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Article: Non-dysbaric arterial gas embolism associated with chronic necrotizing pneumonia, bullae and coughing: a case report.

Ceponis, Peter J / Fox, William / Tailor, Tina D / Hurwitz, Lynne M / Amrhein, Timothy J / Moon, Richard E

Undersea & hyperbaric medicine : journal of the Undersea and Hyperbaric Medical Society, Inc

2017 Volume 44, Issue 1, Page(s) 73–77

Abstract: Arterial gas embolism (AGE) can be clinically devastating, and is most often associated with exposure to changes in ambient pressure, medical procedure or congenital malformation. Here we report a case of AGE in a 78-year-old male without these ... ...

Abstract	Arterial gas embolism (AGE) can be clinically devastating, and is most often associated with exposure to changes in ambient pressure, medical procedure or congenital malformation. Here we report a case of AGE in a 78-year-old male without these traditional risk factors. Rather, the patient's history included chronic obstructive pulmonary disease, necrotizing pneumonia, bullous disease and coughing. He was safely treated with hyperbaric oxygen (HBO₂) therapy for AGE, with initial clinical improvement, but ultimately died from his underlying condition. Pathophysiology is discussed. This case illustrates the possibility that AGE can occur due to rupture of lung tissue in the absence of traditional risk factors. HBO₂ therapy should be considered in the management of such patients.
MeSH term(s)	Aged ; Blister/complications ; Chronic Disease ; Cough/complications ; Embolism, Air/diagnostic imaging ; Embolism, Air/etiology ; Embolism, Air/therapy ; Fatal Outcome ; Humans ; Hyperbaric Oxygenation ; Male ; Pneumonia, Necrotizing/complications ; Pneumonia, Necrotizing/diagnostic imaging ; Pulmonary Disease, Chronic Obstructive/complications
Language	English
Publishing date	2017-08-02
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	1154414-4
ISSN	1066-2936
ISSN	1066-2936
DOI	10.22462/1.2.2017.16
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Zs.A 1069: Show issues

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Article: Defining mechanisms of interaction between enterohemorrhagic Escherichia coli O157:H7 and host epithelia.

Ceponis, Peter J / Sherman, Philip M

Journal of pediatric gastroenterology and nutrition

2004 Volume 38, Issue 2, Page(s) 230–231

MeSH term(s)	Bacterial Proteins/physiology ; Escherichia coli Infections/metabolism ; Escherichia coli Infections/microbiology ; Escherichia coli O157/pathogenicity ; Escherichia coli O157/physiology ; Gene Expression Regulation, Bacterial ; Humans ; Mutation ; Signal Transduction ; Virulence/genetics ; Virulence/physiology
Chemical Substances	Bacterial Proteins
Language	English
Publishing date	2004-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	603201-1
ISSN	1536-4801 ; 0277-2116
ISSN (online)	1536-4801
ISSN	0277-2116
DOI	10.1097/00005176-200402000-00027
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Zs.A 1728: Show issues

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Article: Epithelial cell signaling responses to enterohemorrhagic Escherichia coli infection.

Ceponis, Peter J M / Riff, Jason D / Sherman, Philip M

Memorias do Instituto Oswaldo Cruz

2005 Volume 100 Suppl 1, Page(s) 199–203

Abstract: Enterohemorrhagic Escherichia coli, including the serotype O157:H7 that is most commonly identified with human disease, cause both sporadic cases and outbreaks of non-bloody diarrhea and hemorrhagic colitis. In about 10% of infected subjects, the ... ...

Abstract	Enterohemorrhagic Escherichia coli, including the serotype O157:H7 that is most commonly identified with human disease, cause both sporadic cases and outbreaks of non-bloody diarrhea and hemorrhagic colitis. In about 10% of infected subjects, the hemolytic uremic syndrome (hemolytic anemic, thrombocytopenia, and acute renal failure) develops, likely as a consequence of systemic spread of bacterial-derived toxins variously referred to as Shiga-like toxin, Shiga toxin, and Verotoxin. Increasing evidence points to a complex interplay between bacterial products--for example, adhesins and toxins--and host signal transduction pathways in mediating responses to infection. Identification of critical signaling pathways could result in the development of novel strategies for intervention to both prevent and treat this microbial infection in humans.
MeSH term(s)	Animals ; Apoptosis/physiology ; Epithelial Cells/microbiology ; Epithelial Cells/physiology ; Escherichia coli Infections/microbiology ; Escherichia coli O157/pathogenicity ; Gastrointestinal Hemorrhage/microbiology ; Humans ; STAT1 Transcription Factor/metabolism ; Signal Transduction/physiology
Chemical Substances	STAT1 Transcription Factor ; STAT1 protein, human
Language	English
Publishing date	2005-06-14
Publishing country	Brazil
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	953293-6
ISSN	1678-8060 ; 0074-0276
ISSN (online)	1678-8060
ISSN	0074-0276
DOI	10.1590/s0074-02762005000900034
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Ud II Zs.33: Show issues

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Article: Modulation of host cell signal transduction pathways by Helicobacter pylori infection.

Ceponis, Peter J M / Jones, Nicola L

Canadian journal of gastroenterology = Journal canadien de gastroenterologie

2005 Volume 19, Issue 7, Page(s) 415–420

Abstract: Bacterial pathogens modulate host cell signal transduction responses to establish infection and cause disease. The purpose of the present summary, first presented at the Canadian Helicobacter Study Group meeting, is to discuss current knowledge of ... ...

Abstract	Bacterial pathogens modulate host cell signal transduction responses to establish infection and cause disease. The purpose of the present summary, first presented at the Canadian Helicobacter Study Group meeting, is to discuss current knowledge of specific Helicobacter pylori factors, including the vacuolating cytotoxin, cytotoxin-associated gene A and the type four secretion system encoded by the cytotoxin-associated gene pathogenicity island and review the host cell signal transduction cascades that they modulate.
MeSH term(s)	Antigens, Bacterial/genetics ; Bacterial Proteins/genetics ; Bacterial Proteins/physiology ; Bacterial Toxins/genetics ; Bacterial Toxins/pharmacology ; Carrier Proteins/genetics ; Carrier Proteins/physiology ; Cytotoxins/genetics ; Cytotoxins/physiology ; Helicobacter Infections/physiopathology ; Helicobacter pylori/genetics ; Helicobacter pylori/physiology ; Humans ; Signal Transduction/physiology
Chemical Substances	Antigens, Bacterial ; Bacterial Proteins ; Bacterial Toxins ; Carrier Proteins ; Cytotoxins ; VacA protein, Helicobacter pylori ; cagA protein, Helicobacter pylori
Language	English
Publishing date	2005-07-05
Publishing country	Canada
Document type	Journal Article ; Review
ZDB-ID	639439-5
ISSN	1916-7237 ; 0835-7900
ISSN (online)	1916-7237
ISSN	0835-7900
DOI	10.1155/2005/731817
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Zs.A 2360: Show issues

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Article: Helicobacter pylori induces apoptosis of macrophages in association with alterations in the mitochondrial pathway.

Menaker, Rena J / Ceponis, Peter J M / Jones, Nicola L

Infection and immunity

2004 Volume 72, Issue 5, Page(s) 2889–2898

Abstract: Helicobacter pylori is a gastric bacterial pathogen that evades host immune responses in vivo and is associated with the development of gastritis, peptic ulcer disease, and gastric cancers. Induction of macrophage apoptosis is a method employed by ... ...

Abstract	Helicobacter pylori is a gastric bacterial pathogen that evades host immune responses in vivo and is associated with the development of gastritis, peptic ulcer disease, and gastric cancers. Induction of macrophage apoptosis is a method employed by multiple pathogens to escape host immune responses. Therefore, we hypothesized that H. pylori induces apoptosis of infected macrophages. RAW 264.7 cells were infected with H. pylori strain 60190, and apoptosis was assessed. Transmission electron microscopy and fluorescence microscopy showed that infected macrophages displayed morphological features characteristic of apoptosis. Quantification by acridine orange-ethidium bromide fluorescent-dye staining showed that apoptosis was dose and time dependent, and apoptosis was further confirmed by increased binding of annexin V-fluorescein isothiocyanate (FITC) to externalized phosphatidylserine of infected but not of control macrophages. Macrophages infected with isogenic mutants of H. pylori strain 60190 deficient in either cagA or vacA induced significantly less apoptosis than the parental strain, as assessed by increased binding of annexin V-FITC. Western blot analysis of whole-cell protein lysates revealed that infection with strain 60190 induced a time-dependent increase in cleavage of procaspase 8 and disappearance of full-length Bid compared with uninfected cells. Furthermore, pharmacological inhibition of caspase 8 caused a decrease in levels of apoptosis. Finally, infection caused a time-dependent increase in mitochondrial-membrane permeability and release of cytochrome c into the cytosol. These results suggest that H. pylori induces apoptosis of macrophages in association with alterations in the mitochondrial pathway. Elimination of this key immunomodulatory cell may represent a mechanism employed by the bacterium to evade host immune responses.
MeSH term(s)	Animals ; Antigens, Bacterial/genetics ; Antigens, Bacterial/physiology ; Apoptosis ; BH3 Interacting Domain Death Agonist Protein ; Bacterial Proteins/genetics ; Bacterial Proteins/physiology ; Carrier Proteins/metabolism ; Caspase 8 ; Caspases/metabolism ; Cell Line ; Cytochromes c/metabolism ; Genes, Bacterial ; Helicobacter Infections/metabolism ; Helicobacter Infections/microbiology ; Helicobacter Infections/pathology ; Helicobacter pylori/genetics ; Helicobacter pylori/pathogenicity ; Helicobacter pylori/physiology ; Macrophages/cytology ; Macrophages/metabolism ; Macrophages/microbiology ; Mice ; Microscopy, Electron ; Mitochondria/metabolism ; Mutation ; Phosphatidylserines/metabolism
Chemical Substances	Antigens, Bacterial ; BH3 Interacting Domain Death Agonist Protein ; Bacterial Proteins ; Bid protein, mouse ; Carrier Proteins ; Phosphatidylserines ; VacA protein, Helicobacter pylori ; cagA protein, Helicobacter pylori ; Cytochromes c (9007-43-6) ; Casp8 protein, mouse (EC 3.4.22.-) ; Caspase 8 (EC 3.4.22.-) ; Caspases (EC 3.4.22.-)
Language	English
Publishing date	2004-02-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218698-6
ISSN	1098-5522 ; 0019-9567
ISSN (online)	1098-5522
ISSN	0019-9567
DOI	10.1128/IAI.72.5.2889-2898.2004
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Zs.A 684: Show issues

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Article: Cytoskeletal rearrangements in gastric epithelial cells in response to Helicobacter pylori infection.

Su, Bin / Ceponis, Peter J M / Sherman, Philip M

Journal of medical microbiology

2003 Volume 52, Issue Pt 10, Page(s) 861–867

Abstract: Helicobacter pylori causes host epithelial cell cytoskeletal rearrangements mediated by the translocation and tyrosine phosphorylation of an outer-membrane protein, CagA, and by the vacuolating cytotoxin, VacA. However, the mechanisms by which H. pylori ... ...

Abstract	Helicobacter pylori causes host epithelial cell cytoskeletal rearrangements mediated by the translocation and tyrosine phosphorylation of an outer-membrane protein, CagA, and by the vacuolating cytotoxin, VacA. However, the mechanisms by which H. pylori mediates cytoskeletal rearrangements in infected host cells need to be more clearly defined. The aim of this study was to determine the effects of H. pylori isolates from children on the architecture of host gastric epithelial cells. Gastric epithelial (AGS) cells were infected with type I (cagE(+), cagA(+), VacA(+)) H. pylori, a type II H. pylori strain (cagE(-), cagA(-), VacA(-)) or a cagE isogenic mutant. Double-labelled immune fluorescence was used to detect adherent H. pylori and the distribution of F-actin, alpha-actinin and Arp3. Both type I and type II H. pylori strains induced stress fibres in gastric epithelial cells that were not observed in uninfected cells. Type I H. pylori also induced cell elongation (hummingbird phenotype) after 4 h of infection, whereas the type II H. pylori strain did not. Less elongation occurred when AGS cells were exposed to a cagE isogenic mutant, compared with the parental strain. Confocal microscopy showed Arp3 accumulation in AGS cells infected with wild-type H. pylori, but not in response to infection with the cagE mutant. These findings indicate that type I H. pylori induce a stress fibre-like phenotype in infected gastric epithelia by a mechanism that is different from the induction of host-cell elongation. In addition to CagA and VacA, cagE also impacts on the morphology of infected gastric epithelial cells.
MeSH term(s)	Actin-Related Protein 3 ; Bacterial Adhesion/physiology ; Cell Line, Tumor ; Child ; Cytoskeletal Proteins/metabolism ; Cytoskeleton/metabolism ; Cytoskeleton/microbiology ; Cytoskeleton/pathology ; Duodenal Ulcer/metabolism ; Duodenal Ulcer/microbiology ; Duodenal Ulcer/pathology ; Epithelial Cells/metabolism ; Epithelial Cells/microbiology ; Epithelial Cells/pathology ; Gastric Mucosa/metabolism ; Gastric Mucosa/microbiology ; Gastric Mucosa/pathology ; Helicobacter Infections/metabolism ; Helicobacter Infections/pathology ; Helicobacter pylori/physiology ; Humans ; Microscopy, Confocal ; Microscopy, Fluorescence ; Nuclear Proteins/metabolism ; Virulence Factors/metabolism
Chemical Substances	ACTR3 protein, human ; Actin-Related Protein 3 ; Cytoskeletal Proteins ; Nuclear Proteins ; Virulence Factors
Language	English
Publishing date	2003-08-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218356-0
ISSN	1473-5644 ; 0022-2615
ISSN (online)	1473-5644
ISSN	0022-2615
DOI	10.1099/jmm.0.05229-0
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Zs.A 634: Show issues

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Article ; Online: A randomized pilot validation of educational measures in teaching shoulder arthroscopy to surgical residents.

Ceponis, Peter J M / Chan, Denise / Boorman, Richard S / Hutchison, Carol / Mohtadi, Nicholas G H

Canadian journal of surgery. Journal canadien de chirurgie

2007 Volume 50, Issue 5, Page(s) 387–393

Abstract: Background: Injuries to the shoulder joint commonly require the attention of an orthopedic surgeon. Shoulder arthroscopy plays an increasingly important role in the diagnosis and repair of shoulder pathology; however, the most effective manner in which ... ...

Abstract	Background: Injuries to the shoulder joint commonly require the attention of an orthopedic surgeon. Shoulder arthroscopy plays an increasingly important role in the diagnosis and repair of shoulder pathology; however, the most effective manner in which to teach orthopedic residents fundamental knowledge of diagnostic shoulder arthroscopy before entering the operating room is unclear. We aimed to compare the existing cadaver-based teaching of diagnostic shoulder arthroscopy knowledge with a method that combines model- and video-based teaching to orthopedic surgery residents in a randomized pilot trial. Methods: A composite (model/video teaching) method was designed, using prepared teaching videos and the commercially available ALEX shoulder arthroscopy model. First- and second-year orthopedic surgery residents from the University of Calgary were consented, surveyed for their arthroscopy experience and randomized to either cadaver or composite teaching. Subjects wrote a pretest before their teaching session and a posttest afterwards to assess their knowledge of diagnostic arthroscopy. The tests were multiple choice, containing text and pictorial-based questions. The posttest was modified to minimize recall bias. Subjects were also surveyed for their comments regarding the teaching sessions. Results: Nine of 10 subjects increased their test scores after the teaching sessions, with 4 of 5 in the cadaver-based and 5 of 5 in the composite groups. There were no differences between the teaching groups on their mean pre- or posttest scores. The composite group, but not the cadaver-based group, had a statistically significant increase in posttest scores. When the text- and pictorial-based question sections were analyzed separately, both groups significantly improved their mean text-based score, whereas only the composite group increased their mean pictorial-based questions score. Surveying the residents elicited positive comments regarding both manners of teaching. Conclusion: This pilot trial suggests that a composite teaching curriculum is at least as effective as a cadaver-based environment for teaching orthopedic surgery residents fundamental knowledge of diagnostic shoulder arthroscopy.
MeSH term(s)	Arm Injuries/diagnosis ; Arm Injuries/surgery ; Arthroscopy/methods ; Arthroscopy/standards ; Cadaver ; Canada ; Humans ; Internship and Residency/methods ; Orthopedics/education ; Orthopedics/methods ; Pilot Projects ; Shoulder Fractures/diagnosis ; Shoulder Fractures/surgery ; Shoulder Joint/injuries ; Shoulder Joint/surgery ; Teaching/standards
Language	English
Publishing date	2007-10-10
Publishing country	Canada
Document type	Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't ; Validation Study
ZDB-ID	410651-9
ISSN	1488-2310 ; 0008-428X
ISSN (online)	1488-2310
ISSN	0008-428X
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Zs.A 221: Show issues

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Article: Interleukin-4- and -13-induced hypercontractility of human intestinal muscle cells-implication for motility changes in Crohn's disease.

Akiho, Hirotada / Lovato, Paola / Deng, Yikang / Ceponis, Peter J M / Blennerhassett, Patricia / Collins, Stephen M

American journal of physiology. Gastrointestinal and liver physiology

2005 Volume 288, Issue 4, Page(s) G609–15

Abstract: Crohn's disease is an idiopathic inflammatory condition. However, little is known about the changes that occur in the muscularis externa, despite the fact that this tissue contributes to motility changes and stricture formation. We characterized immune ... ...

Abstract	Crohn's disease is an idiopathic inflammatory condition. However, little is known about the changes that occur in the muscularis externa, despite the fact that this tissue contributes to motility changes and stricture formation. We characterized immune activity in the muscularis externa from intestinal segments of Crohn's disease patients and evaluated the role of IL-4 and -13 as well as signal transducer and activator of transcription (STAT)6 in the contractility of the cultured human intestinal smooth muscle cells. CD3+ve cells (P < 0.01) and IL-4 protein (P < 0.01) were significantly increased in the muscularis externa of Crohn's disease patients compared with noninflamed controls. Preincubation of human cultured smooth muscle cells with IL-4 (P < 0.001) or IL-13 (P < 0.05) significantly enhanced carbachol-induced contraction, and this was significantly inhibited by the STAT6 inhibitor leflunomide (P < 0.0001). A similar profile was observed in muscle cells isolated from Crohn's disease patients. Both IL-4 and IL-13 increased specific STAT6-DNA binding in control cells, and this was inhibited by anti-STAT6 Ab (P < 0.05) or leflunomide (P < 0.05). IL-4 and IL-13 mediate the hypercontractility of intestinal muscle via a STAT6 pathway at the level of the smooth muscle cell. The STAT6 pathway may contribute to the hypercontractility of intestinal muscle in Crohn's disease.
MeSH term(s)	Adult ; CD3 Complex/metabolism ; Carbachol/pharmacology ; Case-Control Studies ; Cells, Cultured ; Crohn Disease/immunology ; Crohn Disease/pathology ; Crohn Disease/physiopathology ; DNA/metabolism ; Female ; Gastrointestinal Motility/drug effects ; Humans ; Interferon-gamma/metabolism ; Interleukin-13/metabolism ; Interleukin-13/pharmacology ; Interleukin-4/metabolism ; Interleukin-4/pharmacology ; Intestines/physiopathology ; Male ; Middle Aged ; Myocytes, Smooth Muscle/drug effects ; STAT6 Transcription Factor ; Tissue Distribution ; Trans-Activators/metabolism ; Trans-Activators/physiology
Chemical Substances	CD3 Complex ; Interleukin-13 ; STAT6 Transcription Factor ; STAT6 protein, human ; Trans-Activators ; Interleukin-4 (207137-56-2) ; Interferon-gamma (82115-62-6) ; Carbachol (8Y164V895Y) ; DNA (9007-49-2)
Language	English
Publishing date	2005-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603840-2
ISSN	1522-1547 ; 0193-1857
ISSN (online)	1522-1547
ISSN	0193-1857
DOI	10.1152/ajpgi.00273.2004
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Uc I Zs.89: Show issues

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Article: Helicobacter pylori disrupts STAT1-mediated gamma interferon-induced signal transduction in epithelial cells.

Mitchell, David J / Huynh, Hien Q / Ceponis, Peter J M / Jones, Nicola L / Sherman, Philip M

Infection and immunity

2003 Volume 72, Issue 1, Page(s) 537–545

Abstract: Infection with Helicobacter pylori is chronic despite a vigorous mucosal immune response characterized by gastric T-helper type 1 cell expansion and gamma interferon (IFN-gamma) production. IFN-gamma signals by activation and nuclear translocation of ... ...

Abstract	Infection with Helicobacter pylori is chronic despite a vigorous mucosal immune response characterized by gastric T-helper type 1 cell expansion and gamma interferon (IFN-gamma) production. IFN-gamma signals by activation and nuclear translocation of signal transducer and activator of transcription 1 (STAT1); however, the effect of H. pylori infection on IFN-gamma-STAT1 signaling is unknown. We infected human gastric (MKN45 and AGS) and laryngeal (HEp-2) epithelial cell lines with type 1 and type 2 H. pylori strains and then stimulated them with IFN-gamma. Western blotting of whole-cell protein extracts revealed that infection with live, but not heat-killed, H. pylori time-dependently decreased IFN-gamma-induced STAT1 tyrosine phosphorylation. Electrophoretic mobility shift assay of nuclear protein extracts demonstrated that H. pylori infection reduced IFN-gamma-induced STAT1 DNA binding. STAT1 was unable to translocate from the cytoplasm to the nucleus in H. pylori-infected HEp-2 cells examined by immunofluorescence, and reverse transcription-PCR showed that IFN-gamma-induced interferon regulatory factor 1 expression was inhibited. These effects were independent of the cagA, cagE, and VacA status of the infecting H. pylori strain. Furthermore, neither H. pylori culture supernatants nor conditioned medium from H. pylori-infected MKN45 cells inhibited IFN-gamma-induced STAT1 tyrosine phosphorylation, suggesting that inhibition is independent of a soluble epithelial or bacterial factor but is dependent on bacterial contact with epithelial cells. H. pylori disruption of IFN-gamma-STAT1 signaling in epithelial cells may represent a mechanism by which the bacterium modifies mucosal immune responses to promote its survival in the human host.
MeSH term(s)	Animals ; Cell Line, Transformed ; Cell Nucleus/metabolism ; Culture Media ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Epithelial Cells/microbiology ; Helicobacter pylori/immunology ; Helicobacter pylori/pathogenicity ; Humans ; Interferon Regulatory Factor-1 ; Interferon-gamma/metabolism ; Mice ; Phosphoproteins/genetics ; Phosphoproteins/metabolism ; STAT1 Transcription Factor ; Signal Transduction/physiology ; Trans-Activators/metabolism
Chemical Substances	Culture Media ; DNA-Binding Proteins ; IRF1 protein, human ; Interferon Regulatory Factor-1 ; Irf1 protein, mouse ; Phosphoproteins ; STAT1 Transcription Factor ; STAT1 protein, human ; Stat1 protein, mouse ; Trans-Activators ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2003-11-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218698-6
ISSN	1098-5522 ; 0019-9567
ISSN (online)	1098-5522
ISSN	0019-9567
DOI	10.1128/IAI.72.1.537-545.2004
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Zs.A 684: Show issues

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Article: Phosphatidylinositol 3'-kinase is a critical mediator of interferon-gamma-induced increases in enteric epithelial permeability.

McKay, Derek M / Watson, James L / Wang, Arthur / Caldwell, Jackie / Prescott, David / Ceponis, Peter M J / Di Leo, Vincenza / Lu, Jun

The Journal of pharmacology and experimental therapeutics

2007 Volume 320, Issue 3, Page(s) 1013–1022

Abstract: The epithelial lining of mucosal surfaces acts as a barrier to regulate the entry of antigen and pathogens. Nowhere is this function of the contiguous epithelium more important than in the gut, which is continually exposed to a huge antigenic load and, ... ...

Abstract	The epithelial lining of mucosal surfaces acts as a barrier to regulate the entry of antigen and pathogens. Nowhere is this function of the contiguous epithelium more important than in the gut, which is continually exposed to a huge antigenic load and, in the colon, an immense commensal microbiota. We assessed the intracellular signaling events that underlie interferon (IFN) gamma-induced increases in epithelial permeability using monolayers of the human colonic T84 epithelial cell line. Confluent epithelial monolayers on semipermeable supports were treated with IFNgamma (20 ng/ml), and barrier function was assessed 48 h later by measuring transepithelial electrical resistance (TER: reflects passive ion flux), fluxes of (51)Cr-EDTA and horseradish peroxidase (HRP), and transcytosis of noninvasive, nonpathogenic Escherichia coli (strain HB101). Exposure to IFNgamma decreased barrier function as assessed by all four markers. The phosphatidylinositol 3'-kinase (PI-3K) inhibitors, LY294002 [2-(4-morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one hydrochloride] and wortmannin, did not affect baseline permeability characteristics but completely blocked the drop in TER, increased fluxes of (51)Cr-EDTA and HRP, and significantly reduced E. coli transcytosis evoked by IFNgamma. In addition, use of the pan-protein kinase C (PKC) inhibitor, bisindolylmaleimide I (5 muM), but not rottlerin (blocks PKCdelta), partially ameliorated the drop in TER and inhibited increased E. coli transcytosis. Addition of the PI-3K and PKC inhibitors to epithelia 6 h after IFNgamma exposure still prevented the increase in paracellular permeability but not E. coli transcytosis. Thus, IFNgamma-induced increases in epithelial paracellular and transcellular permeability are critically dependent on PI-3K activity, which may represent an epithelial-specific target to treat immune-mediated loss of barrier function.
MeSH term(s)	Bacterial Translocation/drug effects ; Cell Line ; Cell Membrane Permeability/drug effects ; Cell Membrane Permeability/immunology ; Colon/drug effects ; Colon/enzymology ; Colon/immunology ; Colon/microbiology ; Enzyme Inhibitors/pharmacology ; Epithelial Cells/drug effects ; Epithelial Cells/enzymology ; Epithelial Cells/immunology ; Epithelial Cells/microbiology ; Escherichia coli/physiology ; Humans ; Interferon-gamma/immunology ; Interferon-gamma/pharmacology ; Intestinal Absorption/drug effects ; Intestinal Absorption/immunology ; Intestinal Mucosa/drug effects ; Intestinal Mucosa/enzymology ; Intestinal Mucosa/immunology ; Intestinal Mucosa/microbiology ; Phosphatidylinositol 3-Kinases/antagonists & inhibitors ; Phosphatidylinositol 3-Kinases/physiology
Chemical Substances	Enzyme Inhibitors ; Interferon-gamma (82115-62-6) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-)
Language	English
Publishing date	2007-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3106-9
ISSN	1521-0103 ; 0022-3565
ISSN (online)	1521-0103
ISSN	0022-3565
DOI	10.1124/jpet.106.113639
Database	MEDical Literature Analysis and Retrieval System OnLINE

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