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Clinical Immunology

Colonic Immunopathogenesis of Clostridium difficile Infections

Charles Darkoh, Bradley P. Turnwald, Hoonmo L. Koo, Kevin W. Garey, Zhi-Dong Jiang, Samuel L. Aitken, Herbert L. DuPont
M. F. Pasetti, Editor
Charles Darkoh
aThe University of Texas Health Science Center, School of Public Health, Center for Infectious Diseases, Houston, Texas, USA
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Bradley P. Turnwald
eOhio Wesleyan University, Delaware, Ohio, USA
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Hoonmo L. Koo
dBaylor College of Medicine, Department of Medicine, Houston, Texas, USA
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Kevin W. Garey
aThe University of Texas Health Science Center, School of Public Health, Center for Infectious Diseases, Houston, Texas, USA
cSt. Luke's Medical Center, Internal Medicine, Houston, Texas, USA
fUniversity of Houston College of Pharmacy, Houston, Texas, USA
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Zhi-Dong Jiang
aThe University of Texas Health Science Center, School of Public Health, Center for Infectious Diseases, Houston, Texas, USA
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Samuel L. Aitken
fUniversity of Houston College of Pharmacy, Houston, Texas, USA
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Herbert L. DuPont
aThe University of Texas Health Science Center, School of Public Health, Center for Infectious Diseases, Houston, Texas, USA
bThe University of Texas Medical School, Houston, Texas, USA
cSt. Luke's Medical Center, Internal Medicine, Houston, Texas, USA
dBaylor College of Medicine, Department of Medicine, Houston, Texas, USA
fUniversity of Houston College of Pharmacy, Houston, Texas, USA
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M. F. Pasetti
Roles: Editor
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DOI: 10.1128/CVI.00770-13
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ABSTRACT

There are major gaps in our understanding of the immunopathogenesis of Clostridium difficile infections (CDIs). In this study, 36 different biomarkers were examined in the stools of CDI and non-CDI patients using the Proteome Profiler human cytokine array assay and quantitative enzyme-linked immunosorbent assay. Diarrheal stools from patients with CDI (CDI-positive diarrheal stools) showed higher relative amounts of the following inflammatory markers than the diarrheal stools from CDI-negative patients (CDI-negative diarrheal stools): C5a, CD40L, granulocyte colony-stimulating factor, I-309, interleukin-13 (IL-13), IL-16, IL-27, monocyte chemoattractant protein 1, tumor necrosis factor alpha, and IL-8. IL-8 and IL-23 were present in a larger number of CDI-positive diarrheal stools than CDI-negative diarrheal stools. Th1 and Th2 cytokines were not significantly different between the CDI-positive and CDI-negative diarrheal stools. Lactoferrin and calprotectin concentrations were also higher in the CDI-positive diarrheal stools. Our results demonstrate that CDI elicits a proinflammatory host response, and we report for the first time that IL-23 is a major marker in CDI-positive diarrheal stools. IL-23 may explain the lack of a robust immunological response exhibited by a proportion of CDI patients and may relate to recurrence; the IL-23 levels induced during CDI in these patients may be inadequate to sustain the cellular immunity conferred by this cytokine in promoting the induction and proliferation of effector memory T cells.

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Colonic Immunopathogenesis of Clostridium difficile Infections
Charles Darkoh, Bradley P. Turnwald, Hoonmo L. Koo, Kevin W. Garey, Zhi-Dong Jiang, Samuel L. Aitken, Herbert L. DuPont
Clinical and Vaccine Immunology Mar 2014, 21 (4) 509-517; DOI: 10.1128/CVI.00770-13

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Colonic Immunopathogenesis of Clostridium difficile Infections
Charles Darkoh, Bradley P. Turnwald, Hoonmo L. Koo, Kevin W. Garey, Zhi-Dong Jiang, Samuel L. Aitken, Herbert L. DuPont
Clinical and Vaccine Immunology Mar 2014, 21 (4) 509-517; DOI: 10.1128/CVI.00770-13
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