The article title supplied—Environment shapes gut microbiome and determines susceptibility to DSS-colitis in Adamdec1-/- mice—reports that environmental factors influence the gut microbiome and affect susceptibility to chemically induced colitis in Adamdec1-/- mice. The publication is listed under Frontiers in Immunology. From the title, the principal claims are that housing or other environmental variables change intestinal microbial communities and that those changes are associated with altered outcomes following dextran sodium sulfate (DSS) exposure in a genetically modified mouse model lacking Adamdec1.
The content provided for rewriting consisted solely of Frontiers website navigation and repeated site sections; it did not include the article abstract, introduction, methods, results, figures, tables, or discussion. Consequently, the following critical details were not present in the supplied material and cannot be stated or paraphrased here because they are not in the source:
Where the full article is needed for these specifics, those details were not reported in the supplied source text and therefore are not included in this summary.
Adamdec1 (A Disintegrin And Metalloproteinase Domain-Like Decysin 1) is identified in the article title as the gene knocked out in the mouse model (Adamdec1-/-). The title links the genotype to altered responses to DSS-induced colitis via an environmental influence on the gut microbiome. DSS-colitis is an established experimental model to study epithelial injury and innate immune–driven intestinal inflammation; environmental modulation of microbiota composition is a plausible modifier of DSS susceptibility in many murine systems. However, the provided source did not include any mechanistic or experimental evidence to confirm or detail these relationships.
Based only on the title, the study implies several clinically and experimentally relevant points:
The interaction between host genotype (Adamdec1-/-) and environment can shape microbial community structure in the intestine.
Changes in the gut microbiome relate to differential susceptibility to DSS-induced colitis, suggesting a gene–environment–microbiome axis affects colitis outcomes.
Environmental factors may mask or reveal phenotypes associated with genetic modifications, which has implications for reproducibility of preclinical studies that examine host–microbe interactions.
These findings, if supported by the full dataset, could inform experimental design (for example, the need to control environmental variables) and may point to microbiome-targeted strategies to modify colitis risk in specific genetic contexts.
Because the source text did not include supporting data or analysis, these implications are inferential and rest on the title rather than the article’s reported evidence.
Given the absence of the article body in the provided source, the following categories of information were not available and therefore are not reported here:
Consult the full Frontiers in Immunology article to obtain experimental details, datasets, figures, and the authors’ interpretation; those elements were not present in the supplied source snippet.
When interpreting genotype–microbiome–environment studies, look for experimental controls such as cohousing, cross-fostering, or fecal transfer that can support causal links between microbiota composition and phenotype.
For reproducibility, examine the manuscript for clear reporting of husbandry and environmental variables (housing facility, bedding, diet, water source) and for statistical methods and sample sizes.
Note: All statements beyond the article title are contextual or explanatory. Specific experimental outcomes, methods, and numeric results were not reported in the supplied source text and therefore are not included here. To report precise findings and evidence, the original published article should be consulted.