Reactivation of Antigen‐Induced Arthritis in Mice by Oral Administration of Lipopolysaccharide

Abstract

We examined whether oral administration of lipopolysaccharide (LPS) from Escherichia coli reactivated antigen-induced arthritis (AIA) in mice that is one of models of human rheumatoid arthritis. To induce AIA, mice were immunized by subcutaneous injection of ovalbumin (OVA) emulsified with complete Freund's adjuvant into the base of the tail (day 0) followed by intraarticular injection of OVA on day 21. To investigate the ability of LPS to reactivate AIA, varying doses of LPS were p.o. administered 48 h after the challenge injection. The results showed that administration of LPS was followed by reactivation of AIA in a dose-related fashion. The reactivation of AIA by LPS was associated with increases in interferon-g, interleukin-1b and tumour necrosis factor-a. Polymyxin B sulfate given immediately before administration of LPS suppressed the reactivation of AIA. These findings suggest that LPS from intestinal bacteria may play a role in the reactivation of joint inflammation in which immune responses to pathogenic antigens are involved.

Effects of bacteriophages on free radical production and phagocytic functions

“…ROS are important second messengers whose production constitutes a major pathway leading to NF jB activation; blocking LPS-macrophage interaction can lead to inhibition of these pathways [30]. Furthermore, anti-LPS antibodies protected mice from challenge with E. coli and the sera of pretreated animals did not present any detectable proinflammatory cytokine [28]; moreover, polymyxin B suppresses LPS-induced activation of inflammation and proinflammatory cytokine production in mice [38]. Thus, phages can decrease LPS effects on target cells mimicking the effects of anti-LPS antibodies or LPS-binding agents.…”

Suppression of collagen-induced arthritis by intra-articular lentiviral vector-mediated delivery of Toll-like receptor 7 short hairpin RNA gene

“…13 -15 In addition, systemic administration of lipopolysaccharide, signaling through the TLR4, has been demonstrated to reactivate arthritis in different mouse models. 16,17 Increased expressions of TLR2 and TLR4 were found in synovial macrophages from RA patients, and enhanced activation by stimulation with TLR ligands were also demonstrated in these cells. 18 Expression of TLRs on B cells were augmented following the stimula-tion of B-cell receptors, and the subsequent ligation of TLRs contributed to the production of rheumatoid factor.…”

Shift from toll‐like receptor 2 (TLR‐2) toward TLR‐4 dependency in the erosive stage of chronic streptococcal cell wall arthritis coincident with TLR‐4–mediated interleukin‐17 production

“…In this context, bacterial-derived TLR ligands such as double-stranded RNA, lipopolysaccharide (LPS) and CpG-containing DNA, which signal through TLR-3, TLR-4, and TLR-9, respectively, have frequently been used to provoke or accelerate experimental arthritis (7)(8)(9). LPS circumvents the IL-1 dependence of the K/BxN serum-transfer model of arthritis (10) and intraarticular injection of cell wall fragments of Streptococcus pyogenes has recently been reported to induce arthritis through the TLR-2/ myeloid differentiation factor 88 (MyD88) pathway (11).…”