Purpose: Amniotic membrane has been applied to the ocular surface to restore corneal function. The beneficial effect of amniotic membrane transplantation may be due to the immunosuppressive effects of amniotic epithelial cells. The purpose of this study was to determine whether amniotic epithelial cells (AECs) secrete anti-inflammatory and antiproliferative factors that affect the chemotaxis of neutrophils and macrophages and suppress both T- and B-cell proliferation in vitro.
Methods: Human amniotic cells were isolated from human amniotic membrane and cultured in vitro. The supernatants from AEC cultures were collected after 48 hours of incubation. Neutrophil and macrophage chemotactic activity was tested in the presence of AEC supernatant, using 24-well migration assay chambers. Lymphocyte proliferation was tested by H(3)-thymidine incorporation. Apoptosis was examined by caspase-3 and annexin V assays, and expression of cytokines was assessed by RT-PCR.
Results: AEC supernatant significantly inhibited the chemotactic activity of neutrophils and macrophages toward macrophage inflammatory protein (MIP)-2 (P < 0.05). The supernatant significantly reduced the proliferation of both T and B cells after mitogenic stimulation (P < 0.05). Caspase-3 assays revealed that the supernatant induced apoptosis of T and B cells, but not of corneal epithelial cells and liver cells. In contrast to lymphocytes, macrophages and neutrophils were resistant to apoptosis induced by AEC supernatant. The AECs expressed message for TNFalpha, Fas ligand (FasL), TRAIL (tumor necrosis factor-related apoptosis-inducing ligand), TGFbeta, and macrophage migration-inhibitory factor (MIF). However, AEC induction of apoptosis was inhibited (50%) by anti-FasL antibody but not by anti-TRAIL or anti-TNFalpha antibodies. Moreover, AEC supernatant inhibited macrophage migration in vitro.
Conclusions: AECs secrete soluble factors that inhibit cells in both the innate and adaptive immune systems.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1167/iovs.04-0495 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Cell-cell crosstalk in the pathogenesis of acute lung injury and acute respiratory distress syndrome.
Tissue Barriers
January 2025
Sepsis Translational Medicine Key Laboratory of Hunan Province, Department of Pathophysiology, School of Basic Medicine Science, Central South University, Changsha, Hunan, PR China.
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are the result of an exaggerated inflammatory response triggered by a variety of pulmonary and systemic insults. The lung tissues are comprised of a variety of cell types, including alveolar epithelial cells, pulmonary vascular endothelial cells, macrophages, neutrophils, and others. There is mounting evidence that these diverse cell populations within the lung interact to regulate lung inflammation in response to both direct and indirect stimuli.
View Article and Find Full Text PDFPiezo1-Induced Nasal Epithelial Barrier Dysfunction in Allergic Rhinitis.
Inflammation
January 2025
Department of Otolaryngology-Head and Neck Surgery, Shandong Provincial ENT Hospital, Shandong University, Duanxing West Road, Jinan, 250000, Shandong, China.
This study aimed to investigate the role of Piezo1 in nasal epithelial barrier dysfunction in allergic rhinitis (AR) using both in vitro and in vivo experimental methods. A total of 79 human nasal mucosal samples were collected, including 43 from AR patients and 36 from healthy controls. Additionally, 12 BALB/c mice were used for the in vivo experiments.
View Article and Find Full Text PDFEffect of CFTR modulators Elexacaftor/Tezacaftor/Ivacaftor on lipid metabolism in human bronchial epithelial cells.
Glycoconj J
January 2025
Department of Medical Biotechnology and Translational Medicine, University of Milano, Milan, Italy.
Cystic Fibrosis (CF) is a life-threatening hereditary disease resulting from mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene that encodes a chloride channel essential for ion transport in epithelial cells. Mutations in CFTR, notably the prevalent F508del mutation, impair chloride transport, severely affecting the respiratory system and leading to recurrent infections. Recent therapeutic advancements include CFTR modulators such as ETI, a combination of two correctors (Elexacaftor and Tezacaftor) and a potentiator (Ivacaftor), that can improve CFTR function in patients with the F508del mutation.
View Article and Find Full Text PDFIL-33, a neutrophil extracellular trap-related gene involved in the progression of diabetic kidney disease.
Inflamm Res
January 2025
Department of Nephrology, First Affiliated Hospital of Naval Medical University, Shanghai Changhai Hospital, Shanghai, China.
Background: Chronic inflammation is well recognized as a key factor related to renal function deterioration in patients with diabetic kidney disease (DKD). Neutrophil extracellular traps (NETs) play an important role in amplifying inflammation. With respect to NET-related genes, the aim of this study was to explore the mechanism of DKD progression and therefore identify potential intervention targets.
View Article and Find Full Text PDFSynthetic rational design of live-attenuated Zika viruses based on a computational model.
Nucleic Acids Res
January 2025
SynVaccine Ltd, Ramat Hachayal, 3 Golda Meir Street, Science Park, Nes Ziona 7403648, Israel.
Many viruses of the Flaviviridae family, including the Zika virus (ZIKV), are human pathogens of significant public health concerns. Despite extensive research, there are currently no approved vaccines available for ZIKV and specifically no live-attenuated Zika vaccine. In this current study, we suggest a novel computational algorithm for generating live-attenuated vaccines via the introduction of silent mutation into regions that undergo selection for strong or weak local RNA folding or into regions that exhibit medium levels of sequence conservation.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!