Murine allergic airway disease (AAD), like human eosinophilic asthma, is characterized by AHR, eosinophilia, goblet cell metaplasia (GCM), smooth muscle hypercontractility, and increased production of IL-4 and IL-13-cytokines that induce these characteristics by binding to the IL-4Rα chain.
Subjects were recruited into a COPD (emphysema versus airway disease [EvA]) or asthma cohort (Unbiased BIOmarkers in PREDiction of respiratory disease outcomes, U-BIOPRED).
We evaluated the epithelial and smooth muscle IL-4Rα-dependent contributions to AHR of BALB/c mice that possessed 0-2 functional IL-4Rα alleles and had airway disease induced by house dust mite extract (HDM) or exogenous IL-13.
We used Rosa<sup>creERT2</sup> IL-4Rα<sup>-/lox</sup> mice, a tamoxifen (TAM) inducible IL-4Rα knockdown model to investigate the role of IL-4/IL-13 signaling prior to the onset of the disease and during the effector phase in the ovalbumin-induced allergic airway disease.
Further studies are needed to identify the pathogenetic differences accounting for the gender distribution of RA-ILD among Black and White populations.Key Points• First study to assess ILD among predominantly Black RA patients.• The prevalence of RA-associated ILD was 6.36%, affecting mostly women in their sixth decade with seropositive disease.• COPD was the most common airway disease among non-RA-ILD Black population.• GERD was found in approximately one-third of patients with RA-associated ILD versus one-fifth of those RA patients without any lung disease.
Asthma is a chronic inflammatory airway disease associated with type 2 cytokines interleukin-4 (IL-4), IL-5, and IL-13, which promote airway eosinophilia, mucus overproduction, bronchial hyperresponsiveness (BHR), and immunogloubulin E (IgE) synthesis.
This AAD histopathology was associated with a T helper type 2 (Th2) transcription profile in the lungs, including IL-4, IL-5, IL-9, and IL-25, known inducers of Th2-driven AAD.
<i>Chlamydia</i>-infected mice responded with robust airway neutrophil infiltration and upon induction of AAD increased their production of IL-4, IL-5, and IL-13 by >3 fold compared to unsensitized groups.
COPD is a distinct disease from adult-onset asthma; however, some patients with COPD may present with several forms of airway disease described as asthma-COPD overlap (ACO).
The IL-13 receptor α2 (IL-13Rα2) is a receptor for IL-13 which has conflicting roles in mediating IL-13 responses in the lower airway, with little known about its impact on upper airway diseases.
COPD is an inflammatory airway disease characterised by progressive airflow limitation and air trapping, leading to lung hyperinflation and exercise limitation.
We used the Longitudinal Health Insurance Database to select patients aged 20 years and older with chronic airway diseases (asthma and COPD) between 2000 and 2011 as the base cohort.
Poly-ADP ribose polymerase-14 (PARP14 or ARTD8) was initially identified as a transcriptional co-activator for signal transducer and activator of transcription 6 (Stat6), where the presence of interleukin-4 (IL-4) and activated Stat6 induces the enzymatic activity of PARP14 that promotes T helper type 2 differentiation and allergic airway disease.
We believe that this regulation is of special importance in the pulmonary system, since both factors, glucocorticoids and IL-4/13, play a role in airway diseases such as asthma.
Because we find 2-3 fold lower basal IL-4 production in CD1d- mice than in wild-type (WT) mice, we hypothesized that the contribution made by NKT cells to AAD would depend on the strength of the stimulus used to induce the disease.
Because asthma and COPD are both inflammatory chronic obstructive airway diseases, there are several clinical expressions which can cause confusion, such as: eosinophilic asthma with fixed obstruction, which is a risk factor and might progress to COPD; eosinophilic COPD; COPD with partial reversible obstruction with no asthmatic component and also eosinophilic asthma-COPD overlap syndrome (ACOS).