Asthma induced with anti-allergen IgE antibodies is characterized by allergen-induced early and late asthmatic responses, airway hyper-responsiveness (AHR) and airway inflammation. A typical mouse asthma model exhibiting these symptoms is induced by sensitization with ovalbumin (OVA) and aluminum hydroxide adjuvant (Alum) by an intraperitoneal injection, followed by repeated intratracheal OVA challenges. However, this model requires several weeks to induce asthma (Figure 1 Top). To minimize this hindrance in asthma research, Chondrex, Inc. introduces a novel mouse asthma model (1, 2) using an anti-OVA IgE monoclonal antibody rather than OVA sensitization, resulting in a one week study (Figure 1 bottom).
Note 1: Dr. Saika et al., recently introduced a new protocol for inducing nasal hypersensitivity in C57BL/6 mice using Chondrex Inc’s anti-OVA IgE monoclonal antibody, E-C1. For more information, see the following report!
Note 2: In recent references, mouse anti OVA monoclonal IgE antibody, E-C1 (catalog# 3006), has been refered to by the clone name "OE-1" and mouse anti OVA monoclonal IgG antibody, L71 (catalog# 3008), has been refered to by the clone name "O1-10".
Dust mite extract from D.pteronyssinus
|Product||Catalog #||Price (USD)|
|Dust Mite Extract from D. farinae||3040||299.00|
|Dust Mite Extract from D. pteronyssinus||3033||99.00|
Mouse Anti-OVA IgE and IgG Monoclonal Antibodies
|Product||In Vitro Application||In Vivo Application||Quantity||Catalog #||Price (USD)|
|Mouse Anti OVA Monoclonal IgG1 Antibody L71||No||1 mg, lyophilized||3008||406.00|
|Mouse Anti OVA Monoclonal IgE Antibody E-C1||Mast Cell Activation||Hyper-Sensitivity Reaction||1 mg, lyophilized||3006||812.00|
|Mouse Anti OVA Monoclonal IgE Antibody E-G5||No||No||1 mg, lyophilized||3007||406.00|
Ovalbumin From Chick Egg White
|Product||Catalog #||Price (USD)|
|Low Endotoxin Ovalbumin From Chick Egg White, 10 mg||3022||129.00|
|Ovalbumin From Chick Egg White, 50 mg||30211||42.00|
Anti-OVA monoclonal IgE and IgG antibodies
The type I hypersensitivity reaction mediated by IgE is a typical clinical feature of allergic diseases, such as asthma, eczema, hay fever, and urticaria. OVA is widely used as an antigen for studying the IgE-mediated allergic reaction in mice. Chondrex, Inc. provides allergenic and non-allergenic mouse anti-OVA IgE and IgG monoclonal antibodies for studying allergic diseases, such as in vivo hyper-sensitivity reactions, and related kits for in vitro and in vivo experiments.
OVA is the predominant protein in chicken egg whites. This glycoprotein is routinely used as an allergen to study mucosal immunity (3) and allergic asthma animal models, such as airway hyper-responsiveness (AHR)(4-7). In addition, OVA is a common reference protein for biochemical assays such as Western blots and ELISAs. Chondrex, Inc. provides purified OVA for in vitro and in vivo experiments as well as anti-OVA antibody ELISAs and anti-OVA antibodies.
Figure 1. Typical protocols for induction of asthma in Balb/c mice
Figure 2. Comparison of OVA/Alum and Anti-OVA IgE (E-C1)-induced Asthma Model (Left) and Effect of Treatment with the Inhibitor in E-C1-induced Asthma Model (Right).
Specific airway resistance (sRaw) was measured in conscious mice using a two-chambered, double flow plethysmograph system (Pulmos-I; M.I.P.S) Mizutani, et al. (2012) (1)
Allergenic and Non-Allergenic Antibodies
In general, the cross-linkage of two adjacent IgE antibody molecules, which are attached to IgE
receptors on mast cells by a polyvalent allergen, is required to trigger degranulation (also known
as activation) of mast cells (Figure 3a). Alternatively, IgG antibodies to an allergen can also
trigger the degranulation of mast cells by forming cross-linkage of the allergen molecules
captured by IgE antibodies on mast cells (Figure 3b).
Figure 3 - Two mechanisms of mast cell-bound IgE cross-linking. a) Cross-linkage by a single allergen and b) Cross-linkage by a single IgG antibody to two allergen molecules. A mouse IgE monoclonal antibody, Clone E-C1, is capable of inducing degranulation of mast cells in vitro (Figure 4a and 4b) and severe hypersensitivity in vivo (Figure 5), suggesting that clone E-C1 might recognize the repetitive epitopes of OVA. Furthermore, it has been reported that aggregated OVA carrying multiple epitopes increases the formation of cross-linkage of IgE molecules on mast cell surfaces. On the other hand, Clone E-G5 is not capable of inducing these allergic reactions in vitro or in vivo (Figures 4a, 4b, and 5), and can be used as a control.
Figure 4 - Degranulation of mast cells by monoclonal IgE antibodya) Comparison of E-C1 and E-G5 and b) Dose response of E-C1
Figure 5 - Foot pad hypersensitivity reaction induced by E-C1 in Balb/c mice
1. N. Mizutani, H. Goshima, T. Nabe, S. Yoshino, Establishment and characterization of a murine model for allergic asthma using allergen-specific IgE monoclonal antibody to study pathological roles of IgE. Immunol Lett 141, 235-245 (2012).
2. N. Mizutani, H. Goshima, T. Nabe, S. Yoshino, Complement C3a-induced IL-17 plays a critical role in an IgE-mediated late-phase asthmatic response and airway hyperresponsiveness via neutrophilic inflammation in mice. J Immunol 188, 5694-5705 (2012).
6. C. Chen, N. Sun, Y. Li, X. Jia, A BALB/c mouse model for assessing the potential allergenicity of proteins: Comparison of allergen dose, sensitization frequency, timepoint and sex. Food Chem Toxicol 62c, 41-47 (2013).
7. K. Tsuchiya, S. Siddiqui, P. A. Risse, N. Hirota, J. G. Martin, The presence of LPS in OVA inhalations affects airway inflammation and AHR but not remodeling in a rodent model of asthma. Am J Physiol Lung Cell Mol Physiol 303, L54-63 (2012).