Related Experiment Video

Updated: Aug 13, 2026

Non-invasive In Vivo Fluorescence Optical Imaging of Inflammatory MMP Activity Using an Activatable Fluorescent Imaging Agent
06:46

Non-invasive In Vivo Fluorescence Optical Imaging of Inflammatory MMP Activity Using an Activatable Fluorescent Imaging Agent

Published on: May 8, 2017

Infliximab therapy does not modify MMP-2 and MMP-9 serum concentrations in chronic arthritis

G Giannelli1, F Iannone, F Marinosci

  • 1Department of Internal Medicine, Immunology, and Infectious Diseases, Section of Internal Medicine, University of Bari Medical School, Bari, Italy. g.giannelli@intmed.uniba.it

Clinical and Experimental Rheumatology
|January 7, 2006
PubMed
Abstract

Insights

Infliximab effectively manages chronic arthritis, but does not alter serum levels of matrix metalloproteinases-2 and -9 (MMP-2, MMP-9). These enzymes may not be reliable systemic markers for monitoring anti-TNF therapy in arthritis.

Area of Science:

  • Rheumatology and Immunology
  • Biochemistry and Molecular Biology

Background:

  • Matrix metalloproteinases-2 (MMP-2) and -9 (MMP-9) are crucial in tissue remodeling, particularly in joint destruction associated with rheumatoid arthritis.
  • Their expression levels may indicate disease activity and serve as potential biomarkers for assessing therapeutic efficacy in arthritis management.

Purpose of the Study:

  • To evaluate the serum concentrations of MMP-2 and MMP-9 in patients with chronic arthritis undergoing treatment with infliximab, a tumor necrosis factor-alpha (TNFα) inhibitor.
  • To determine if infliximab therapy modulates MMP-2 and MMP-9 serum levels, potentially serving as surrogate markers for treatment response.

Main Methods:

  • Fifty patients with chronic arthritis (26 rheumatoid arthritis, 24 undifferentiated) received infliximab (3 mg/kg).
  • Serum MMP-2 and MMP-9 levels were measured using gelatine zymography at baseline, and at 2 and 14 weeks post-treatment.
  • Disease activity and clinical response were assessed using DAS-28 and ACR criteria, with 24 healthy donors as controls.

Main Results:

  • Infliximab treatment led to a statistically significant reduction in DAS-28 scores and improved ACR clinical response.
  • Despite clinical improvements, serum concentrations of MMP-2 and MMP-9 did not show significant modulation during infliximab therapy.

Conclusions:

  • Blocking TNFα with infliximab is an effective strategy for managing chronic arthritis.
  • Serum MMP-2 and MMP-9 levels do not appear to be modified by infliximab therapy, suggesting localized rather than systemic changes at the joint inflammation site.
  • Further investigation into soluble factors reflecting joint damage is recommended for monitoring anti-TNFα therapy effectiveness.

Related Concept Videos

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab (Humira),...
Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents01:29

Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel Disease...
Inflammatory Bowel Disease IV: Pharmacological Management01:29

Inflammatory Bowel Disease IV: Pharmacological Management

Upon diagnosis, managing Inflammatory Bowel Disease (IBD) involves addressing several crucial aspects. The primary goals include resting the bowel, correcting malnutrition, and providing symptomatic relief. Resting the bowel may consist of medications to reduce inflammation and promote healing. Correcting malnutrition is essential, often requiring dietary adjustments and nutritional supplements. Symptomatic relief aims to ease pain, diarrhea, and other discomforts in IBD.
Pharmacologic...
Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids01:21

Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids

Glucocorticoids, a class of anti-inflammatory drugs, are pivotal in treating moderate to severe Crohn's disease by inducing remission. They exhibit their anti-inflammatory action by inhibiting the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, and chemokines like IL-8. In addition, they reduce the expression of inflammatory cell adhesion molecules and inhibit gene transcription of nitric oxide synthase, phospholipase A2, cyclooxygenase-2 (COX-2),...
Drugs for Treatment of Ulcerative Colitis in IBD01:29

Drugs for Treatment of Ulcerative Colitis in IBD

Ulcerative colitis is a chronic inflammatory condition primarily affecting the colon and rectum. The primary drugs used in the treatment of ulcerative colitis are aminosalicylates. They exhibit anti-inflammatory and immunosuppressive properties. They modulate inflammatory mediators and inhibit the activity of nuclear factor κB (NF-κB). Aminosalicylates also reduce inflammation by inhibiting prostaglandin and leukotriene production and decreasing neutrophil chemotaxis and superoxide generation. 
Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...