Background. Optimal management of pediatric patients with inflammatory bowel disease (IBD) requires early diagnosis. Aim of the study is to compare fecal lactoferrin (FL) as biomarker of intestinal inflammation to CRP in pediatric patients with new-onset IBD. Methods. FL was measured by ELISA in stool specimens collected prior to endoscopy for IBD (IBD-SCAN; TechLab, Blacksburg; normal < 7.3 µg/g feces). CRP was detected in serum (normal < 5 mg/L). Three patient groups were determined: n = 21 (mean age 13.2) with Crohn's disease (CD), n = 15 (mean age 10.9) with ulcerative colitis (UC), and n = 20 (mean age 11.9) in whom IBD was ruled out. In CD patients the endoscopic severity score SES-CD was correlated with the FL levels. Results. (Mean ± SEM). CRP levels were 27.18 ± 4.2 for CD-cases, 20.8 ± 9.5 for UC, and 0.24 ± 0.06 for non-IBD patients. FL levels were 313.6 ± 46.4 in CD, 370.7 ± 46.9 in UC, and 1.3 ± 0.5 in non-IBD patients. Sensitivity of CRP to detect IBD was 75% with specificity of 100%, positive predictive value of 100%, and negative predictive value of 69%. Sensitivity of FL was 100% with specificity of 95%, positive predictive value of 97.3%, and negative predictive value of 100%. In CD, FL levels correlated positively (R (2) = 0.42) with disease severity as judged by the SES-CD. Conclusions. Elevated FL corresponds to intestinal inflammation, even in patients with normal CRP. With high probability, normal FL excludes intestinal inflammation.
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http://dx.doi.org/10.1155/2015/578527 | DOI Listing |
Sci Transl Med
January 2025
Department of Medicine 1, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91052 Erlangen, Germany.
Dysregulation at the intestinal epithelial barrier is a driver of inflammatory bowel disease (IBD). However, the molecular mechanisms of barrier failure are not well understood. Here, we demonstrate dysregulated mitochondrial fusion in intestinal epithelial cells (IECs) of patients with IBD and show that impaired fusion is sufficient to drive chronic intestinal inflammation.
View Article and Find Full Text PDFJ Appl Physiol (1985)
January 2025
Department of Medical Education, Paul L Foster School of Medicine, Texas Tech University Health Science Center, El Paso, TX, USA.
There is growing interest in understanding the complex relationship between psychosocial stress and the human gastrointestinal microbiome (GIM). This review explores the potential physiological pathways connecting these two and how they contribute to a pro-inflammatory environment that can lead to the development and progression of the disease. Exposure to psychosocial stress triggers the activation of the sympathetic nervous system (SNS) and hypothalamic-pituitary axis (HPA), leading to various physiological responses essential for survival and coping with the stressor.
View Article and Find Full Text PDFClin Exp Med
January 2025
The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, Sichuan, China.
Upon stimulation and activation, mast cells (MCs) release soluble mediators, including histamine, proteases, and cytokines. These mediators are often stored within cytoplasmic granules in MCs and may be released in a granulated form. The secretion of cytokines and chemokines occurs within hours following activation, with the potential to result in chronic inflammation.
View Article and Find Full Text PDFFASEB J
January 2025
Department of Pharmacy, College of Pharmacy, Kangwon National University, Chuncheon, South Korea.
Metabolic dysfunction-associated steatohepatitis (MASH) is characterized by severe liver inflammation and fibrosis due to an imbalanced immune response caused by enhanced bacterial components. The progression of MASH is closely linked to increased permeability of intestinal mucosal barrier facilitating enter of bacterial components into hepatic portal venous system. B cells are important immune cells for adaptive responses and enhance hepatic inflammation through cytokine production and T cell activation.
View Article and Find Full Text PDFGut Microbes
December 2025
Beijing Institute of Clinical Pharmacy, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Metformin is the first-line pharmacotherapy for type 2 diabetes mellitus; however, many patients respond poorly to this drug in clinical practice. The potential involvement of microbiota-mediated intestinal immunity and related signals in metformin responsiveness has not been previously investigated. In this study, we successfully constructed a humanized mouse model by fecal transplantation of the gut microbiota from clinical metformin-treated - responders and non-responders, and reproduced the difference in clinical phenotypes of responsiveness to metformin.
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