Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Cysteinyl leukotrienes regulate Th2 cell-dependent pulmonary inflammation.

Daniel C Kim1, F Ida Hsu, Nora A Barrett

  • 1Department of Medicine, Harvard Medical School, Boston, MA 02115, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|March 21, 2006
PubMed
Summary

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Tuft cells shape airway remodeling by eliciting OXGR1- and SOX9-dependent stem cell programs.

Nature communications·2026
Same author

Regulation of basal and tumour necrosis factor α-induced fibroblast gene expression by peptidylarginine deiminase 2.

The Journal of physiology·2026
Same author

Altered perivascular diffusivity in glioblastoma: integrating DTI-ALPS index with radio-pathomic and histopathologic correlates.

Journal of neuro-oncology·2026
Same author

Author Correction: Human cerebrospinal fluid net flow enhanced by respiration during the awake state.

Nature communications·2026
Same author

Novel Mixed Cancer-Cell Models Designed to Capture Inter-Patient Tumor Heterogeneity for Accurate Evaluation of Drug Combinations.

International journal of molecular sciences·2026
Same author

Altered Perivascular Diffusivity in Glioblastoma:Integrating DTI-ALPS Index with Radio-Pathomicand Histopathologic Correlates.

Research square·2026

Cysteinyl leukotrienes (cys-LTs) are key regulators of Th2 cell-driven asthma inflammation. Mice lacking leukotriene C(4) synthase (LTC(4)S) showed reduced allergic lung inflammation, indicating cys-LTs drive asthma pathology.

Area of Science:

  • Immunology
  • Pulmonary Medicine
  • Allergy Research

Background:

  • Asthma involves Th2 cell-dependent inflammation, with cysteinyl leukotrienes (cys-LTs) playing a known role in airway constriction.
  • Additional roles of cys-LTs in pulmonary inflammation pathobiology require elucidation.

Purpose of the Study:

  • To investigate the role of cys-LTs in regulating Th2 cell-dependent pulmonary inflammation in a mouse model of asthma.
  • To determine the impact of leukotriene C(4) synthase (LTC(4)S) deficiency on allergic airway responses.

Main Methods:

  • Utilized a mouse model with a deficiency in leukotriene C(4) synthase (LTC(4)S) using an ovalbumin (OVA) sensitization and challenge protocol.
  • Assessed pulmonary inflammation markers, including eosinophil infiltration, goblet cell hyperplasia, mucus hypersecretion, and mast cell activation.

Related Experiment Videos

  • Measured antigen-specific IgE and IgG1, Th2 cytokine mRNA expression, airway hyperresponsiveness, and lymph node cell cytokine production ex vivo.

    • Main Results:

    • LTC(4)S-null mice exhibited significantly reduced Ag-induced pulmonary inflammation compared to wild-type controls.
    • Key indicators of Th2 response, including serum IgE/IgG1, lung Th2 cytokine mRNA, and airway hyperresponsiveness, were markedly decreased in LTC(4)S-null mice.
    • Impaired Th2 cell activation and cytokine generation were observed in lymph nodes of LTC(4)S-null mice, while Th1 responses remained intact.

    Conclusions:

    • Cysteinyl leukotrienes (cys-LTs) play a critical role in the initiation and/or amplification of Th2 cell-dependent pulmonary inflammation in asthma.
    • Targeting LTC(4)S or cys-LT pathways may represent a therapeutic strategy for managing allergic asthma.
    • These findings highlight cys-LTs as significant mediators in the complex pathobiology of asthma.