Production of Murine Collagen‐Induced Arthritis Using <i>Klebsiella pneumoniae</i> O3 Lipopolysaccharide as a Potent Immunological Adjuvant

Takahashi, K.; Kato, Yasuhiro; Sugiyama, Tsuyoshi; Koide, Naoki; Kikuchi, Makoto; Fukada, Masako; Yoshida, Tomoaki; Yokochi, Takashi

doi:10.1111/j.1348-0421.1999.tb02472.x

Cited by 12 publications

(8 citation statements)

References 28 publications

(9 reference statements)

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“…In the present study, we detected a second increase in gene expression of some inflammatory mediators 2-8 hrs after LPS injection, this interval of time being just after the increase in serum anti-CII IgG. Additionally, a previous study has shown that LPS injection of mice without CII immunization does not induce arthritis (23,26). Thus, production of anti-CII antibody and the consequent induction of continuous expression of inflammatory mediators may be necessary for acute onset of LPS-CIA.…”

Section: Discussionsupporting

confidence: 69%

Lipopolysaccharide accelerates collagen‐induced arthritis in association with rapid and continuous production of inflammatory mediators and anti‐type II collagen antibody

Tanaka¹,

Toki²,

Akimoto

et al. 2013

Microbiology and Immunology

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Collagen-induced arthritis (CIA) is an animal model for rheumatoid arthritis (RA). Lipopolysaccharide (LPS) is known to accelerate CIA; however, the pathogenetic mechanisms are not yet fully understood. In this study, type II collagen (CII)-immunized mice were found to have marked increases in degree of expression of mRNA of inflammatory mediators such as tumor necrosis factor alpha (TNF-a), interleukin (IL)-1b, and macrophage inflammatory protein-2 (MIP-2) in their arthritic paws and of serum anti-CII antibody concentration before the onset of arthritis induced by LPS injection. The gene expression was rapid and continuous after direct activation of nuclear factor kB. The amounts of mRNA of TNF-a, IL-1b, and MIP-2, as well as of matrix metalloproteinases and the receptor activator of nuclear factor kB ligand, increased with the development of arthritis, correlated positively with clinical severity and corresponded with histopathological changes. Moreover, anti-TNF-a neutralizing antibody inhibited the development of LPS-accelerated CIA and a single injection of recombinant mouse TNF-a induced increases in anti-CII antibody concentrations, suggesting TNF-a may contribute to the development of arthritis by both initiation of inflammation and production of autoantibodies. These data suggest that exacerbation of RA by LPS is associated with rapid and continuous production of inflammatory mediators and autoantibodies.Key words anti-type II collagen antibody, collagen-induced arthritis, inflammatory mediators, lipopolysaccharide.Rheumatoid arthritis is a systemic autoimmune disease that is characterized by chronic inflammation of joints, leading to synovial hyperplasia, infiltration of leukocytes and progressive destruction of cartilage and bone (1). Various humoral factors are involved in the development of RA. One of these is autoantibodies, which activate complement systems by formation of immune complexes in combination with self-antigens and induce recruitment of inflammatory cells into synovium (1, 2). Another important factor is inflammatory mediators such as Correspondence Shinji Tanaka, Frontier Research Laboratories, Daiichi Sankyo Co., Ltd., 1-2-58 Hiromachi, Shinagawa-ku, Tokyo 140-8710, Japan. Tel: þ81 3 3492 3131; fax: þ81 3 5740 3644; email: tanaka.shinji.fv@daiichisankyo.co.jp List of Abbreviations: CIA, collagen-induced arthritis; CII, type II collagen; E. coli, Escherichia coli; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; IkBa, inhibitor of nuclear factor kB alpha; IL, interleukin; LPS, lipopolysaccharide; LPS-CIA, lipopolysaccharide-accelerated collageninduced arthritis; MIP-2, macrophage inflammatory protein-2; MMP, matrix metalloproteinase; ND, not detected; NF-kB, nuclear factor kB; RA, rheumatoid arthritis; RANKL, receptor activator of nuclear factor kB ligand; SEM, standard error of the mean; TLR, Toll-like receptor; TNF-a, tumor necrosis factor alpha.

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Section: Discussionsupporting

confidence: 69%

Lipopolysaccharide accelerates collagen‐induced arthritis in association with rapid and continuous production of inflammatory mediators and anti‐type II collagen antibody

Tanaka¹,

Toki²,

Akimoto

et al. 2013

Microbiology and Immunology

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“…Required for leukocyte endothelial interactions in vivo [78] Eosinophils Expression of MIF [6] Expression of MIF [79,80] B lymphocytes Growth factor [76,81] Expression of MIF [70] Induce cPLA2, COX-2, IL-1, IL-6, IL-8, MMPs [52,82,84] Induce proliferation, inhibit apoptosis [23,85] Synovial or other fibroblasts Activate MAP kinases [47,85] gen-induced arthritis model [21]. In this study, neutralisation of MIF using a monoclonal antibody resulted in delayed onset and lowered frequency of arthritis.…”

Section: Mif Is a Pro-inflammatory Mediator In A Range Of Immune-medimentioning

confidence: 99%

Macrophage Migration Inhibitory Factor: A Therapeutic Target Across Inflammatory Diseases

Hoi¹,

Iskander²,

Morand

2007

IADT

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Macrophage migration inhibitory factor (MIF), a cytokine originally reported in the 1960s as the prototypic T lymphokine, has emerged in recent years as a key factor regulating inflammatory responses. Both by directly activating immune cells, and by participating in activation entrained by other stimuli, MIF is important in innate and adaptive immune responses as well as tissue-specific mechanisms of damage. As a consequence of its involvement in multiple stages of the immune-inflammatory response, MIF has the potential to be involved in the pathogenesis of a range of immune-mediated inflammatory diseases affecting multiple organ systems. Diseases in which a role for MIF has been strongly validated include rheumatoid arthritis, inflammatory bowel disease, multiple sclerosis, atherosclerosis, asthma, inflammatory liver disease, and most recently systemic lupus erythematosus. Recent data have provided mechanisms of action for MIF which further support its suitability as a therapeutic target. Finally, MIF has a unique relationship with glucocorticoids, acting to counter-regulate their anti-inflammatory effects, such that MIF antagonist therapy may be a direct route to 'steroid-sparing'. Methods of targeting MIF therapeutically have also emerged in recent years, based on the unique protein structure of MIF which affords opportunities for direct antagonism by small molecules, as well as by protein therapeutics such as monoclonal antibodies. Clinical trials of MIF antagonist therapies are likely before the end of the current decade.

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“…Collagen-induced enterocolitis [42] as well as arthritis [43] has been observed in experimental animals when immunized with homologous colonic extracts and collagen type II together with Klebsiella lipopolysaccharides.…”

Section: Aetiopathogenesismentioning

confidence: 99%

The Role ofKlebsiellain Crohn’s Disease with a Potential for the Use of Antimicrobial Measures

Rashid

Ebringer

Wilson

2013

International Journal of Rheumatology

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There is a general consensus that Crohn's disease (CD) develops as the result of immune-mediated tissue damage triggered by infections with intestinal microbial agents. Based on the results of existing microbiological, molecular, and immunological studies, Klebsiella microbe seems to have a key role in the initiation and perpetuation of the pathological damage involving the gut and joint tissues in patients with CD. Six different gastroenterology centres in the UK have reported elevated levels of antibodies to Klebsiella in CD patients. There is a relationship between high intake of starch-containing diet, enhanced growth of gut microbes, and the production of pullulanases by Klebsiella. It is proposed that eradication of these microbes by the use of antibiotics and low starch diet, in addition to the currently used treatment, could help in alleviating or halting the disease process in CD.

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Production of Murine Collagen‐Induced Arthritis Using Klebsiella pneumoniae O3 Lipopolysaccharide as a Potent Immunological Adjuvant

Cited by 12 publications

References 28 publications

Lipopolysaccharide accelerates collagen‐induced arthritis in association with rapid and continuous production of inflammatory mediators and anti‐type II collagen antibody

Lipopolysaccharide accelerates collagen‐induced arthritis in association with rapid and continuous production of inflammatory mediators and anti‐type II collagen antibody

Macrophage Migration Inhibitory Factor: A Therapeutic Target Across Inflammatory Diseases

The Role ofKlebsiellain Crohn’s Disease with a Potential for the Use of Antimicrobial Measures

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