Campylobacter jejuni Modulates Reactive Oxygen Species Production and NADPH Oxidase 1 Expression in Human Intestinal Epithelial Cells

Author:

Hong Geunhye1,Davies Cadi1,Omole Zahra1,Liaw Janie1,Grabowska Anna D.2ORCID,Canonico Barbara3ORCID,Corcionivoschi Nicolae45ORCID,Wren Brendan W.1ORCID,Dorrell Nick1ORCID,Elmi Abdi1ORCID,Gundogdu Ozan1ORCID

Affiliation:

1. Faculty of Infectious and Tropical Diseases, London School of Hygiene & Tropical Medicine, Keppel Street, London WC1E 7HT, UK

2. Department of Biophysics, Physiology and Pathophysiology, Medical University of Warsaw, Warsaw 02-004, Poland

3. Department of Biomolecular Sciences, University of Urbino Carlo Bo, Urbino 61029, Italy

4. Bacteriology Branch, Veterinary Sciences Division, Agri-Food and Biosciences Institute (AFBI), Belfast BT9 5PX, UK

5. Faculty of Bioengineering of Animal Resources, University of Life Sciences King Mihai I from Timisoara, Timisoara 300645, Romania

Abstract

Campylobacter jejuni is the major bacterial cause of foodborne gastroenteritis worldwide. Mechanistically, how this pathogen interacts with intrinsic defence machinery of human intestinal epithelial cells (IECs) remains elusive. To address this, we investigated how C. jejuni counteracts the intracellular and extracellular reactive oxygen species (ROS) in IECs. Our work shows that C. jejuni differentially regulates intracellular and extracellular ROS production in human T84 and Caco-2 cells. C. jejuni downregulates the transcription and translation of nicotinamide adenine dinucleotide phosphate (NAPDH) oxidase (NOX1), a key ROS-generating enzyme in IECs and antioxidant defence genes CAT and SOD1. Furthermore, inhibition of NOX1 by diphenylene iodonium (DPI) and siRNA reduced C. jejuni ability to interact, invade, and intracellularly survive within T84 and Caco-2 cells. Collectively, these findings provide mechanistic insight into how C. jejuni modulates the IEC defence machinery.

Publisher

Hindawi Limited

Subject

Virology,Immunology,Microbiology

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