Loss of IL-33 enhances elastase-induced and cigarette smoke extract-induced emphysema in mice.

ABSTRACT:

Background

IL-33, which is known to induce type 2 immune responses via group 2 innate lymphoid cells, has been reported to contribute to neutrophilic airway inflammation in chronic obstructive pulmonary disease. However, its role in the pathogenesis of emphysema remains unclear.

Methods

We determined the role of interleukin (IL)-33 in the development of emphysema using porcine pancreas elastase (PPE) and cigarette smoke extract (CSE) in mice. First, IL-33^-/- mice and wild-type (WT) mice were given PPE intratracheally. The numbers of inflammatory cells, and the levels of cytokines and chemokines in the bronchoalveolar lavage (BAL) fluid and lung homogenates, were analyzed; quantitative morphometry of lung sections was also performed. Second, mice received CSE by in

SUBMITTER: Morichika D 

PROVIDER: S-EPMC8122555 | biostudies-literature | 2021 May

REPOSITORIES: biostudies-literature