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(B6)IL-10 KO interleukin-10 mouse

Jiangsu Aniphe BioLab, leveraging a high‑standard laboratory animal platform, maintains an on‑hand inventory of (B6) IL‑10 knockout mice. As a gold‑standard model for studying inflammatory bowel disease (IBD), intestinal mucosal immunity, and autoimmune disorders, our gene‑knockout mice feature well‑defined genotypes and a pure genetic background. With a robust breeding system and ample stock, we help you bypass the time‑consuming processes of breeding and genotyping, enabling you to swiftly launch research into immune and inflammatory mechanisms.

Strain Introduction

Interleukin‑10 (IL‑10) is a central anti‑inflammatory mediator that maintains intestinal and systemic immune homeostasis. In this strain, the Il10 gene has been knocked out on a pure C57BL/6 background, resulting in spontaneous chronic colitis that recapitulates the core pathological features of human inflammatory bowel disease (IBD), while also exhibiting a systemic hyperimmune phenotype. This model serves as a flagship system for studying immune regulation and gut–microbiota interactions.

Product Advantages

The knockout phenotype is stable and well-defined.

Global Il10 knockout abolishes IL‑10–mediated anti‑inflammatory signaling; mice maintained under standard housing conditions develop spontaneous chronic colitis, with pathological features highly reminiscent of human Crohn’s disease.

Pure B6 genetic background

Purified on a C57BL/6J genetic background to avoid immune biases arising from heterozygous backgrounds, making it suitable for B6‑based immunological experiments such as bone marrow transplantation and adoptive cell transfer.

Inflammation depends on the gut microbiota.

In the SPF environment, disease onset is dependent on the gut microbiota, and germ-free conditions or antibiotic treatment can suppress inflammation; fecal microbiota transplantation and single‑strain colonization are feasible, allowing for deliberate modulation of the timing and severity of inflammatory episodes.

Systemic multiple immune abnormalities

It is not limited to intestinal inflammation; rather, it encompasses impaired pathogen clearance, excessive lymphocyte activation, a shift toward humoral immunity, and a propensity for lymphoproliferation, making it relevant to research across multiple domains, including anti-inflammatory therapies, cancer immunotherapy, and immune aging.

The disease course can be predicted, facilitating the evaluation of therapeutic efficacy.

Under standard housing conditions, typical intestinal lesions develop steadily between 10 and 12 weeks of age, facilitating the establishment of pharmacokinetic–pharmacodynamic windows for preventive and therapeutic dosing in drug evaluation.

 

Data parameters

Strain Name B6.129P2-Il10^tm1Cgn^/J (abbreviated as B6-IL-10 KO)
Targeted gene Il10 (Interleukin 10)
Mutant site A portion of exon 1 was replaced by the neomycin resistance gene (neo), resulting in the complete loss of functional IL‑10.
Types of gene editing Constitutive Knockout
Genetic background C57BL/6J (backcrossed for at least N≥10 generations)
Microbial Grade SPF grade

Validate data

Intestinal commensal bacteria drive colonic inflammation in IL-10-deficient mice.

In this study, histological examination was performed on mid‑colon tissue from three groups of mice: SPF‑conditioned IL‑10–deficient mice (Figure a) exhibited marked mucosal hyperplasia, extensive inflammatory cell infiltration in the lamina propria, and crypt abscesses (indicated by arrows), demonstrating typical pathological features of colonic inflammation; germfree IL‑10–deficient mice (Figure b) showed intact colonic mucosal architecture, with no evidence of mucosal hyperplasia, inflammatory cell infiltration, or crypt abscesses; and SPF‑grade wild‑type mice (Figure c) displayed normal colonic tissue structure, without spontaneous intestinal inflammatory lesions. These findings suggest that IL‑10 gene deficiency alone is insufficient to induce colonic inflammation, and that resident gut commensal bacteria are essential for the development of colitis in IL‑10–deficient mice.

 

 

Colonic Inflammation Quantitative Score

The results of the quantitative colitis scoring demonstrated that SPF‑conditioned IL‑10‑deficient mice exhibited significantly higher inflammation scores than germ‑free IL‑10‑deficient mice, germ‑free heterozygous mice, and SPF wild‑type mice (P<0.05). In contrast, the remaining three groups all displayed low inflammation scores, with no overt signs of inflammation. These quantitative data support the notion that the gut microbiota is an indispensable factor in the development of colitis in IL‑10‑deficient mice.

 

 

Histological observation results

Histological analysis revealed that the cecum of SPF wild-type mice exhibited no inflammatory damage; IL‑10–deficient mice maintained in an SPF environment from weaning onward showed only mild cecal inflammation; whereas IL‑10–deficient mice colonized with SPF microbiota only after adulthood developed markedly more severe cecal inflammation, characterized by prominent mucosal hyperplasia, transmural inflammation, and crypt abscesses. These findings suggest that the timing of microbial colonization can influence the severity of cecal inflammation in IL‑10–deficient mice, with colonization occurring in adulthood eliciting a more robust inflammatory response.

 

 

Immunoglobulin test results

The results of immunoglobulin assays in the culture supernatants of colon tissue showed that, in SPF‑raised IL‑10–deficient mice, the local colonic secretion levels of IgG2a, IgG1, and IgA were significantly higher than those in germ‑free IL‑10–deficient mice, germ‑free heterozygous mice, and SPF wild‑type mice. These findings indicate that the gut microbiota can induce activation of local humoral immunity in the colon of IL‑10–deficient mice.

 

Application areas

● Pathogenesis and Treatment of Inflammatory Bowel Disease (IBD): As a spontaneous model of chronic colitis, it is used for evaluating the efficacy of anti-inflammatory drugs, investigating targets for intestinal barrier repair, and studying the mechanisms underlying probiotic interventions.
● Intestinal–Microbiota–Immune Interactions: Leveraging aseptic, germ‑free, and fecal microbiota transplantation approaches, we screen for functional gut bacterial strains and elucidate the molecular mechanisms by which microbial metabolites regulate host immunity.
● Infection and Immune Response: Investigate the negative regulatory effects of IL‑10 on pathogen clearance, sepsis, and vaccine responses, and elucidate the signaling pathways through which IL‑10 deficiency triggers excessive inflammatory injury.
● Tumor Immunology and Autoimmunity: It is suitable for investigating the dual effects of IL‑10 imbalance: enhancing anti‑tumor immunity while increasing the risk of autoimmune disease; it can also be used in studies of Treg/Tr1 functional defects and immune checkpoint inhibitor‑associated colitis.
● Food Safety and Environmental Toxicology: This strain exhibits high intestinal immune sensitivity, enabling the assessment of subclinical intestinal immune damage induced by environmental factors such as food additives, pesticides, and nanomaterials.

Breeding Techniques and Precautions

Strictly control inbreeding systems to mitigate genetic disparities.

Strictly control the microbial environment.

SPF‑grade housing is a prerequisite for phenotypic stability. It is essential to avoid the introduction of highly pro‑inflammatory microbial communities, such as Helicobacter and segmented filamentous bacteria; when necessary, imported mice should undergo embryo‑level pathogen clearance followed by re‑colonization with a standardized SPF microbiota.

 

Strictly control environmental stimuli to reduce experimental stress.

Reproductive strategy

Conventional breeding employs heterozygote × heterozygote mating; homozygotes are also viable, but inflammatory conditions may affect litter size and lactation capacity. It is recommended to prioritize using heterozygotes from the same litter as wild-type controls.

 

Standardize breeding management to improve the survival rate of pups.

Feed and Water

It is recommended to use standard breeding feed; do not arbitrarily add high-fat or high‑allergen ingredients, as this may exacerbate intestinal inflammation. The administration of pressurized acidic water or, when necessary, antibiotic solutions must be clearly documented as experimental variables.

 

Monitor age-related spontaneous lesions and eliminate experimental confounding.

Health Monitoring

Body weight, perianal cleanliness, and stool characteristics should be monitored at least twice weekly. If rectal prolapse, progressive weight loss, or lethargy occurs, the experiment shall be terminated in accordance with animal welfare guidelines.

 

Literature support

References: Resident Enteric Bacteria Are Necessary for Development of Spontaneous Colitis and Immune System Activation in Interleukin-10-Deficient Mice.

Frequently Asked Questions

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Q1: Will IL-10 knockout mice invariably develop colitis at X weeks of age?

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A: Under standard SPF conditions, histological inflammation can be detected as early as 10–12 weeks of age; however, the onset and severity of disease are strongly influenced by the composition of the resident microbiota within the animal facility. For the same strain, differences across facilities may range from 2 to 4 weeks; therefore, it is recommended to first conduct small-scale pilot studies to establish an appropriate time window.

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Q2: Why choose a global knockout rather than a conditional knockout?

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A: Whole-body KO is the preferred approach for IBD mechanistic studies and initial drug screening, as it fully recapitulates the shared effects of IL‑10 deficiency across multiple immune cell types (T cells, macrophages, B cells) without requiring additional transgenic mouse breeding. To dissect cell‑type–specific contributions, one can further cross Il10‑flox mice with Cre‑expressing conditional knockout mice.

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Q3: How can we distinguish whether colitis is caused by gene knockout or by infection?

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A: The diagnosis can be based on the following three criteria: ① SPF sentinel mice and their littermate controls are healthy and exhibit no inflammation; ② Colonic histopathology reveals multifocal inflammation throughout the entire colon, rather than isolated infectious ulcers; ③ Following antibiotic treatment or germ-free conditions, the inflammation completely resolves, returning to wild-type levels.

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