Gastroenterology Research and Practice

Gastrointestinal Inflammation and Repair: Role of Microbiome, Infection, and Nutrition


Publishing date
16 Sep 2016
Status
Published
Submission deadline
29 Apr 2016

Lead Editor

1University of KY Medical Center, Lexington, USA

2University of Toronto, Toronto, Canada

3Taipei Medical University, Taipei, Taiwan


Gastrointestinal Inflammation and Repair: Role of Microbiome, Infection, and Nutrition

Description

Gastrointestinal Inflammation is a complex biological response to injury as a result of different stimuli such as pathogens, damaged cells, or irritants. Symbiotic microbiome in digestive tract is considered to protect gut by removing harmful stimuli and to enhance healing process. Altered microbiome or absence can lead to exacerbated type 2 immunity and allergic/infectious inflammations including parasites. Thus, the microbiota regulates type 2 responses and acts as a key element in harmonizing immune responses at mucosal surfaces. While the mechanism by which microbiota regulates type 2 immunity is unclear, it is known as a strong inducer of proinflammatory T helper 17 cells and regulatory T cells (Tregs) in the intestine.

The signals at the sites of inflammation mediate rapid cell recruitment and differentiation in order to remove inflammatory inducers and promote tissue homeostasis restoration. However, persistent inflammatory stimuli or dysregulation of mechanisms of the restoration can lead to chronic inflammation. Different stressors can affect immune system and increase risk for infectious diseases, such as gastritis in post infectious IBS, and vice versa. As IBS patients have increased susceptibility to develop infectious gastroenteritis. Various viral (e.g., norovirus), microbial (e.g., Campylobacter jejuni, Clostridium, Mycobacterium), and parasitic agents (e.g., Giardia, helminths) are known to be involved in the development of chronic inflammatory bowel diseases. Yet, the mechanisms of action are not well known and there is no available cure. Additionally, nutritional elements, such as antioxidants, probiotics, and prebiotics directly and indirectly modulate GI immunity. Diets high in fat change the populations of innate microbiome in digestive tract and alter signaling to the brain and satiety, leading to obesity and inflammation.

We are inviting investigators to submit original research papers and review articles that will stimulate the continuing efforts in following areas.

Potential topics include, but are not limited to:

  • Studies of the mechanisms of inflammatory pathways and microbiome involved in GI diseases (e.g., gastritis colitis, hepatitis, and pancreatitis) in patients and experimental models
  • The role of altered microbiome/ infectious agents and mechanisms of interactions between various mediators involved in regulating the immune response in GI inflammation
  • Breakthroughs in GI repair management and anti-inflammatory properties: biological, chemical, pharmaceutical, and nutraceutical ones
  • New challenges in the effect of antibiotics and antibiotic resistance on GI microbiome and inflammation
  • Translational preclinical and clinical pilot studies regarding the feasibility and safety profiles of anti-inflammatory compounds, biological agents relevant to GI inflammatory disease
  • Elucidation role/mechanism of microbiome, nutrients, and metabolites during acute or chronic GI inflammation and malignancies
  • New findings relevant to a specific nutrient or food component intervention alone or in combination on the modulation of GI immunity in health and disease

Articles

  • Special Issue
  • - Volume 2016
  • - Article ID 6516708
  • - Editorial

Gastrointestinal Inflammation and Repair: Role of Microbiome, Infection, and Nutrition

Helieh S. Oz | Sung-Ling Yeh | Manuela G. Neuman
  • Special Issue
  • - Volume 2016
  • - Article ID 3952534
  • - Research Article

Selective Induced Altered Coccidians to Immunize and Prevent Enteritis

Helieh S. Oz
  • Special Issue
  • - Volume 2016
  • - Article ID 3019362
  • - Review Article

Nutrition and Helicobacter pylori: Host Diet and Nutritional Immunity Influence Bacterial Virulence and Disease Outcome

Kathryn P. Haley | Jennifer A. Gaddy
  • Special Issue
  • - Volume 2016
  • - Article ID 4210462
  • - Research Article

Molecular Diversity of Sapovirus Infection in Outpatients Living in Nanjing, China (2011–2013)

Hong-ying Zhang | Meng-kai Qiao | ... | Hei-ying Jin
  • Special Issue
  • - Volume 2016
  • - Article ID 9686238
  • - Review Article

Research Advance in Intestinal Mucosal Barrier and Pathogenesis of Crohn’s Disease

Kuan Wang | Lu-yi Wu | ... | Hui-rong Liu
  • Special Issue
  • - Volume 2016
  • - Article ID 5789232
  • - Research Article

Prebiotic Effects of Xylooligosaccharides on the Improvement of Microbiota Balance in Human Subjects

Shyh-Hsiang Lin | Liang-Mao Chou | ... | Ching-I Lin
  • Special Issue
  • - Volume 2016
  • - Article ID 4514687
  • - Research Article

Tea and Recurrent Clostridium difficile Infection

Martin Oman Evans II | Brad Starley | ... | Joseph John Salama
  • Special Issue
  • - Volume 2016
  • - Article ID 6421351
  • - Research Article

Suppressing Syndecan-1 Shedding Ameliorates Intestinal Epithelial Inflammation through Inhibiting NF-κB Pathway and TNF-α

Yan Zhang | Zhongqiu Wang | ... | Ye Chen
  • Special Issue
  • - Volume 2016
  • - Article ID 4969163
  • - Research Article

Helicobacter pylori CagA and IL-1β Promote the Epithelial-to-Mesenchymal Transition in a Nontransformed Epithelial Cell Model

Haruki Arévalo-Romero | Isaura Meza | ... | Ezequiel M. Fuentes-Pananá
  • Special Issue
  • - Volume 2016
  • - Article ID 3126280
  • - Research Article

Synergic Interaction of Rifaximin and Mutaflor (Escherichia coli Nissle 1917) in the Treatment of Acetic Acid-Induced Colitis in Rats

Artur Dembiński | Zygmunt Warzecha | ... | Peter Christopher Konturek
Gastroenterology Research and Practice
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Acceptance rate5%
Submission to final decision98 days
Acceptance to publication22 days
CiteScore3.900
Journal Citation Indicator0.370
Impact Factor2.0
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