Role Of Elafin Research Articles

Clinical Significance of Serum Elafin in Children with Inflammatory Bowel Disease.

The role of elafin in the pathophysiology of inflammatory bowel disease (IBD) has not been not elucidated. We aimed to evaluate serum elafin in children with IBD and assess its relationship with disease activity. We enrolled children with IBD in the study group and children with functional abdominal pain in the control group. We evaluated serum elafin using enzyme-linked immunosorbent assay kits. In children with IBD, serum elafin (mean ± SD: 4.192 ± 1.424 ng/mL) was significantly elevated compared with controls (mean ± SD: 3.029 ± 1.366 ng/mL) (p = 0.0005). Elafin was significantly increased in children in the active phase of IBD (mean ± SD: 4.424 ± 1.449 ng/mL) compared with the control group (p = 0.0003). In IBD remission, only children with ulcerative colitis (mean ± SD: 4.054 ± 1.536 ng/mL) had elevated elafin compared with controls (p = 0.004). ROC analysis revealed that the area under the curve (AUC) of serum elafin was 0.809 while discriminating patients with ulcerative colitis from the control group, and the AUC was 0.664 while differentiating patients with Crohn's disease from the control group. Serum elafin was found to be elevated in our cohort of children with IBD, depending on disease activity. Serum elafin was increased in the active phases of both ulcerative colitis and Crohn's disease, but only in the remission of ulcerative colitis. Elafin appears to be a potential candidate for a biomarker of ulcerative colitis.

Elafin promotes tumour metastasis and attenuates the anti-metastatic effects of erlotinib via binding to EGFR in hepatocellular carcinoma

BackgroundElafin is a serine protease inhibitor critical for host defence. We previously reported that Elafin was associated with the recurrence of early-stage hepatocellular carcinoma (HCC) after surgery. However, the exact role of Elafin in HCC remains obscure.MethodsHCC tissue microarrays were used to investigate the correlation between Elafin expression and the prognosis of HCC patients. In vitro migration, invasion and wound healing assays and in vivo lung metastasis models were used to determine the role of Elafin in HCC metastasis. Mass spectrometry, co-immunoprecipitation, western blotting, and immunofluorescence staining assays were performed to uncover the mechanism of Elafin in HCC. Dual-luciferase reporter and chromatin immunoprecipitation assays were employed to observe the transcriptional regulation of Elafin.ResultsElafin expression was frequently increased in HCC tissues compared to normal tissues, and high Elafin expression in HCC tissues was correlated with aggressive tumour phenotypes and a poor prognosis in HCC patients. Elafin dramatically enhanced the metastasis of HCC cells both in vitro and in vivo by interacting with EGFR and activating EGFR/AKT signalling. Moreover, Elafin attenuated the suppressive effects of erlotinib on HCC metastasis. Besides, Elafin was transcriptionally regulated by Sp1 in HCC cells. Clinically, Elafin expression was positively correlated with Sp1, Vimentin, and EGFR signalling in both our HCC tissue microarrays and TCGA database analysis.ConclusionsUpregulation of Elafin by Sp1 enhanced HCC metastasis via EGFR/AKT pathway, and overexpression of Elafin attenuated the anti-metastatic effects of erlotinib, suggesting a valuable prognostic biomarker and therapeutic target for HCC.

Sheep lung segmental delivery strategy demonstrates adenovirus priming of local lung responses to bacterial LPS and the role of elafin as a response modulator.

Viral lung infections increase susceptibility to subsequent bacterial infection. We questioned whether local lung administration of recombinant adenoviral vectors in the sheep would alter the susceptibility of the lung to subsequent challenge with bacterial lipopolysaccharide (LPS). We further questioned whether local lung expression of elafin, a locally produced alarm anti-LPS/anti-bacterial molecule, would modulate the challenge response. We established that adenoviral vector treatment primed the lung for an enhanced response to bacterial LPS. Whereas this local effect appeared to be independent of the transgene used (Ad-o-elafin or Ad-GFP), Ad-o-elafin treated sheep demonstrated a more profound lymphopenia in response to local lung administration of LPS. The local influence of elafin in modulating the response to LPS was restricted to maintaining neutrophil myeloperoxidase activity, and levels of alveolar macrophage and neutrophil phagocytosis at higher levels post-LPS. Adenoviral vector-bacterial synergism exists in the ovine lung and elafin expression modulates such synergism both locally and systemically.