IL-4 induces ICAM-1 expression in human bronchial epithelial cells and potentiates TNF-α

Střı́ž, Ilja; Mio, Tadashi; Adachi, Yuichi; Heires, Peggy; Robbins, Richard; Spurzem, John R.; Illig, Mary; Romberger, Debra J.; Rennard, Stephen I.

doi:10.1152/ajplung.1999.277.1.l58

Cited by 33 publications

(36 citation statements)

References 40 publications

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“…By 48 and 72 h exposure, the level of ICAM-1 mRNA was significantly greater in cytokine-treated than in control cultures. No ICAM-1 was detectable in vehicle-treated HAE cultures, consistent with previously published data (Striz et al, 1999). After 24 h exposure to cytokines, there was a significant increase in ICAM-1 mRNA expression, which increased further to 214 Ϯ 14.5% of the 24-h level by 48 h and 242 Ϯ 8.5% at 72 h. To correlate the changes in mRNA expression after cytokine exposure with protein levels, we performed an enzymelinked immunosorbent assay (ELISA) on vehicle and cytokine-treated cultures for 24, 48, or 72 h (Figure 7).…”

Section: Cytokine Exposure and Jam And Icam-1 Expressionsupporting

confidence: 92%

Regulation of Airway Tight Junctions by Proinflammatory Cytokines

Coyne¹,

Vanhook²,

Gambling

et al. 2002

MBoC

262

233

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Epithelial tight junctions (TJs) provide an important route for passive electrolyte transport across airway epithelium and provide a barrier to the migration of toxic materials from the lumen to the interstitium. The possibility that TJ function may be perturbed by airway inflammation originated from studies reporting (1) increased levels of the proinflammatory cytokines interleukin-8 (IL-8), tumor necrosis factor ␣ (TNF-␣), interferon ␥ (IFN-␥), and IL-1␤ in airway epithelia and secretions from cystic fibrosis (CF) patients and (2) abnormal TJ strands of CF airways as revealed by freeze-fracture electron microscopy. We measured the effects of cytokine exposure of CF and non-CF well-differentiated primary human airway epithelial cells on TJ properties, including transepithelial resistance, paracellular permeability to hydrophilic solutes, and the TJ proteins occludin, claudin-1, claudin-4, junctional adhesion molecule, and ZO-1. We found that whereas IL-1␤ treatment led to alterations in TJ ion selectivity, combined treatment of TNF-␣ and IFN-␥ induced profound effects on TJ barrier function, which could be blocked by inhibitors of protein kinase C. CF bronchi in vivo exhibited the same pattern of expression of TJ-associated proteins as cultures exposed in vitro to prolonged exposure to TNF-␣ and IFN-␥. These data indicate that the TJ of airway epithelia exposed to chronic inflammation may exhibit parallel changes in the barrier function to both solutes and ions.

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Section: Cytokine Exposure and Jam And Icam-1 Expressionsupporting

confidence: 92%

Regulation of Airway Tight Junctions by Proinflammatory Cytokines

Coyne¹,

Vanhook²,

Gambling

et al. 2002

MBoC

262

233

View full text Add to dashboard Cite

show abstract

“…It is also likely that IL-4 has proinflammatory effects on nonhemopoietic cells. Colonic epithelial cells express IL-4R and can increase ICAM-1 expression in response to IL-4, and thus may contribute to the exacerbation of disease in this model (47,55).…”

Section: Discussionmentioning

confidence: 90%

IL-4 Exacerbates Disease in a Th1 Cell Transfer Model of Colitis

Fort¹,

Lesley²,

Davidson³

et al. 2001

The Journal of Immunology

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IL-4 is associated with Th2-type immune responses and can either inhibit or, in some cases, promote Th1-type responses. We tested the effect of IL-4 treatment on the development of inflammation in the CD4+CD45RBhigh T cell transfer model of colitis, which has been characterized as a Th1-dependent disease. IL-4 treatment significantly accelerated the development of colitis in immunodeficient recipients (recombinase-activating gene-2 (Rag2)−/−) of CD4+CD45RBhigh T cells. Quantitative analysis of mRNA expression in the colons of IL-4-treated mice showed an up-regulation of both Th1- and Th2-associated molecules, including IFN-γ, IP-10, MIG, CXCR3, chemokine receptor-8, and IL-4. However, cotreatment with either IL-10 or anti-IL-12 mAb effectively blocked the development of colitis in the presence of exogenous IL-4. These data indicate that IL-4 treatment exacerbates a Th1-mediated disease rather than induces Th2-mediated inflammation. As other cell types besides T cells express the receptor for IL-4, the proinflammatory effects of IL-4 on host cells in Rag2−/− recipients were assessed. IL-4 treatment was able to moderately exacerbate colitis in Rag2−/− mice that were reconstituted with IL-4Rα-deficient (IL-4Rα−/−) CD4+CD45RBhigh T cells, suggesting that the IL-4 has proinflammatory effects on both non-T and T cells in this model. IL-4 did not cause colitis in Rag2−/− mice in the absence of T cells, but did induce an increase in MHC class II expression in the lamina propria of the colon, which was blocked by cotreatment with IL-10. Together these results indicate that IL-4 can indirectly promote Th1-type inflammation in the CD4+CD45RBhigh T cell transfer model of colitis.

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“…Adhesion molecules and chemokines are expressed by various airway cells including eosinophils, bronchial epithelium cells, endothelial cells, T cells, mast cells, and alveolar macrophages (Wardlaw et al, 1994;Bisset and Schmid-Grendelmeier, 2005). Expression of ICAM-1 or VCAM-1 is modulated by Th2 cytokines in airway inflammation (Bochner et al, 1995;Striz et al, 1999;Henderson et al, 2000). Th2 cytokines are also able to stimulate the production of chemokines in airway cells (Mochizuki et al, 1998;Li et al, 1999;Teran et al, 1999;Bisset and Schmid-Grendelmeier, 2005).…”

Section: Discussionmentioning

confidence: 99%

Change of connexin 37 in allergen-induced airway inflammation

et al. 2007

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Gap junction channels formed with connexins directly link to the cytoplasm of adjacent cells and have been implicated in intercellular signaling. Connexin 37 (Cx37) is expressed in the gas-exchange region of the lung. Recently, Cx37 has been reported to be involved in the pathogenesis of inflammatory disease. However, no data are available on the role of Cx37 in allergic airway inflammatory disease. In the present study, we used a murine model of ovalbumin (OVA)-induced allergic airway disease and primary murine epithelial cells to examine the change of Cx37 in allergic airway disease. These mice develop the following typical pathophysiological features of asthma: airway hyperresponsiveness, airway inflammation, and increased IL-4, IL-5, IL-13, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, eotaxin, and RANTES levels in lungs. Cx37 protein and mRNA expression were decreased in OVA-induced allergic airway disease. Immunoreactive Cx37 localized in epithelial layers around the bronchioles in control mice, which dramatically disappeared in allergen-induced asthmatic lungs. Moreover, the levels of Cx37 protein in lung tissues showed significantly negative correlations with airway inflammation, airway responsiveness, and levels of Th2 cytokines in lungs. These findings indicate that change of Cx37 may be associated with the asthma phenotype.

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IL-4 induces ICAM-1 expression in human bronchial epithelial cells and potentiates TNF-α

Cited by 33 publications

References 40 publications

Regulation of Airway Tight Junctions by Proinflammatory Cytokines

Regulation of Airway Tight Junctions by Proinflammatory Cytokines

IL-4 Exacerbates Disease in a Th1 Cell Transfer Model of Colitis

Change of connexin 37 in allergen-induced airway inflammation

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