Cystic Fibrosis Pathogens Activate Ca2+-dependent Mitogen-activated Protein Kinase Signaling Pathways in Airway Epithelial Cells

Ratner, Adam J.; Bryan, Ruth; Weber, Adam J.; Nguyen, Stephen; Barnes, Derrick; Pitt, Allyson; Gelber, Shari E.; Cheung, Ambrose L.; Prince, Alice

doi:10.1074/jbc.m007703200

Cited by 157 publications

(169 citation statements)

References 37 publications

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“…Pseudomonas aeruginosa rapidly and transiently activates ERK in human cells via contact-dependent ligation of host cell asialo-GM1 receptors and intracellular calcium transients (75); whether a similar mechanism applies to H. pylori remains to be determined. A second, delayed ERK activation peak was induced only by cagA ϩ H. pylori strains, and greatly increased in the presence of the CagA tyrosine phosphorylation site, indicating that contact with the cagI-encoded structures is necessary, and that CagA phosphorylation is required for the maximal effect.…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori Stimulates Gastric Epithelial Cell MMP-1 Secretion via CagA-dependent and -independent ERK Activation

Pillinger

Marjanović

Kim

et al. 2007

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 99%

Helicobacter pylori Stimulates Gastric Epithelial Cell MMP-1 Secretion via CagA-dependent and -independent ERK Activation

Pillinger

Marjanović

Kim

et al. 2007

Journal of Biological Chemistry

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“…91 These Ca 2þ fluxes are sufficient to activate NF-kB and generate IL-8 and GM-CSF expression. 58,92 Several other Ca 2þ dependent transcription factors are also activated by bacterial ligands leading to local cytokine expression and mucin production. 81 Peptidoglycan activates the leucine zipper containing transcription factors cAMP-responsive element binding protein (CREB)/ATF and AP-1.…”

Section: Signaling Pathways Involved In Chemokine and Cytokine Producmentioning

confidence: 99%

Airway epithelial cell signaling in response to bacterial pathogens

Gómez

Prince

2007

Pediatric Pulmonology

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Summary. The airway epithelium represents a primary site for the introduction and deposition of potentially pathogenic microorganisms into the body, through inspired air. The epithelial mucosa is an important component of the innate immune system that recognizes conserved structures in microorganisms and initiates appropriate signaling to recruit and activate phagocytic cells to the airways. This review focuses on how airway epithelial cells sense and respond to the presence of bacterial pathogens. The major signaling cascades initiated by epithelial receptors that lead to phagocyte recruitment to the airways as well as the ability of the epithelium to regulate inflammation are discussed.

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“…Stringaris et al (14) reported activation of p38 MAPK and calciumdependent cell death in neuroblastoma cells treated with purified Ply and speculated on its relevance to the pathogenesis of pneumococcal meningitis. Likewise, S. aureus activation of host p38 MAPK has been recognized but not attributed to the pore-forming nature of its ␣-hemolysin (15). S. pyogenes has been reported to activate osteoblasts and keratinocytes via p38 MAPK, but the importance of streptolysin O (SLO) in these systems is not addressed (16,17).…”

Section: Pft Are Necessary and Sufficient For Activation Of P38 Mapk-mentioning

confidence: 99%

Epithelial Cells Are Sensitive Detectors of Bacterial Pore-forming Toxins

Ratner

Hippe

Aguilar

et al. 2006

Journal of Biological Chemistry

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Epithelial cells act as an interface between human mucosal surfaces and the surrounding environment. As a result, they are responsible for the initiation of local immune responses, which may be crucial for prevention of invasive infection. Here we show that epithelial cells detect the presence of bacterial pore-forming toxins (including pneumolysin from Streptococcus pneumoniae, ␣-hemolysin from Staphylococcus aureus, streptolysin O from Streptococcus pyogenes, and anthrolysin O from Bacillus anthracis) at nanomolar concentrations, far below those required to cause cytolysis. Phosphorylation of p38 MAPK appears to be a conserved response of epithelial cells to subcytolytic concentrations of bacterial poreforming toxins, and this activity is inhibited by the addition of high molecular weight osmolytes to the extracellular medium. By sensing osmotic stress caused by the insertion of a sublethal number of pores into their membranes, epithelial cells may act as an early warning system to commence an immune response, while the local density of toxin-producing bacteria remains low. Osmosensing may thus represent a novel innate immune response to a common bacterial virulence strategy.

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Cystic Fibrosis Pathogens Activate Ca2+-dependent Mitogen-activated Protein Kinase Signaling Pathways in Airway Epithelial Cells

Cited by 157 publications

References 37 publications

Helicobacter pylori Stimulates Gastric Epithelial Cell MMP-1 Secretion via CagA-dependent and -independent ERK Activation

Helicobacter pylori Stimulates Gastric Epithelial Cell MMP-1 Secretion via CagA-dependent and -independent ERK Activation

Airway epithelial cell signaling in response to bacterial pathogens

Epithelial Cells Are Sensitive Detectors of Bacterial Pore-forming Toxins

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