Biomere

CRO Expertise

INFLAMMATORY BOWEL DISEASE (IBD)

Inflammation is a vital part of the body’s immune response. It is the body’s attempt to heal itself after an injury; defend itself against foreign invaders, such as viruses and bacteria; and repair damaged tissue. Biomere’s interest in inflammatory disease stems from our expertise in autoimmunity.

We offer models of systemic lupus erythematosus (SLE) as well as antigen induced infl ammation such as collagen induced arthritis and myelin peptide-induced experimental autoimmune encephalomyelitis (EAE) as a model of multiple sclerosis. Additionally we offer chemically induced models of infl ammatory bowel disease (IBD)/ulcerative colitis and Type 1 diabetes.

INDUCIBLE MODELS

Acute 2,4 6-trinitrobenzenesulfonic acid (TNBS) hapten including IFN-γ, TNF-α, IL-2, IL-12 and IL-18

Mediated by Th1 and Th17 cells locally producing excessive proinflammatory cytokines

Acute dextran sulfate sodium (DSS)

Suggested epithelial cell toxicity, increased intestinal permeability, and macrophage activation

IBD Readouts

IBD Disease Activity Index

Body weight
Rectal bleeding scoring (hemoccult kit)
Stool scoring

Additional Analyses

Interim blood collections for PK/PD evaluation
Histology
Collections for PK/PD evaluation

Colon Evaluation

Colon length and weight measures
Macroscopic colon scoring index
0 – 10 graded morphologic scoring

Microscopic Colon Scoring

Histopathology assessment by an unbiased pathologist
Inflammation and morphological damage

DSS Induced IBD in Mice

8 -10 animals per group
Induction with 5% DSS in drinking water for consecutive days
~100% induction rate
Disease onset on Day 3
Peak disease on Day 8 – 10
Positive control is available

TNBS-Induced IBD in Mice

8 -10 animals per group
I~100% induction rate, low mortality
Prophylactic or therapeutic treatment
Intrarectal induction with TNBS hapten
Study duration 5 to 8 days
– ~Day 5 is the peak of diseases severity
– Day 8 represents a recovery phase