization period in the facility before sampling.…”

Section: Discussionmentioning

confidence: 99%

Induction of CD8⁺ immune memory and enhanced inflammation in a skin inflammation model through pre‐immunization with inactivated pathogens

Falkenberg,

Bartholdy,

Koch

et al. 2023

Clinical Translational Sci

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Laboratory mice live in specific pathogen‐free (SPF) conditions, resulting in an immature immune system comparable to that of newborns rather than adult humans or mice from pet shops. This condition may compromise their translational value. Reintroducing pathogens would lead to the uncontrolled spread of infections and associated diseases, so research facilities should seek safer alternatives. We immunized laboratory mice with a cocktail of pathogens, which were inactivated by ultraviolet irradiation and mixed with the adjuvant AddaVax. This immunization resulted in a higher percentage of CD8+ effector memory T cells compared to untreated mice, although the response was not as robust as in pet shop mice. In a model of skin inflammation, pre‐immunization led to an increased skin inflammatory response compared to non‐immunized mice. All immunized mice seroconverted to the pathogens in the mixture, while none of the non‐immunized mice housed together seroconverted to the pathogens applied to the pre‐immunized mice. In conclusion, pre‐immunization of mice impacts the immune system, which includes increasing the levels of CD8+ effector memory T cells.

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The microbiome and rodent models of immune mediated diseases

Cited by 12 publications

References 132 publications

The influences of microbial colonisation and germ-free status on the chicken TCRβ repertoire

The influences of microbial colonisation and germ-free status on the chicken TCRβ repertoire

Controlling the uncontrolled variation in the diet induced obese mouse by microbiomic characterization

Induction of CD8⁺ immune memory and enhanced inflammation in a skin inflammation model through pre‐immunization with inactivated pathogens

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The microbiome and rodent models of immune mediated diseases

Cited by 12 publications

References 132 publications

The influences of microbial colonisation and germ-free status on the chicken TCRβ repertoire

The influences of microbial colonisation and germ-free status on the chicken TCRβ repertoire

Controlling the uncontrolled variation in the diet induced obese mouse by microbiomic characterization

Induction of CD8+ immune memory and enhanced inflammation in a skin inflammation model through pre‐immunization with inactivated pathogens

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Product

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Induction of CD8⁺ immune memory and enhanced inflammation in a skin inflammation model through pre‐immunization with inactivated pathogens