scholarly journals MUC1 expression by human airway epithelial cells mediates pseudomonas aeruginosa adhesion

10.2741/e67 ◽  
2010 ◽  
Vol E2 (1) ◽  
pp. 68-77 ◽  
Author(s):  
Kwang Chul Kim
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Muc1 Expression ◽  
Airway Epithelial ◽  
Human Airway ◽  
Human Airway Epithelial Cells

scholarly journals Flagellin From Pseudomonas Aeruginosa Stimulates ATB0,+ Transporter for Arginine and Neutral Amino Acids in Human Airway Epithelial Cells

2021 ◽  
Vol 12 ◽  
Author(s):  
Amelia Barilli ◽  
Rossana Visigalli ◽  
Francesca Ferrari ◽  
Giuseppe Borsani ◽  
Valeria Dall'Asta ◽  
...  
Keyword(s):  
Amino Acids ◽  
Pseudomonas Aeruginosa ◽  
Epithelial Cells ◽  
Cellular Responses ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Bronchial Epithelial ◽  
Human Airway ◽  
Expression And Activity ◽  
Human Airway Epithelial Cells

At present, the central role played by arginine in the modulation of the inflammatory cellular responses is well-recognized, and many pro-inflammatory stimuli are known to modulate the expression and activity of its transmembrane transporters. In this regard, we have addressed the effects of bacterial flagellin from Pseudomonas aeruginosa (FLA-PA) on the uptake of the amino acid in human epithelial respiratory cells. Among the arginine transporters, only ATB0,+, y+L, and y+ were operative in bronchial epithelial Calu-3 cells under control conditions; however, only the expression and activity of ATB0,+ were stimulated upon incubation with flagellin, whereas those of systems y+L and y+ were not stimulated. As a result, this induction, in turn, led to an increase in the intracellular content of arginine without making any change to its metabolic pathway. In addition, flagellin upregulated the amount of other amino acids substrates of ATB0,+, in particular, all the essential amino acids, such as valine, isoleucine, and leucine, along with the non-essential glutamine. At the molecular level, these effects were directly referable to the stimulation of a toll-like receptor-5 (TLR5) signaling pathway and to the induction of nuclear factor-κB (NF-κB) transcription factor. An induction of ATB0,+ expression has been observed also in EpiAirway™, a model of primary human normal tracheal-bronchial epithelial cells that mimics the in vitro pseudostratified columnar epithelium of the airways. In this tissue model, the incubation with flagellin is associated with the upregulation of messenger RNAs (mRNAs) for the chemokine IL-8 and for the cytokines IL-6 and interleukin-1β (IL-1β); as for the latter, a marked secretion in the extracellular medium was also observed due to the concomitant activation of caspase-1. The overall findings indicate that, in human respiratory epithelium, flagellin promotes cellular responses associating the increase of intracellular amino acids through ATB0,+ with the activation of the inflammasome. Given the role of the ATB0,+ transporter as a delivery system for bronchodilators in human airway epithelial cells, its induction under inflammatory conditions gains particular relevance in the field of respiratory pharmacology.

scholarly journals Transcriptome Analysis of Pseudomonas aeruginosa after Interaction with Human Airway Epithelial Cells

2004 ◽  
Vol 72 (9) ◽  
pp. 5433-5438 ◽  
Author(s):  
Anders Frisk ◽  
Jill R. Schurr ◽  
Guoshun Wang ◽  
Donna C. Bertucci ◽  
Luis Marrero ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pseudomonas Aeruginosa ◽  
Epithelial Cells ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Human Airway ◽  
Normal Human ◽  
Human Airway Epithelial Cells

ABSTRACT The transcriptional profile of Pseudomonas aeruginosa after interactions with primary normal human airway epithelial cells was determined using Affymetrix GeneChip technology. Gene expression profiles indicated that various genes involved in phosphate acquisition and iron scavenging were differentially regulated.

scholarly journals Human Airway Epithelial Cells Sense Pseudomonas aeruginosa Infection via Recognition of Flagellin by Toll-Like Receptor 5

2005 ◽  
Vol 73 (11) ◽  
pp. 7151-7160 ◽  
Author(s):  
Zhe Zhang ◽  
Jean-Pierre Louboutin ◽  
Daniel J. Weiner ◽  
Joanna B. Goldberg ◽  
James M. Wilson
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Epithelial Cells ◽  
Inflammatory Responses ◽  
Airway Epithelial Cells ◽  
Respiratory Pathogen ◽  
Luciferase Reporter ◽  
Apical Surface ◽  
Airway Epithelial ◽  
Human Airway ◽  
Human Airway Epithelial Cells

ABSTRACT Pseudomonas aeruginosa, an opportunistic respiratory pathogen that infects the majority of patients with cystic fibrosis, initiates host inflammatory responses through interaction with airway epithelial cells. The Toll-like receptors (TLRs) are a family of pathogen pattern recognition receptors that play key roles in host innate immunity. In this study we aimed to determine whether TLRs mediate the interaction between P. aeruginosa and airway epithelial cells. Individual murine TLRs (TLR1 to TLR9) and dual combinations of these TLRs that activate an NF-κB-driven luciferase reporter in response to PAO1 were screened in HEK 293 cells. TLR5, TLR2, a combination of TLR1 and TLR2, or a combination of TLR2 and TLR6 responded to PAO1. Another P. aeruginosa strain, strain PAK, activated TLR5 similarly, while the isogenic flagellin-deficient strain PAK/fliC and the flagellum-free bacterium Haemophilus influenzae failed to activate TLR5. Reverse transcription-PCR was used to probe the presence of multiple TLRs (including TLR5) in primary human airway epithelial cells (HAECs). Immunostaining with TLR5 antibodies showed that TLR5 was expressed in HAECs and on the apical surface of the human trachea epithelium. In HAECs, PAO1, PAK, and Burkholderia cepacia, but not flagellin-deficient strain PAK/fliC or a B. cepacia fliC mutant, activated the NF-κB reporter. Dominant negative TLR5 specifically blocked the response to P. aeruginosa but not to the response to lipoteichoic acid, a specific ligand of TLR2. We also determined that MyD88, IRAK, TRAF6, and Toll-interacting protein (Tollip), but not TIRAP, were involved in the TLR-mediated response to P. aeruginosa in HAECs. These findings demonstrate that the airway epithelial receptor TLR5 senses P. aeruginosa through its flagellin protein, which may have an important role in the initiation of the host inflammatory reaction to clear the invading pathogen.

scholarly journals Pseudomonas aeruginosa Inhibition of Flagellin-Activated NF-κB and Interleukin-8 by Human Airway Epithelial Cells

2009 ◽  
Vol 77 (7) ◽  
pp. 2857-2865 ◽  
Author(s):  
Jose Pena ◽  
Zhu Fu ◽  
Christian Schwarzer ◽  
Terry E. Machen
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Epithelial Cells ◽  
Conditioned Medium ◽  
Primary Cultures ◽  
Airway Epithelial Cells ◽  
Interleukin 8 ◽  
Airway Epithelial ◽  
Human Airway ◽  
Basolateral Side ◽  
Human Airway Epithelial Cells

ABSTRACT Pseudomonas aeruginosa-induced activation of NF-κB and secretion of proinflammatory cytokines by airway epithelial cells require that the bacteria express flagellin. We tested whether P. aeruginosa and human airway epithelial cells secrete factors that modulated this response. Experiments were performed with both the Calu-3 cell line and primary cultures of tracheal epithelial cells. P. aeruginosa strain PAK ΔfliC (flagellin knockout) did not activate NF-κB or interleukin-8 (IL-8) but inhibited flagellin-activated NF-κB by 40 to 50% and IL-8 secretion by 20 to 25%. PAK ΔfliC also inhibited NF-κB induced by IL-1β and Toll-like receptor 2 agonist Pam3CSK4. Similar inhibitions were observed with strains PAK, PAO1, and PA14. The inhibitory factor was present in conditioned medium isolated from PAK ΔfliC or Calu-3 plus PAK ΔfliC, but it was not present in conditioned medium isolated from Calu-3 cells alone or from PAK ΔfliC that had been heat treated. Inhibition by PAK ΔfliC-conditioned medium was exerted from either the apical or the basolateral side of the epithelium, was enhanced in simple Ringer's solution over that in tissue culture medium, and did not result from altered pH or depletion of glucose. The inhibitory effect of conditioned medium was abolished by boiling and appeared from filtration studies to result from effects of a factor with a molecular mass of <3 kDa. These and further studies with isogenic mutants led to the conclusion that the NF-κB and IL-8 response of airway epithelial cells to P. aeruginosa results from a balance of proinflammatory effects of flagellin and antiinflammatory effects of a small (<3-kDa), heat-sensitive factor(s) that is not lipopolysaccharide, C12 homoserine lactone, alginate, CIF, or exotoxin A, S, T, U, or Y.

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