TACI-Ig prevents the development of airway hyperresponsiveness in a murine model of asthma

Clin Exp Allergy. 2008 Dec;38(12):1959-68. doi: 10.1111/j.1365-2222.2008.03099.x.

Abstract

Background: Increased levels of serum IgE are associated with greater asthma prevalence and disease severity. IgE depletion using an anti-IgE monoclonal antibody has met with success in the treatment of moderate-to-severe and severe persistent allergic asthma.

Objective: To test whether B cell-targeted therapy is a more effective treatment for airway hyperresponsiveness (AHR) in a murine model compared with IgE-depletion.

Methods: We delivered soluble mTACI-Ig, a receptor for the B cell survival factors BLyS (B Lymphocyte Stimulator) and APRIL (A PRoliferation-Inducing Ligand), or anti-IgE to allergen-sensitized mice before airway challenge with allergen.

Results: mTACI-Ig treatment reduced circulating mature B cell levels in the blood, while anti-IgE treatment had no effect on B cell counts. Both mTACI-Ig and anti-IgE decreased the levels of total and allergen-specific IgE in the serum. Histopathologic analysis of lungs showed a reduction in disease severity scores for both treatment groups, but results were more pronounced in mTACI-Ig-treated mice. Neutrophil and eosinophil numbers in the bronchoalveolar lavage (BAL) were significantly reduced following mTACI-Ig treatment, but not after anti-IgE delivery. BLyS and APRIL blockade also resulted in a significant decrease in IL-4 and eotaxin mRNA and IL-4 and KC protein levels in total lung homogenates and BAL fluid, respectively. Finally, mTACI-Ig treatment was more effective than anti-IgE treatment in reducing AHR to inhaled antigen.

Conclusions: Our data demonstrate that delivery of mTACI-Ig is a more effective treatment than anti-IgE mAb in a murine model of AHR.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Allergens / adverse effects
  • Animals
  • Antibodies, Monoclonal / administration & dosage
  • Antibodies, Monoclonal / therapeutic use
  • Asthma / blood
  • Asthma / etiology
  • Asthma / immunology
  • Asthma / prevention & control*
  • B-Cell Activating Factor / genetics
  • B-Lymphocytes / immunology
  • Bronchoalveolar Lavage Fluid / immunology
  • Chemokines / genetics
  • Chemokines / metabolism
  • Disease Models, Animal
  • Eosinophils / immunology
  • Immunoglobulin E / blood
  • Immunoglobulin E / immunology
  • Inflammation / pathology
  • Injections, Intraperitoneal
  • Interleukin-4 / genetics
  • Interleukin-4 / metabolism
  • Lung / metabolism
  • Lung / pathology
  • Mice
  • Mice, Inbred BALB C
  • Neutrophils / immunology
  • Ovalbumin / adverse effects
  • RNA, Messenger / genetics
  • Recombinant Fusion Proteins / administration & dosage
  • Recombinant Fusion Proteins / therapeutic use*
  • Tumor Necrosis Factor Ligand Superfamily Member 13 / genetics

Substances

  • Allergens
  • Antibodies, Monoclonal
  • B-Cell Activating Factor
  • Chemokines
  • RNA, Messenger
  • Recombinant Fusion Proteins
  • Tnfsf13 protein, mouse
  • Tumor Necrosis Factor Ligand Superfamily Member 13
  • keratinocyte-derived chemokines
  • Interleukin-4
  • Immunoglobulin E
  • Ovalbumin
  • TACI receptor-IgG Fc fragment fusion protein