Abstract
Successful colonization of the intestine requires that bacteria interact with the innate immune system and, in particular, neutrophils. Progression of inflammatory bowel diseases (IBD) is associated with alterations in gut microbiota, and dysbiosis in Crohn’s disease (CD) patients is often associated with an expansion of Escherichia coli. Here, we investigated the ability of such E. coli isolates to avoid neutrophil activation and to utilize reactive oxygen species. Neutrophil activation was detected in vitro in normal human blood via luminol chemiluminescence (CL) induced by reactive oxygen and halogen species generated by neutrophils. No significant difference in neutrophil activation in vitro was detected between isolates from inflamed (23 isolates) vs healthy intestines (5 isolates), with 10‐fold variation within both groups (2.9–61.2 mV). CL activity of isolates from the same patient differed by 1.5–5 times. Twenty‐four isolates from ileal aspirate, biopsy, and feces of seven patients with CD and one patient with no intestine inflammation were tested for extracellular peroxidase and catalase activity and cell surface hydrophobicity. Average values between patients varied from 26 ± 3 to 73 ± 18 µmol·g−1 of air dry weight for peroxidase activity, from 15 ± 2 to 189 ± 56 mmol·g−1 of air dry weight for catalase activity, and from 5 ± 3 to 105 ± 9 a.u. for the hydrophobic probe fluorescence. Extracellular peroxidase activity and hydrophobicity of bacterial cell surface correlated negatively with stimulated neutrophil CL. The ability of some isolates to avoid neutrophil activation and to utilize reactive oxygen species may provide a strategy to survive assault by the innate immune system.
Highlights
Progression of inflammatory bowel diseases (IBD) is associated with alterations in gut microbiota, and dysbiosis in Crohn’s disease (CD) patients is often associated with an expansion of Escherichia coli
Antibodies to E. coli were found in biopsy samples from ulcer, erosion, and granuloma of patients with Crohn’s disease, Abbreviations ANS, 1-anilino-8-naphthalenesulfonate; CD, Crohn’s disease; CFU, colony-forming units; CL, chemiluminescence; DMC, 4dimethylaminochalcone; DMEM, Dulbecco’s modified Eagle’s medium; DW, dry weight; FBS, fetal bovine serum; IBD, inflammatory bowel disease; KRB, Krebs–Ringer bicarbonate; OD, optical density; PBS, phosphate-buffered saline; PMA, phorbol 12-myristate 13-acetate; RHS, reactive halogen species; ROS, reactive oxygen species
Neutrophil CL was activated by bacterial suspensions in diluted blood of healthy volunteers, without leukocyte isolation [37] in order to imitate in vivo conditions
Summary
Progression of inflammatory bowel diseases (IBD) is associated with alterations in gut microbiota, and dysbiosis in Crohn’s disease (CD) patients is often associated with an expansion of Escherichia coli. We investigated the ability of such E. coli isolates to avoid neutrophil activation and to utilize reactive oxygen species. Twenty-four isolates from ileal aspirate, biopsy, and feces of seven patients with CD and one patient with no intestine inflammation were tested for extracellular peroxidase and catalase activity and cell surface hydrophobicity. The ability of some isolates to avoid neutrophil activation and to utilize reactive oxygen species may provide a strategy to survive assault by the innate immune system. Dysbiosis often observed in CD patients is associated with an expansion of Escherichia coli capable of various adaptive reactions [1–3] One of these reactions is surviving the attack of human immune system. Neutrophil activation by E. coli from CD patients suggesting the presence of bacteria at the very spot of acute inflammation [4]
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