Published: Vol 7, Iss 1, Jan 5, 2017 DOI: 10.21769/BioProtoc.2096 Views: 8452
Reviewed by: Ivan ZanoniMeenal SinhaBenoit Chassaing
Protocol Collections
Comprehensive collections of detailed, peer-reviewed protocols focusing on specific topics
Related protocols
A Participant-Derived Xenograft Mouse Model to Decode Autologous Mechanisms of HIV Control and Evaluate Immunotherapies
Emma Falling Iversen [...] R. Brad Jones
Apr 5, 2025 1274 Views
Analysis of Vascular Permeability by a Modified Miles Assay
Hilda Vargas-Robles [...] Michael Schnoor
Apr 5, 2025 1150 Views
PBMC-Humanized Mouse Model for Multiple Sclerosis: Studying Immune Changes and CNS Involvement
Anastasia Dagkonaki [...] Lesley Probert
May 20, 2025 2024 Views
Abstract
The aryl hydrocarbon receptor (AHR) is known as a sensor for dioxins that mediates their toxicity, and also has important biophysiological roles such as circadian rhythms, cell differentiation and immune responses. 6-formylindolo(3,2-b)carbazole (FICZ), which is derived through the metabolism of L-tryptophan by ultraviolet B irradiation, is one of putative physiological ligands for AHR (Smirnova et al., 2016). It has recently been shown that endogenously-activated AHR signaling modulates innate immune response during viral infection (Yamada et al., 2016). This section describes how to treat mice with FICZ and to infect them with virus.
Keywords: Aryl hydrocarbon receptorBackground
The role of AHR had so far been investigated mainly on the basis of experiments with dioxin treatment. On the other hand, it has been shown that AHR-mediated signaling is activated by endogenous tryptophan metabolites (FICZ, Kynurenine, etc.), heme metabolites (bilirubin etc.), and eicosanoids (Lipoxin A etc.). In particular, it was demonstrated that FICZ is a physiological high affinity ligand for AHR, and many accumulating reports have shown that FICZ is involved in various basic biological processes including adaptive responses to ultraviolet light, immune responses, genomic instability, and homeostasis of stem cells. Recently, Yamada et al. (2016) demonstrated its role in innate immune response: FICZ treatment in vivo suppresses type I interferon (IFN) production in response to viral infection and promotes levels of viral titer in sera of mice.
Materials and Reagents
Equipment
Procedure
Data analysis
Statistical significance between two samples is determined by Student’s t-test. Each sample is prepared in septuplicate (cf. Figure 2d of Yamada et al. [2016]).
Recipes
Acknowledgments
This protocol was adapted from Yamada et al. (2016). This was supported by a grant from the Ministry of Health, Labour and Welfare of Japan, the Ministry of Education, Culture, Sports, Science and Technology of Japan (grant-in-aid for scientific research (A) [25253030] and grant-in-aid for scientific research on innovative areas [25115502, 23112701]), the Kato Memorial Bioscience Foundation, the Yasuda Medical Foundation, the Takeda Science Foundation and the Waksman Foundation of Japan to A.T.
References
Article Information
Copyright
© 2017 The Authors; exclusive licensee Bio-protocol LLC.
How to cite
Yamada, T. and Takaoka, A. (2017). FICZ Exposure and Viral Infection in Mice. Bio-protocol 7(1): e2096. DOI: 10.21769/BioProtoc.2096.
Category
Immunology > Animal model > Mouse
Cell Biology > Cell signaling > Stress response
Do you have any questions about this protocol?
Post your question to gather feedback from the community. We will also invite the authors of this article to respond.
Tips for asking effective questions
+ Description
Write a detailed description. Include all information that will help others answer your question including experimental processes, conditions, and relevant images.
Share
Bluesky
X
Copy link