Undenatured type II collagen protects against collagen-induced arthritis by restoring gut-joint homeostasis and immunity.
Piaopiao PanYilin WangMukanthu H NyirendaZainulabedin SaiyedElnaz Karimian AzariAmy SundermanSimon MillingMargaret M HarnettMiguel A PinedaPublished in: Communications biology (2024)
Oral administration of harmless antigens can induce suppression of reactive immune responses, a process that capitalises on the ability of the gastrointestinal tract to tolerate exposure to food and commensal microbiome without triggering inflammatory responses. Repeating exposure to type II collagen induces oral tolerance and inhibits induction of arthritis, a chronic inflammatory joint condition. Although some mechanisms underlying oral tolerance are described, how dysregulation of gut immune networks impacts on inflammation of distant tissues like the joints is unclear. We used undenatured type II collagen in a prophylactic regime -7.33 mg/kg three times/week- to describe the mechanisms associated with protective oral immune-therapy (OIT) in gut and joint during experimental Collagen-Induced Arthritis (CIA). OIT reduced disease incidence to 50%, with reduced expression of IL-17 and IL-22 in the joints of asymptomatic mice. Moreover, whilst the gut tissue of arthritic mice shows substantial damage and activation of tissue-specific immune networks, oral administration of undenatured type II collagen protects against gut pathology in all mice, symptomatic and asymptomatic, rewiring IL-17/IL-22 networks. Furthermore, gut fucosylation and microbiome composition were also modulated. These results corroborate the relevance of the gut-joint axis in arthritis, showing novel regulatory mechanisms linked to therapeutic OIT in joint disease.
Keyphrases
- rheumatoid arthritis
- wound healing
- oxidative stress
- immune response
- tissue engineering
- high fat diet induced
- gene expression
- high glucose
- poor prognosis
- type diabetes
- drug induced
- risk factors
- dendritic cells
- risk assessment
- lymph node
- endothelial cells
- inflammatory response
- wild type
- climate change
- mesenchymal stem cells
- long non coding rna
- study protocol
- placebo controlled