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Review
. 2022 Jul 15;9(7):321.
doi: 10.3390/bioengineering9070321.

Paradoxical Duel Role of Collagen in Rheumatoid Arthritis: Cause of Inflammation and Treatment

Affiliations
Review

Paradoxical Duel Role of Collagen in Rheumatoid Arthritis: Cause of Inflammation and Treatment

Jeevithan Elango et al. Bioengineering (Basel). .

Abstract

In biology, collagen-biomaterial regulates several signaling mechanisms of bone and immune cells involved in tissue repair and any imbalance in collagen turnover may affect the homeostasis of cells, becoming a major cause of several complications. In this case, the administration of oral collagen may play a potential role in returning cells to their normal function. For several decades, the beneficial effects of collagen have been explored widely, and thus many commercial products are available in cosmetics, food, and biomedical fields. For instance, collagen-based-products have been widely used to treat the complications of cartilage-related-disorders. Many researchers are reporting the anti-arthritogenic properties of collagen-based materials. In contrast, collagen, especially type-II collagen (CII), has been widely used to induce arthritis by immunization in an animal-model with or without adjuvants, and the potentially immunogenic-properties of collagen have been continuously reported for a long time. Additionally, the immune tolerance of collagen is mainly regulated by the T-lymphocytes and B-cells. This controversial hypothesis is getting more and more evidence nowadays from both sides to support its mechanism. Therefore, this review links the gap between the arthritogenic and anti-arthritogenic effects of collagen and explored the actual mechanism to understand the fundamental concept of collagen in arthritis. Accordingly, this review opens-up several unrevealed scientific knots of collagen and arthritis and helps the researchers understand the potential use of collagen in therapeutic applications.

Keywords: arthritis; collagen; collagen peptide; homeostasis; joint treatment; mechanism.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Schematic representation of the chimerism of type II collagen (CII) peptides (256–270) to MHC-II molecules and T cell receptor (TCR) of CD4 + T cells, APC-antigen-presenting cell.
Figure 2
Figure 2
Interaction of type II collagen peptide with B cell in collagen-induced arthritis (CIA) pathogenesis. Collagen with Gly-Arg and hydrophobic amino acids interacts with B cells through repetitive D period (C1, U1 and J1), which releases cytokines and CII-induced antibodies in order to damage the joints during arthritis.
Figure 3
Figure 3
Schematic representation of the anti-arthritic mechanism of collagen and its peptides. Collagens with different molecular weights are obsorbed in the colon and are transported to the arthritic joints by circulation as tri-peptides for healing arthritis.

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