Abstract
Allergic contact dermatitis (ACD) is a common skin disease with high prevalence in work environments. Human allergic contact dermatitis is triggered by the exposure to haptens that leads to an initial phase known as sensitization. During this phase, hapten–protein complexes presented by antigen-presenting cells activate a T-cell-mediated response, leading to the generation of memory cells against the hapten. Upon re-exposure to the same hapten, the elicitation phase is initiated. This phase is characterized by a quicker acute inflammatory response involving activation and/or infiltration of a variety of immune cell populations. Human ACD can be studied through the use of animal models of contact hypersensitivity (CHS). The 2,4-dinitrofluorobenzene (DNFB)-induced CHS model is a commonly used mouse model that has been helpful in the study of the mechanisms as well as potential therapeutic interventions of ACD. In this chapter I will provide a detailed protocol to develop acute DNFB-induced CHS in mice in a period of 7 days. In addition, I will discuss several key considerations for experimental design including best controls, potential expected outcomes, and sample collection.
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Similar content being viewed by others
References
Kaplan DH, Igyártó BZ, Gaspari AA (2012) Early events in the induction of allergic contact dermatitis. Nat Rev Immunol 12(2):114–124
Holmdahl M, Ahlfors SR, Holmdahl R et al (2008) Structure-immune response relationships of hapten-modified collagen II peptides in a T-cell model of allergic contact dermatitis. Chem Res Toxicol 21(8):1514–1523
Christensen AD, Haase C (2012) Immunological mechanisms of contact hypersensitivity in mice. APMIS 120(1):1–27
Gaide O, Emerson RO, Jiang X et al (2015) Common clonal origin of central and resident memory T cells following skin immunization. Nat Med 21(6):647–653
Martin SF, Esser PR, Weber FC et al (2011) Mechanisms of chemical-induced innate immunity in allergic contact dermatitis. Allergy 66(9):1152–1163
Vocanson M, Hennino A, Rozières A et al (2009) Effector and regulatory mechanisms in allergic contact dermatitis. Allergy 64(12):1699–1714
Dilulio NA, Engeman T, Armstrong D et al (1999) Groalpha-mediated recruitment of neutrophils is required for elicitation of contact hypersensitivity. Eur J Immunol 29(11):3485–3495
Dudeck A, Dudeck J, Scholten J et al (2011) Mast cells are key promoters of contact allergy that mediate the adjuvant effects of haptens. Immunity 34(6):973–984
Takanami-Ohnishi Y, Amano S, Kimura S et al (2002) Essential role of p38 mitogen-activated protein kinase in contact hypersensitivity. J Biol Chem 277(40):37896–37903
Kish DD, Gorbachev AV, Parameswaran N et al (2012) Neutrophil expression of Fas ligand and perforin directs effector CD8 T cell infiltration into antigen-challenged skin. J Immunol 189(5):2191–2202
Honda T, Matsuoka T, Ueta M et al (2009) Prostaglandin E(2)-EP(3) signaling suppresses skin inflammation in murine contact hypersensitivity. J Allergy Clin Immunol 124(4):809–18.e2
Manresa MC, Smith L, Casals-Diaz L et al (2019) Pharmacologic inhibition of hypoxia-inducible factor (HIF)-hydroxylases ameliorates allergic contact dermatitis. Allergy 74(4):753–766
Dudeck J, Medyukhina A, Fröbel J et al (2017) Mast cells acquire MHCII from dendritic cells during skin inflammation. J Exp Med 214(12):3791–3811
Bell BD, Kitajima M, Larson RP et al (2013) STAT5 is critical in dendritic cells for development of TH2- but not TH1-dependent Immunity. Nat Immunol 14(4):364–371
Takamori A, Nambu A, Sato K et al (2018) IL-31 is crucial for induction of pruritus, but not inflammation, in contact hypersensitivity. Sci Rep 8(1):6639
Takeshita K, Yamasaki T, Akira S et al (2004) Essential role of MHC II-independent CD4+ T cells, IL-4 and STAT6 in contact hypersensitivity induced by fluorescein isothiocyanate in the mouse. Int Immunol 16(5):685–695
Howard HL, McLaughlin-Taylor E, Hill RL (1990) The effect of mouse euthanasia technique on subsequent lymphocyte proliferation and cell mediated lympholysis assays. Lab Anim Sci 40(5):510–514
Al-Mousawi AM, Kulp GA, Branski LK et al (2010) Impact of anesthesia, analgesia, and euthanasia technique on the inflammatory cytokine profile in a rodent model of severe burn injury. Shock 34(3):261–268
Author information
Authors and Affiliations
Corresponding author
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2021 Springer Science+Business Media, LLC, part of Springer Nature
About this protocol
Cite this protocol
Manresa, M.C. (2021). Animal Models of Contact Dermatitis: 2,4-Dinitrofluorobenzene-Induced Contact Hypersensitivity. In: Nagamoto-Combs, K. (eds) Animal Models of Allergic Disease. Methods in Molecular Biology, vol 2223. Humana, New York, NY. https://doi.org/10.1007/978-1-0716-1001-5_7
Download citation
DOI: https://doi.org/10.1007/978-1-0716-1001-5_7
Published:
Publisher Name: Humana, New York, NY
Print ISBN: 978-1-0716-1000-8
Online ISBN: 978-1-0716-1001-5
eBook Packages: Springer Protocols