Interleukin-8 expression by mammary gland endothelial and epithelial cells following experimental mastitis infection with E. coli

2006 ◽  
Vol 29 (2-3) ◽  
pp. 127-137 ◽  
Author(s):  
David McClenahan ◽  
Rebecca Krueger ◽  
Haa-Yung Lee ◽  
Chet Thomas ◽  
Marcus E. Kehrli ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Epithelial Cells ◽  
Interleukin 8 ◽  
E Coli

scholarly journals Staphylococcus aureus Phenol-Soluble Modulins Impair Interleukin Expression in Bovine Mammary Epithelial Cells

2016 ◽  
Vol 84 (6) ◽  
pp. 1682-1692 ◽  
Author(s):  
Martine Deplanche ◽  
Ludmila Alekseeva ◽  
Ksenia Semenovskaya ◽  
Chih-Lung Fu ◽  
Frederic Dessauge ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Mammary Gland ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Dendritic Cell Maturation ◽  
Mammary Epithelial ◽  
Content Type ◽  
Bovine Mammary Epithelial Cells ◽  
E Coli ◽  
Infected Cells

The role of the recently described interleukin-32 (IL-32) inStaphylococcus aureus-induced mastitis, an inflammation of the mammary gland, is unclear. We determined expression of IL-32, IL-6, and IL-8 inS. aureus- andEscherichia coli-infected bovine mammary gland epithelial cells. Using live bacteria, we found that inS. aureus-infected cells, induction of IL-6 and IL-8 expression was less pronounced than inE. coli-infected cells. Notably, IL-32 expression was decreased inS. aureus-infected cells, while it was increased inE. coli-infected cells. We identified the staphylococcal phenol-soluble modulin (PSM) peptides as key contributors to these effects, as IL-32, IL-6, and IL-8 expression by epithelial cells exposed topsmmutant strains was significantly increased compared to that in cells exposed to the isogenicS. aureuswild-type strain, indicating that PSMs inhibit the production of these interleukins. The use of genetically complemented strains confirmed this observation. Inasmuch as the decreased expression of IL-32, which is involved in dendritic cell maturation, impairs immune responses, our results support a PSM-dependent mechanism that allows for the development of chronicS. aureus-related mastitis.

Production of interleukin-6 and interleukin-8 by human mammary gland epithelial cells

1994 ◽  
Vol 26 (1) ◽  
pp. 57-64 ◽  
Author(s):  
Kimberly H. Palkowetz ◽  
Cassandre L. Royer ◽  
Roberto Garofalo ◽  
Helen E. Rudloff ◽  
Frank C. Schmalstieg ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Epithelial Cells ◽  
Interleukin 6 ◽  
Interleukin 8 ◽  
Human Mammary Gland ◽  
Mammary Gland Epithelial Cells

scholarly journals Flagellin of Enteropathogenic Escherichia coli Stimulates Interleukin-8 Production in T84 Cells

2003 ◽  
Vol 71 (4) ◽  
pp. 2120-2129 ◽  
Author(s):  
Xin Zhou ◽  
Jorge A. Girón ◽  
Alfredo G. Torres ◽  
J. Adam Crawford ◽  
Erasmo Negrete ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Luria Bertani ◽  
Interleukin 8 ◽  
Epec Strain ◽  
T84 Cells ◽  
E Coli ◽  
Luria Bertani Broth ◽  
Mitogen Activated Protein ◽  
K 12

ABSTRACT The type III secretion system (TTSS) of enteropathogenic Escherichia coli (EPEC) has been associated with the ability of these bacteria to induce secretion of proinflammatory cytokines, including interleukin-8 (IL-8), in cultured epithelial cells. However, the identity of the effector molecule directly involved in this event is unknown. In this study, we determined that the native flagellar filament and its flagellin monomer are activators of IL-8 release in T84 epithelial cells. Supernatants of wild-type EPEC strain E2348/69 and its isogenic mutants deficient in TTSS (escN) and in production of intimin (eae), grown in Luria-Bertani broth, elicited similar amounts of IL-8 secretion by T84 cells. In contrast, supernatants of EPEC fliC mutants and of B171, a nonflagellated EPEC strain, were defective in inducing IL-8 release, a phenotype that was largely restored by complementation of the fliC gene in the mutant lacking flagella. Purified flagella from E. coli K-12, EPEC serotypes H6 and H34, and enterohemorrhagic E. coli serotype H7 all induced IL-8 release in T84 cells. Induction of IL-8 by purified flagella or His-tagged FliC from EPEC strain E2348/69 was dose dependent and was blocked by a polyclonal anti-H6 antibody. Finally, the mitogen-activated protein kinases (Erk1 and -2 and Jnk) were phosphorylated in flagellin-treated T84 cells, and inhibition of the p38 and Erk pathways significantly decreased the IL-8 response induced by EPEC flagellin. Our data clearly indicate that FliC of EPEC is sufficient to induce IL-8 release in T84 cells and that activation of the Erk and p38 pathways is required for IL-8 induction.

scholarly journals Interleukin-8, CXCL1, and MicroRNA miR-146a Responses to Probiotic Escherichia coli Nissle 1917 and Enteropathogenic E. coli in Human Intestinal Epithelial T84 and Monocytic THP-1 Cells after Apical or Basolateral Infection

2016 ◽  
Vol 84 (9) ◽  
pp. 2482-2492 ◽  
Author(s):  
Harshana Sabharwal ◽  
Christoph Cichon ◽  
Tobias A. Ölschläger ◽  
Ulrich Sonnenborn ◽  
M. Alexander Schmidt
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Pathogenic Bacteria ◽  
Interleukin 8 ◽  
Model Systems ◽  
Probiotic Properties ◽  
Content Type ◽  
E Coli ◽  
Apical Side ◽  
Basolateral Side

Bacterium-host interactions in the gut proceed via directly contacted epithelial cells, the host's immune system, and a plethora of bacterial factors. Here we characterized and compared exemplary cytokine and microRNA (miRNA) responses of human epithelial and THP-1 cells toward the prototype enteropathogenicEscherichia coli(EPEC) strain E2348/69 (O127:H6) and the probiotic strainEscherichia coliNissle 1917 (EcN) (O6:K5:H1). Human T84 and THP-1 cells were used as cell culture-based model systems for epithelial and monocytic cells. Polarized T84 monolayers were infected apically or basolaterally. Bacterial challenges from the basolateral side resulted in more pronounced cytokine and miRNA responses than those observed for apical side infections. Interestingly, the probiotic EcN also caused a pronounced transcriptional increase of proinflammatory CXCL1 and interleukin-8 (IL-8) levels when human T84 epithelial cells were infected from the basolateral side. miR-146a, which is known to regulate adaptor molecules in Toll-like receptor (TLR)/NF-κB signaling, was found to be differentially regulated in THP-1 cells between probiotic and pathogenic bacteria. To assess the roles of flagella and flagellin, we employed several flagellin mutants of EcN. EcN flagellin mutants induced reduced IL-8 as well as CXCL1 responses in T84 cells, suggesting that flagellin is an inducer of this cytokine response. Following infection with an EPEC type 3 secretion system (T3SS) mutant, we observed increased IL-8 and CXCL1 transcription in T84 and THP-1 cells compared to that in wild-type EPEC. This study emphasizes the differential induction of miR-146a by pathogenic and probioticE. colistrains in epithelial and immune cells as well as a loss of probiotic properties in EcN interacting with cells from the basolateral side.

N-acetyl- L-cysteine inhibits bleomycin-induced interleukin-8 secretion by bronchial epithelial cells

Respirology ◽  
2000 ◽  
Vol 5 (4) ◽  
pp. 309-313 ◽  
Author(s):  
Yasuhiro Gon ◽  
Shu Hashimoto ◽  
Tomoko Nakayama ◽  
Ken Matsumoto ◽  
Toshiya Koura ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Interleukin 8 ◽  
Bronchial Epithelial

scholarly journals Mammary gland adipocytes in lactation cycle, obesity and breast cancer

2021 ◽  
Author(s):  
Georgia Colleluori ◽  
Jessica Perugini ◽  
Giorgio Barbatelli ◽  
Saverio Cinti
Keyword(s):  
Breast Cancer ◽  
Mammary Gland ◽  
Epithelial Cells ◽  
Close Association ◽  
Critical Role ◽  
Exocrine Gland ◽  
Plastic Properties ◽  
Lactation Cycle ◽  
Gland Development

AbstractThe mammary gland (MG) is an exocrine gland present in female mammals responsible for the production and secretion of milk during the process of lactation. It is mainly composed by epithelial cells and adipocytes. Among the features that make the MG unique there are 1) its highly plastic properties displayed during pregnancy, lactation and involution (all steps belonging to the lactation cycle) and 2) its requirement to grow in close association with adipocytes which are absolutely necessary to ensure MG’s proper development at puberty and remodeling during the lactation cycle. Although MG adipocytes play such a critical role for the gland development, most of the studies have focused on its epithelial component only, leaving the role of the neighboring adipocytes largely unexplored. In this review we aim to describe evidences regarding MG’s adipocytes role and properties in physiologic conditions (gland development and lactation cycle), obesity and breast cancer, emphasizing the existing gaps in the literature which deserve further investigation.

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