Airway epithelial cells modify immune responses by inducing an anti-inflammatory microenvironment

Yang, X.-q., Wang, L., Li, H.-t. and Liu, D. 2015. Immune responses of porcine airway epithelial cells to poly(I:C), a synthetic analogue of viral double-stranded RNA. Can. J. Anim. Sci. 95: 13–20. Swine respiratory disease (SRD) is one of the most economically important diseases affecting the pig industry. The main infectious agents that cause SRD are viruses, but the molecular pathogenesis of viral SRD has not been extensively studied. Here, using digital gene expression tag profiling, the global transcriptional responses to poly(I:C), a synthetic analogue of viral double-stranded RNA, was analyzed in porcine airway epithelial cells (PAECs). The profiling analysis revealed numerous differentially expressed genes (DEGs), including unknown sequences in the porcine nucleotide databases. Gene ontology enrichment analysis showed that DEGs were mainly enriched in response to stress (GO: 0006950), of which, defense response is one sub-process. Poly(I:C) challenge induced a general inflammation response as indicated by marked upregulation of a variety of pathogen recognition receptors, interferon-stimulated genes, proinflammatory cytokines, and chemokines, together with the significant downregulation of anti-inflammatory molecules. Furthermore, the antiapoptotic pathway was triggered, as demonstrated by the significant suppression of molecules involved in the induction of apoptosis, together with the significant stimulation of putative inhibitor of apoptosis. The results indicate that PAECs initiated defense against poly(I:C) challenge through the inflammation responses, whereas poly(I:C) can utilize antiapoptotic pathway to evade host defense.

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Anti-Inflammatory Properties of Fructo-Oligosaccharides in a Calf Lung Infection Model and in Mannheimia haemolytica-Infected Airway Epithelial Cells

Nutrients ◽

10.3390/nu13103514 ◽

2021 ◽

Vol 13 (10) ◽

pp. 3514

Author(s):

Yang Cai ◽

Myrthe S. Gilbert ◽

Walter J. J. Gerrits ◽

Gert Folkerts ◽

Saskia Braber

Keyword(s):

Epithelial Cells ◽

A549 Cells ◽

Airway Epithelial Cells ◽

Mannheimia Haemolytica ◽

Epithelial Barrier ◽

Infection Model ◽

Airway Epithelial ◽

Clinical Scores ◽

Lung Infections ◽

Anti Inflammatory

Emerging antimicrobial-resistant pathogens highlight the importance of developing novel interventions. Here, we investigated the anti-inflammatory properties of Fructo-oligosaccharides (FOS) in calf lung infections and in airway epithelial cells stimulated with pathogens, and/or bacterial components. During a natural exposure, 100 male calves were fed milk replacer with or without FOS for 8 weeks. Then, immune parameters and cytokine/chemokine levels in the bronchoalveolar lavage fluid (BALF) and blood were measured, and clinical scores were investigated. Calf primary bronchial epithelial cells (PBECs) and human airway epithelial cells (A549) were treated with Mannheimia haemolytica, lipopolysaccharides (LPS), and/or flagellin, with or without FOS pretreatment. Thereafter, the cytokine/chemokine levels and epithelial barrier function were examined. Relative to the control (naturally occurring lung infections), FOS-fed calves had greater macrophage numbers in BALF and lower interleukin (IL)-8, IL-6, and IL-1β concentrations in the BALF and blood. However, FOS did not affect the clinical scores. At slaughter, FOS-fed calves had a lower severity of lung lesions compared to the control. Ex vivo, FOS prevented M. haemolytica-induced epithelial barrier dysfunction. Moreover, FOS reduced M. haemolytica- and flagellin-induced (but not LPS-induced) IL-8, TNF-α, and IL-6 release in PBECs and A549 cells. Overall, FOS had anti-inflammatory properties during the natural incidence of lung infections but had no effects on clinical symptoms.

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Olodaterol and anti-inflammatory effects on differentiated air-liquid interface cultures of airway epithelial cells

10.1183/1393003.congress-2017.pa1000 ◽

2017 ◽

Author(s):

Gurpreet Singhera ◽

Roxana Yan ◽

Delbert Dorscheid ◽

Don Sin ◽

Michael Pieper

Keyword(s):

Epithelial Cells ◽

Airway Epithelial Cells ◽

Liquid Interface ◽

Airway Epithelial ◽

Anti Inflammatory ◽

Air Liquid Interface

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Anti-inflammatory effects of resveratrol in lung epithelial cells: molecular mechanisms

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00110.2004 ◽

2004 ◽

Vol 287 (4) ◽

pp. L774-L783 ◽

Cited By ~ 211

Author(s):

Louise E. Donnelly ◽

Robert Newton ◽

Gina E. Kennedy ◽

Peter S. Fenwick ◽

Rachel H. F. Leung ◽

...

Keyword(s):

Epithelial Cells ◽

A549 Cells ◽

Airway Epithelial Cells ◽

Airway Epithelial ◽

Colony Stimulating Factor ◽

Macrophage Colony Stimulating Factor ◽

Anti Inflammatory ◽

Macrophage Colony ◽

Stimulating Factor ◽

Factor Release

Resveratrol (3,4′,5-trihydroxystilbene) is a polyphenolic stilbene found in the skins of red fruits, including grapes, that may be responsible for some of the health benefits ascribed to consumption of red wine. Resveratrol has been shown to have antioxidant properties and can act as an estrogen agonist. This study examined the anti-inflammatory effects of resveratrol on human airway epithelial cells. Resveratrol and the related molecule quercetin, but not deoxyrhapontin, inhibited IL-8 and granulocyte-macrophage colony-stimulating factor release from A549 cells. Neither the estrogen receptor antagonist tamoxifen nor the glucocorticoid antagonist mifepristone altered the inhibitory effect of resveratrol. The mechanism of resveratrol action was investigated further using luciferase reporter genes stably transfected into A549 cells. Resveratrol and quercetin inhibited NF-κB-, activator protein-1-, and cAMP response element binding protein-dependent transcription to a greater extent than the glucocorticosteroid dexamethasone. These compounds also had no significant effect on acetylation or deacetylation of core histones. Resveratrol, but not estradiol or N-acetyl cysteine, inhibited cytokine-stimulated inducible nitric oxide synthase expression and nitrite production (IC50 = 3.6 ± 2.9 μM) in human primary airway epithelial cells. Resveratrol also inhibited granulocyte-macrophage colony-stimulating factor release (IC50 = 0.44 ± 0.17 μM), IL-8 release (IC50 = 4.7 ± 3.3 μM), and cyclooxygenase-2 expression in these cells. This study demonstrates that resveratrol and quercetin have novel nonsteroidal anti-inflammatory activity that may have applications for the treatment of inflammatory diseases.

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