P2Y6 Receptor Contributes to Neutrophil Recruitment to Inflamed Intestinal Mucosa by Increasing Cxc Chemokine Ligand 8 Expression in an AP-1-dependent Manner in Epithelial Cells

2012 ◽  
Vol 18 (8) ◽  
pp. 1456-1469 ◽  
Author(s):  
Djordje M. Grbic ◽  
Émilie Degagné ◽  
Jean-François Larrivée ◽  
Maude S. Bilodeau ◽  
Valérie Vinette ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Mucosa ◽  
Neutrophil Recruitment ◽  
Dependent Manner ◽  
Cxc Chemokine ◽  
Chemokine Ligand ◽  
P2y6 Receptor

scholarly journals Intestinal Inflammation Increases the Expression of the P2Y6 Receptor on Epithelial Cells and the Release of CXC Chemokine Ligand 8 by UDP

2008 ◽  
Vol 180 (4) ◽  
pp. 2659-2668 ◽  
Author(s):  
Djordje M. Grbic ◽  
Émilie Degagné ◽  
Christine Langlois ◽  
Andrée-Anne Dupuis ◽  
Fernand-Pierre Gendron
Keyword(s):  
Epithelial Cells ◽  
Intestinal Inflammation ◽  
Cxc Chemokine ◽  
Chemokine Ligand ◽  
P2y6 Receptor

Endothelin-1 induces neutrophil recruitment in adaptive inflammation via TNFα and CXCL1/CXCR2 in mice

2012 ◽  
Vol 90 (2) ◽  
pp. 187-199 ◽  
Author(s):  
Ana C. Zarpelon ◽  
Larissa G. Pinto ◽  
Thiago M. Cunha ◽  
Silvio M. Vieira ◽  
Vanessa Carregaro ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Peritoneal Cavity ◽  
Neutrophil Migration ◽  
Neutrophil Recruitment ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dependent Manner ◽  
Endothelin 1 ◽  
Cxc Chemokine ◽  
Chemokine Ligand ◽  
Factor Α

Endothelin mediates neutrophil recruitment during innate inflammation. Herein we address whether endothelin-1 (ET-1) is involved in neutrophil recruitment in adaptive inflammation in mice, and its mechanisms. Pharmacological treatments were used to determine the role of endothelin in neutrophil recruitment to the peritoneal cavity of mice challenged with antigen (ovalbumin) or ET-1. Levels of ET-1, tumour necrosis factor α (TNFα), and CXC chemokine ligand 1 (CXCL1) were determined by enzyme-linked immunosorbent assay. Neutrophil migration and flow cytometry analyses were performed 4 h after the intraperitoneal stimulus. ET-1 induced dose-dependent neutrophil recruitment to the peritoneal cavity. Treatment with the non-selective ETA/ETB receptor antagonist bosentan, and selective ETA or ETB receptor antagonists BQ-123 or BQ-788, respectively, inhibited ET-1- and ovalbumin-induced neutrophil migration to the peritoneal cavity. In agreement with the above, the antigen challenge significantly increased levels of ET-1 in peritoneal exudates. The ET-1- and ovalbumin-induced neutrophil recruitment were reduced in TNFR1 deficient mice, and by treatments targeting CXCL1 or CXC chemokine receptor 2 (CXCR2); further, treatment with bosentan, BQ-123, or BQ-788 inhibited ET-1- and antigen-induced production of TNFα and CXCL1. Furthermore, ET-1 and ovalbumin challenge induced an increase in the number of cells expressing the Gr1+ markers in the granulocyte gate, CD11c+ markers in the monocyte gate, and CD4+ and CD45+ (B220) markers in the lymphocyte gate in an ETA- and ETB-dependent manner, as determined by flow cytometry analysis, suggesting that ET-1 might be involved in the recruitment of neutrophils and other cells in adaptive inflammation. Therefore, the present study demonstrates that ET-1 is an important mediator for neutrophil recruitment in adaptive inflammation via TNFα and CXCL1/CXCR2-dependent mechanism.

scholarly journals Interleukin-1β Regulates CXCL8 Release and Influences Disease Outcome in Response to Streptococcus pneumoniae, Defining Intercellular Cooperation between Pulmonary Epithelial Cells and Macrophages

2011 ◽  
Vol 80 (3) ◽  
pp. 1140-1149 ◽  
Author(s):  
Helen M. Marriott ◽  
Kate A. Gascoyne ◽  
Ravi Gowda ◽  
Ian Geary ◽  
Martin J. H. Nicklin ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Epithelial Cells ◽  
Cell Line ◽  
A549 Cells ◽  
Neutrophil Recruitment ◽  
Molecular Networks ◽  
Cellular Interactions ◽  
Chemokine Expression ◽  
Tnf Α ◽  
Cxc Chemokine

The success ofStreptococcus pneumoniae(the pneumococcus) as a pulmonary pathogen is related to its restriction of innate immune responses by respiratory epithelial cells. The mechanisms used to overcome this restriction are incompletely elucidated. Pulmonary chemokine expression involves complex cellular and molecular networks, involving the pulmonary epithelium, but the specific cellular interactions and the cytokines that control them are incompletely defined. We show that serotype 2 or 4 pneumococci induce only modest levels of CXCL8 expression from epithelial cell lines, even in the absence of a polysaccharide capsule. In contrast, coculture of A549 cells with the macrophage-like THP-1 cell line, differentiated with vitamin D, or monocyte-derived macrophages enhanced CXCL8 release. Supernatants from the THP-1 cell line prime A549 cells to release CXCL8 at levels similar to cocultures. Interleukin-1Ra (IL-1Ra) inhibits CXCL8 release from cocultures and reduces the activity of macrophage-conditioned media, but inhibition of tumor necrosis factor alpha (TNF-α) had only a minimal effect on CXCL8 release. Release of IL-1β but not TNF-α was upregulated in cocultures. IL-1 type 1 receptor knockout C57BL/6 and BALB/c mice confirmed the importance of IL-1 signaling in CXC chemokine expression and neutrophil recruitmentin vivo. In fulminant disease, increased IL-1 signaling resulted in increased neutrophils in the airway and more invasive disease. These results demonstrate that IL-1 is an important component of the cellular network involving macrophages and epithelial cells, which facilitates CXC chemokine expression and aids neutrophil recruitment during pneumococcal pneumonia. They also highlight a potential clinical role for anti-IL-1 treatment to limit excessive neutrophilic inflammation in the lung.

scholarly journals Induction of Interleukin-8 from Nasal Epithelial Cells during Bacterial Infection: The Role of IL-8 for Neutrophil Recruitment in Chronic Rhinosinusitis

2010 ◽  
Vol 2010 ◽  
pp. 1-7 ◽  
Author(s):  
Bit-Na Yoon ◽  
Nan-Geum Choi ◽  
Hyun-Sun Lee ◽  
Kyu-Sup Cho ◽  
Hwan-Jung Roh
Keyword(s):  
Endothelial Cells ◽  
Epithelial Cells ◽  
Vascular Endothelial Cells ◽  
Flow Cytometric Analysis ◽  
Neutrophil Recruitment ◽  
Dependent Manner ◽  
Vascular Endothelial ◽  
Flow Cytometric ◽  
Major Factors

Objectives. The aim of this study was to elucidate the role of IL-8 for neutrophil recruitment in nonallergic CRS patients.Methods. After coculture ofStreptococcus pneumoniae(SP) with the mucosal epithelial cells (MECs) from non-CRS patients, at three different SP/MEC (1/1, 10/1, 100/1) ratios, the expression of IL-8 mRNA and the concentration of IL-8 were measured by RT-PCR and ELISA. The expression of CD11b/CD18 on neutrophils and E-selectin/ICAM-1 on endothelial cells and the adherence between neutrophils and human umbilical vascular endothelial cells (HUVECs) were determined by flow cytometric analysis, ELISA, and RIA, respectively.Results. IL-8 concentration and IL-8 mRNA expression continued to increase from 3 hours after incubation in SP number-dependent manner. The expression of CD11b/CD18 on neutrophils and E-selectin/ICAM-1 on HUVECs, and the adherence between neutrophils and HUVECs were significantly increased in 10 SP/MEC-CM, and the increments were significantly blocked by anti-IL-8 antibody.Conclusion. MEC and IL-8 are major factors for neutrophil recruitment in nonallergic CRS.

scholarly journals Cigarette Smoke Stimulates SARS-CoV-2 Internalization by Activating AhR and Increasing ACE2 Expression in Human Gingival Epithelial Cells

2021 ◽  
Vol 22 (14) ◽  
pp. 7669
Author(s):  
Cassio Luiz Coutinho Almeida-da-Silva ◽  
Harmony Matshik Dakafay ◽  
Kaitlyn Liu ◽  
David M. Ojcius
Keyword(s):  
Epithelial Cells ◽  
Oral Cavity ◽  
Cigarette Smoke ◽  
Large Body ◽  
Receptor Expression ◽  
Host Cells ◽  
Dependent Manner ◽  
Gingival Epithelial Cells ◽  
Human Gingival Epithelial Cells ◽  
Oral Cells

A large body of evidence shows the harmful effects of cigarette smoke to oral and systemic health. More recently, a link between smoking and susceptibility to coronavirus disease 2019 (COVID-19) was proposed. COVID-19 is due to infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which uses the receptor ACE2 and the protease TMPRSS2 for entry into host cells, thereby infecting cells of the respiratory tract and the oral cavity. Here, we examined the effects of cigarette smoke on the expression of SARS-CoV-2 receptors and infection in human gingival epithelial cells (GECs). We found that cigarette smoke condensates (CSC) upregulated ACE2 and TMPRSS2 expression in GECs, and that CSC activated aryl hydrocarbon receptor (AhR) signaling in the oral cells. ACE2 was known to mediate SARS-CoV-2 internalization, and we demonstrate that CSC treatment potentiated the internalization of SARS-CoV-2 pseudovirus in GECs in an AhR-dependent manner. AhR depletion using small interference RNA decreased SARS-CoV-2 pseudovirus internalization in CSC-treated GECs compared with control GECs. Our study reveals that cigarette smoke upregulates SARS-CoV-2 receptor expression and infection in oral cells. Understanding the mechanisms involved in SARS-CoV-2 infection in cells of the oral cavity may suggest therapeutic interventions for preventing viral infection and transmission.

scholarly journals Enterococcus faecium PNC01 isolated from the intestinal mucosa of chicken as an alternative for antibiotics to reduce feed conversion rate in broiler chickens

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Yang He ◽  
Xuan Liu ◽  
Yuanyang Dong ◽  
Jiaqi Lei ◽  
Koichi Ito ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Mucosa ◽  
Conversion Rate ◽  
Broiler Chickens ◽  
Intestinal Epithelial Cells ◽  
Relative Length ◽  
Intestinal Epithelial ◽  
Feed Conversion ◽  
Broiler Production ◽  
Feed Conversion Rate

Abstract Background The development and utilization of probiotics had many environmental benefits for replacing antibiotics in animal production. Bacteria in the intestinal mucosa have better adhesion to the host intestinal epithelial cells compared to bacteria in the intestinal contents. In this study, lactic acid bacteria were isolated from the intestinal mucosa of broiler chickens and investigated as the substitution to antibiotic in broiler production. Results In addition to acid resistance, high temperature resistance, antimicrobial sensitivity tests, and intestinal epithelial cell adhesion, Enterococcus faecium PNC01 (E. faecium PNC01) was showed to be non-cytotoxic to epithelial cells. Draft genome sequence of E. faecium PNC01 predicted that it synthesized bacteriocin to perform probiotic functions and bacteriocin activity assay showed it inhibited Salmonella typhimurium from invading intestinal epithelial cells. Diet supplemented with E. faecium PNC01 increased the ileal villus height and crypt depth in broiler chickens, reduced the relative length of the cecum at day 21, and reduced the relative length of jejunum and ileum at day 42. Diet supplemented with E. faecium PNC01 increased the relative abundance of Firmicutes and Lactobacillus, decreased the relative abundance of Bacteroides in the cecal microbiota. Conclusion E. faecium PNC01 replaced antibiotics to reduce the feed conversion rate. Furthermore, E. faecium PNC01 improved intestinal morphology and altered the composition of microbiota in the cecum to reduce feed conversion rate. Thus, it can be used as an alternative for antibiotics in broiler production to avoid the adverse impact of antibiotics by altering the gut microbiota. Graphic Abstract

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