Effective tumour necrosis factor-blocking therapy reduces reactive oxygen metabolite level in rheumatoid arthritis

Fabio Cacciapaglia1, Maria Grazia Anelli2, Daniela Rizzo3

  • 1Internal Medicine Unit and Rheumatology Clinic - N. Melli Hospital, San Pietro Vernotico, Brindisi, Italy f.cacciapaglia@unicampus.it.

Abstract

Insights

Anti-tumour necrosis factor (TNF)-α therapy significantly reduced reactive oxygen metabolites (ROMs) in patients with rheumatoid arthritis (RA). This treatment also correlated with reduced disease activity, indicating its effectiveness in managing RA oxidative stress.

Area of Science:

  • Rheumatology
  • Immunology
  • Biochemistry

Background:

  • Rheumatoid arthritis (RA) is associated with increased oxidative stress.
  • Reactive oxygen metabolites (ROMs) are key markers of oxidative stress.
  • Anti-tumour necrosis factor (TNF)-α therapy is a treatment for active RA.

Purpose of the Study:

  • To evaluate circulating ROM levels in active RA patients before and during anti-TNF-α therapy.
  • To assess the impact of anti-TNF-α therapy on oxidative stress markers in RA.

Main Methods:

  • 40 patients with active RA received subcutaneous anti-TNF-α for 52 weeks.
  • Circulating hydrogen peroxide, a marker of oxidative stress, was quantified.
  • Measurements were taken at baseline, 24 weeks, and 52 weeks.

Main Results:

  • Circulating ROM levels significantly decreased after 24 and 52 weeks of anti-TNF-α treatment compared to baseline.
  • A significant direct correlation was observed between disease activity score and ROM levels.
  • The study included 40 patients, with ROM levels measured in mgH2O2/dl.

Conclusions:

  • Anti-TNF-α therapy effectively controls disease activity in RA patients.
  • TNF-α inhibition leads to a reduction in circulating reactive oxygen species.
  • This suggests a role for anti-TNF-α therapy in mitigating oxidative stress in RA.

Related Concept Videos

T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
3.1K
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...
696
Cancer Therapies02:49

Cancer Therapies

Cancer therapies are various modes of treatment, such as surgery, radiation therapy, and chemotherapy that are administered to cancer patients.
However, cancer treatments can pose several challenges, as therapies used to kill cancer cells are generally also toxic to normal cells. Moreover, cancer cells mutate rapidly and can develop resistance to chemical agents or radiation therapy. Besides, all types of cancer cells may not respond to the same therapy. Some cancer cells respond to one...
10.6K
Tumor Immunotherapy01:27

Tumor Immunotherapy

Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
2.1K
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
19.4K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
13.6K