Interleukin-10 Down-Regulates Cathepsin B Expression in Fetal Rat Alveolar Type II Cells Exposed to Hyperoxia

Lee, Hyeon-Soo; Kim, Chun Ki

doi:10.3349/ymj.2013.54.2.445

Cited by 9 publications

(11 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recently, it was found that IL-10 treatment inhibited inflammatory cytokines released by fetal mouse lung fibroblasts exposed to mechanical stretch (Hawwa et al 2011) and reduced cell death of alveolar type II cells exposed to hyperoxia (Lee & Kim, 2013). Inhaled IL-10 reduced biotrauma and mortality in a model of ventilator-induced lung injury (Hoegl et al 2009).…”

Section: Discussionmentioning

confidence: 99%

Exogenous interleukin‐10 attenuates hyperoxia‐induced acute lung injury in mice

Zhang

Mao

et al. 2015

Experimental Physiology

View full text Add to dashboard Cite

New Findings r What is the central question of this study? It is not known whether treatment with interleukin-10 (IL-10) attenuates hyperoxia-induced acute lung injury in mice. r What is the main finding and its importance? Our results showed that exogenous IL-10 treatment alleviated hyperoxia-induced acute lung injury in mice, possibly by regulating neutrophil recruitment and the subsequent generation of cytokines, nitric oxide and matrix metalloproteinases. Lung injury caused by breathing air enriched with oxygen continues to be a major problem in clinical medicine. Here, we investigated the therapeutic role of interleukin-10 (IL-10) in hyperoxia-induced acute lung injury in mice. In the first experiment, mice were exposed to room air or 95% O 2 and treated with IL-10 simultaneously. In the second experiment, wild-type mice and IL-10 −/− mice were exposed to room air or 95% O 2. Exogenous IL-10 treatment attenuated hyperoxia-induced acute lung injury, evidenced by a reduced ratio of lung weight to body weight, ratio of lung wet weight to dry weight, cell numbers and protein content in bronchoalveolar lavage fluid and cell death. Interleukin-10 treatment markedly prolonged the survival of mice during oxygen exposure. Interleukin-10 treatment reduced the activity of myeloperoxidase and mRNA levels of interleukin-6, tumour necrosis factor-α and macrophage inflammatory protein 2, suppressed nuclear factor-κB activation and decreased inducible nitric oxide synthnase expression and nitric oxide formation in lungs of mice exposed to hyperoxia. Interleukin-10 treatment suppressed activities of matrix metalloproteinase 2 and matrix metalloproteinase 9 and reduced lung permeability in mice during oxygen exposure. Furthermore, absence of IL-10 aggravated hyperoxia-induced acute lung injury and reduced the duration of survival of mice during oxygen exposure, which was attenuated by treatment with IL-10. In conclusion, our results show that exogenous IL-10 treatment alleviates hyperoxia-induced acute lung injury in mice, possibly by regulating neutrophil recruitment and the subsequent generation of cytokines, nitric oxide and matrix metalloproteinases. This suggests that IL-10 treatment may be a promising therapeutic strategy to reduce lung injury in patients exposed to hyperoxia.

show abstract

Section: Discussionmentioning

confidence: 99%

Exogenous interleukin‐10 attenuates hyperoxia‐induced acute lung injury in mice

Zhang

Mao

et al. 2015

Experimental Physiology

View full text Add to dashboard Cite

show abstract

“…Foetal rat lungs were obtained from time‐pregnant Sprague–Dawley rats (Daehan Biolink, Eumsung, South Korea) on E19 (term = 22 days). After extraction of foetal lungs and isolation of type II cells was proceeded as described previously Describing briefly, extracted tissues were finely minced and digested with 0.5 mg/ml collagenase type I and 0.5 mg/ml collagenase type IA (Sigma Chemical Co., St. Louis, MO, USA) with vigorous pipetting for 15 min. at 37°C.…”

Section: Methodsmentioning

confidence: 99%

“…Total RNA was extracted from E19 type II cells exposed to 65%‐hyperoxia for 24 hrs or parallel normoxic samples by a single‐step method and purified further with the Rneasy Mini Kit (Invitrogen, Carlsbad, CA, USA). Fold expressions of the hyperoxic samples relative to the controls were calculated using the ΔΔC T method for relative quantification as described previously . Samples were normalized to the 18S rRNA.…”

Section: Methodsmentioning

confidence: 99%

“…50 μg of protein were separated by SDS‐PAGE and transferred to polyvinylidene difluoride membranes. Blots were hybridized with polyclonal antibodies (p‐JAK1: cat #: CE3331; Cell Signaling, Denvers, MA, USA; p‐TYK2: cat #: SC‐11763; Santa Cruz Biotechnology, Dallas, TX, USA; and p‐STAT3: cat #: CE9131; Cell signaling) as described previously . Anti‐rabbit Ig G was used as secondary antibody, and conjugated with horseradish peroxidase, and blots were developed by exposing them to X‐ray film.…”

Section: Methodsmentioning

confidence: 99%

“…Anti‐rabbit Ig G was used as secondary antibody, and conjugated with horseradish peroxidase, and blots were developed by exposing them to X‐ray film. Membranes were then stripped and reprobed with total antibodies (t‐JAK1: cat #: CE3344s; Cell signaling; t‐TYK2: cat #: SC‐7205; Santa Cruz Biotechnology; and t‐STAT3: cat #: CE9132s; Cell signaling) and actin antibody in an identical manner .…”

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

rIL‐10 enhances IL‐10 signalling proteins in foetal alveolar type II cells exposed to hyperoxia

Lee

2015

J Cellular Molecular Medi

View full text Add to dashboard Cite

Although the mechanisms by which hyperoxia promotes bronchopulmonary dysplasia are not fully defined, the inability to maintain optimal interleukin (IL)-10 levels in response to injury secondary to hyperoxia seems to play an important role. We previously defined that hyperoxia decreased IL-10 production and pre-treatment with recombinant IL-10 (rIL-10) protected these cells from injury. The objectives of these studies were to investigate the responses of IL-10 receptors (IL-10Rs) and IL-10 signalling proteins (IL-10SPs) in hyperoxic foetal alveolar type II cells (FATIICs) with and without rIL-10. FATIICs were isolated on embryonic day 19 and exposed to 65%-oxygen for 24 hrs. Cells in room air were used as controls. IL-10Rs protein and mRNA were analysed by ELISA and qRT-PCR, respectively. IL-10SPs were assessed by Western blot using phospho-specific antibodies. IL-10Rs protein and mRNA increased significantly in FATIICs during hyperoxia, but JAK1 and TYK2 phosphorylation showed the opposite pattern. To evaluate the impact of IL-8 (shown previously to be increased) and the role of IL-10Rs, IL-10SPs were reanalysed in IL-8-added normoxic cells and in the IL-10Rs’ siRNA-treated hyperoxic cells. The IL-10Rs’ siRNA-treated hyperoxic cells and IL-8-added normoxic cells showed the same pattern in IL10SPs with the hyproxic cells. And pre-treatment with rIL-10 prior to hyperoxia exposure increased phosphorylated IL-10SPs, compared to the rIL-10-untreated hyperoxic cells. These studies suggest that JAK1 and TYK2 were significantly suppressed during hyperoxia, where IL-8 may play a role, and rIL-10 may have an effect on reverting the suppressed JAK1 and TYK2 in FATIICs exposed to hyperoxia.

show abstract

Effect of IL-10 in the pathogenesis of HIV/AIDS patients with cryptococcal meningitis

et al. 2022

Mol Cell Biochem

View full text Add to dashboard Cite

Interleukin-10 Down-Regulates Cathepsin B Expression in Fetal Rat Alveolar Type II Cells Exposed to Hyperoxia

Cited by 9 publications

References 25 publications

Exogenous interleukin‐10 attenuates hyperoxia‐induced acute lung injury in mice

Exogenous interleukin‐10 attenuates hyperoxia‐induced acute lung injury in mice

rIL‐10 enhances IL‐10 signalling proteins in foetal alveolar type II cells exposed to hyperoxia

Effect of IL-10 in the pathogenesis of HIV/AIDS patients with cryptococcal meningitis

Contact Info

Product

Resources

About