The effect of graft-versus-host disease on skin endothelial and epithelial cell chimerism in stem-cell transplant recipients.

Background: Recent evidence indicates that bone marrow-derived cells contribute to endothelial and epithelial cell renewal in recipients of an allogeneic stem-cell transplantation (SCT). Controversy remains on the biological significance of these donor-derived cells.

Methods: This study investigated the occurrence of endothelial and epithelial cell chimerism in relation to the conditioning regimen, time interval after SCT, and development of acute and chronic graft-versus-host disease (GVHD).

Renal tubular epithelial cells modulate T-cell responses via ICOS-L and B7-H1.

Background: Renal tubular epithelial cells (TECs) play an active role in renal inflammation. Previous studies have demonstrated the capacity of TECs to modulate T-cell responses both positively and negatively. Recently, new costimulatory molecules [inducible T cell costimulator-L (ICOS-L) and B7-H1] have been described, which appear to be involved in peripheral T-cell activation.

Interactions of the extracellular matrix proteoglycans decorin and biglycan with C1q and collectins.

Decorin and biglycan are closely related abundant extracellular matrix proteoglycans that have been shown to bind to C1q. Given the overall structural similarities between C1q and mannose-binding lectin (MBL), the two key recognition molecules of the classical and the lectin complement pathways, respectively, we have examined functional consequences of the interaction of C1q and MBL with decorin and biglycan. Recombinant forms of human decorin and biglycan bound C1q via both collagen and globular domains and inhibited the classical pathway.

NF-kappaB mediated IL-6 production by renal epithelial cells is regulated by c-jun NH2-terminal kinase.

Tubular epithelial cells (TEC) play an important role in tubulointerstitial inflammation, a hallmark of most renal diseases, via production of cytokines and chemokines. In this study, the role of mitogen-activated protein kinases (MAPK) in regulation of the proinflammatory cytokine IL-6 in cultured human TEC in response to the leukocyte-derived factors IL-1, TNF-alpha, IL-17, and CD40L was investigated. IL-6 production induced by IL-1, TNF-alpha, and IL-17 was specifically inhibited by the c-jun NH(2)-terminal kinase (JNK) inhibitor SP600125, but not by a selective inhibitor of p38 MAPK, and was moderately increased when the ERK1/2 pathway was inhibited.

Meconium is a source of pro-inflammatory substances and can induce cytokine production in cultured A549 epithelial cells.

Inflammation plays an important role in the pathogenesis of meconium aspiration syndrome, and pneumonitis is one of the major characteristics. We have previously shown that meconium has chemotactic properties because of the presence of IL-8. We hypothesize that IL-8 and other proinflammatory substances in meconium may amplify inflammation in meconium aspiration syndrome, inducing endogenous cytokine production by lung epithelial cells.

Steroid responsiveness of renal epithelial cells. Dissociation of transrepression and transactivation.

Glucocorticoids modulate cellular and inflammatory responses via stimulation or inhibition of gene transcription. Inhibition of cytokine gene expression is mediated via repression of transcription factors, including NF-kappaB. Previously we have shown that cytokine production by renal epithelial cells is insensitive to the inhibitory action of dexamethasone.

Production of inflammatory mediators by renal epithelial cells is insensitive to glucocorticoids.

1. In the present study we investigated the effect of glucocorticoids on the activation of renal tubular epithelial cells, which are thought to play an important role in inflammatory processes in the kidney. 2.