BackgroundInnate T helper type 2 (Th2) immune responses mediated by interleukin (IL)-33, thymic stromal lymphopoietin (TSLP), and IL-25 have been shown to play an important role in pulmonary fibrosis of animal models; however, their clinical implications remain poorly understood.MethodsTSLP, IL-25, and IL-33 concentrations were measured in bronchoalveolar lavage fluids obtained from normal controls (NCs; n = 40) and from patients with idiopathic pulmonary fibrosis (IPF; n = 100), non-specific interstitial pneumonia (NSIP; n = 22), hypersensitivity pneumonitis (HP; n = 20), and sarcoidosis (n = 19).ResultsThe TSLP and IL-33 levels were significantly higher in patients with IPF relative to the NCs (p = 0.01 and p = 0.0001, respectively), NSIP (p = 4.95E − 7 and p = 0.0002, respectively), HP (p = 0.00003 and p = 0.000005, respectively), and sarcoidosis groups (p = 0.003 and p = 0.0001, respectively). However, the IL-25 levels were not significantly different between NC and IPF group (p = 0.432). Receiver operating characteristic curves of the TSLP and IL-33 levels revealed clear differences between the IPF and NC groups (AUC = 0.655 and 0.706, respectively), as well as between the IPF and the other lung disease groups (AUC = 0.786 and 0.781, respectively). Cut-off values of 3.52 pg/μg TSLP and 3.77 pg/μg IL-33 were shown to differentiate between the IPF and NC groups with 99.2 and 94.3% accuracy. Cut-off values of 4.66 pg/μg TSLP and 2.52 pg/μg IL-33 possessed 99.4 and 93.2% accuracy for differentiating among the IPF and other interstitial lung disease groups.ConclusionsInnate immune responses may be associated with the development of IPF. Furthermore, the IL-33 and TSLP levels in BAL fluids may be useful for differentiating IPF from other chronic interstitial lung diseases.Electronic supplementary materialThe online version of this article (doi:10.1186/s12890-017-0380-z) contains supplementary material, which is available to authorized users.
SummaryThe purpose of this study is to examine the relationship between dietary algae (seaweed) consumption and the risk of Type 2 diabetes mellitus in the Korean population. We analyzed data from the Korean National Health and Nutrition Examination Survey in 2005, a nationally representative survey. The study participants included 3,405 males and females aged 20-65 y. Participants were classified into four groups according to the quartiles of total algae consumption frequencies. Proportional odds models were used to assess the relationship between algae consumption and the risk of having diabetes or prediabetes, after adjustment for age, family history of diabetes, education, smoking, alcohol consumption, physical activity, body mass index, waist circumference, triglycerides, total energy intake and food group intakes. The frequency of algae consumption was positively correlated to the consumption of legumes, fruits, fish, and dairy products in both genders ( p Ͻ 0.001). The odds ratios (95% confidence interval) for diabetes vs. prediabetes vs. normoglycemia was 0.66 (0.43-0.99) for males and 0.80 (0.51-1.24) for females in the highest quartile of algae consumption compared to the lowest quartile. Our results suggest that dietary algae consumption may decrease the risk of diabetes mellitus in Korean men. A welldesigned prospective study is needed to confirm this association.
IL-25 is associated with bronchospasm after aspirin challenge, possibly via mechanisms other than altered LTC4 and PGD2 production.
Background: Exposure to ozone (O 3) induces neutrophilic inflammation and goblet cell hyperplasia in humans and experimental animals. Because the solute carrier family 26-member 4 (Slc26a4; pendrin) gene induces mucin production and intraluminal acidification in the airways, it was hypothesized to be a key molecule in O 3-induced airway injury. Thus, we evaluated the role of Slc26a4 and the protective effects of ammonium chloride (NH 4 Cl) in O 3-induced airway injury in mice. Methods: Six-week-old female BALB/c mice were exposed to filtered air or O 3 for 21 days (2 ppm for 3 hr/day). NH 4 Cl (0, 0.1, 1, and 10 mM) was administered intratracheally into the airways. Airway resistance was measured using a flexiVent system, and bronchoalveolar lavage fluid (BALF) cells were differentially counted. Slc26a4 and Muc5ac proteins and mRNA were measured via western blotting, real-time polymerase chain reaction, and immunostaining. Tumor necrosis factor (TNF)-α, interferon (IFN)-γ, interleukin (IL)-17, IL-1β, and caspase-1 were analyzed via western blotting. Results: The levels Slc26a4 protein and mRNA significantly increased in lung tissues from Day 7 to Day 21 of O 3 exposure, with concomitant increases in lung resistance, numbers of goblet cells in lung tissues, and inflammatory cells and thiocyanate (SCN −) levels in BALF in a time-dependent manner. Treatment with NH 4 Cl significantly reduced these changes to levels similar to those of sham-treated mice, with a concomitant reduction of Slc26a4 proteins in lung lysates and SCN − levels in BALF. Slc26a4 protein was co-expressed with muc5ac protein in the bronchial epithelium, as indicated by immunofluorescence staining. NH 4 Cl treatment also significantly attenuated the O 3-induced increases in IFN-γ, TNF-α, IL-17, IL-1β, and p20activated caspase-1. Conclusion: Slc26a4 may be involved in O 3-induced inflammatory and epithelial changes in the airways via activation of the inflammasome and the induction of IL-17 and IFN-γ. NH 4 Cl shows a potential as a therapeutic agent for controlling O 3-induced airway inflammation and epithelial damage by modulating Slc26a4 expression.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2025 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.