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Inflammatory Bowel Disease (IBD) affects more than 6 million people worldwide and constitutes not only a debilitating disease for the patients, but also a significant factor for society due to costs for health care and reduced working capacity.
Key factors for Inflammatory Bowel Disease (IBD) are similar worldwide. However, there are genetic, environmental, and microbial differences. These differences influence disease risk and disease progression. They also affect treatment responses. This aspect is often ignored in research.
Inflammatory bowel diseases (IBDs), including ulcerative colitis and Crohn’s disease, are characterized by chronic idiopathic inflammation of the gastrointestinal tract
Although the pathogenesis of Inflammatory Bowel Disease (IBD) remains unknown, intestinal immune dysfunction has been considered the core pathogenesis
Excessive NFKB Activation is linked to the pathogenesis of conditions like Crohn's disease and ulcerative colitis.
Inflammatory bowel disease is characterized by defects in epithelial function and dysregulated inflammatory signaling by lamina propria mononuclear cells including macrophages and dendritic cells in response to microbiota.
The Faroe Islands has the world’s highest incidence of Inflammatory Bowel Disease (IBD)
The pathogenesis of Inflammatory Bowel Disease (IBD) is still unclear.
While cytokines play a major role in the inflammatory processes of both Crohn's disease (CD) and Ulcerative colitis (UC), there are key differences in the specific cytokines involved in the pathobiology of each condition.
A combination of fecal calprotectin and human beta-defensin 2 facilitates diagnosis and monitoring of inflammatory bowel disease
Inflammatory bowel disease (IBD) is a chronic autoimmune condition
IBD is classically associated with gut accumulation of pro-inflammatory Th1 and Th17 cells accompanied by insufficient Treg numbers and Tr1 immune suppression.
Inflammatory T cells guide innate cells to perpetuate a constant hypersensitivity to microbial antigens, tissue injury, and chronic intestinal inflammation.
This annoying disease affects approximately 0.2% of the European population, imposing a heavy economic burden and poorer quality of life on patients.
Inflammatory bowel diseases (IBDs) are a group of multifactorial disorders with significant morbidity and mortality. Abnormal host immune responses to the gut microbiota disrupt homeostasis, leading to their development in genetically susceptible individuals.
Alatab et al. 2020 The Lancet Gastroenterology & Hepatology 5: 17-30
The key players in Inflammatory Bowel Disease (IBD) are:
Permeability of gut barrier (expression of occludin , Zonula Occludens (ZO) Proteins (Zoludins) )
Gut microbiota (i.e., Bifidobacterium / Bifidobacter , Escherichia coli (E. coli) , Lacticaseibacillus (Lactobacillus) ], Staphylococcus aureus , others
Immunological status (i.e., fluctuations in Lymphocytes counts CD4+ Th1 Cells , CD4+ Th2 Cells , CD4+ Th17 Cells - and cytokine levels - Interleukin-17 Family / Interleukin-17 (IL-17) , Tumor Necrosis Factor alfa (TNF-alfa) , Interferon Type II (IFN Type II) / Interferon Gamma (IFN-g) )
Enviromental factors (Food / Diets / Nutrients , Lifestyle / Lifestyle Changes , Tobacco Smoking , antibiotics , air pollution , others)
Genetic agents (e.g., CARD15/NOD2, OCTN1, CD1H, muc2 gene )
Others
Coexistence of environmental and genetic agents, immunological imbalance, permeability of gut barrier, and state of gut microbiota have a great impact on the rise and progress of disease. However, the direct mechanism and cause of Inflammatory Bowel Disease (IBD) remain unclear.
Another key player in Inflammatory Bowel Disease (IBD) is the immunological status of the organism. The most important cells seem to be helper lymphocytes Th (Th1, Th2, Th17) and regulatory T cells
Inflammatory bowel disease (IBD) mainly refers to Crohn's disease & ulcerative colitis
In Crohn's Disease (CD), Th1 skewing is observed, but in Ulcerative colitis (UC), Th2 skewing is common. The population of Th17 cells is decreased regarding the Th1 or Th2 population. The decreased number of Regulatory T Cells (Tregs) and imbalance in Th17 and Treg subpopulations are common in Inflammatory Bowel Disease (IBD). The subpopulation disturbance triggers the loss of microbiota tolerance and the pro-inflammatory processes' privilege. In turn, microbiota modulates the Treg population and has an anti-inflammatory effect
No sex predominance exists in Inflammatory Bowel Disease (IBD) , and the peak age of disease onset is between 17 and 40 years
However, with a westernized diet and lifestyle , a wave of rapidly rising incidence has followed
Inflammatory bowel diseases are common, complex, immune-mediated conditions with a sharply rising global prevalence
A common disease denominator in all Inflammatory Bowel Disease (IBD) patients is the infiltration of inflammatory CD4 + T-cells in intestinal tissue
Inflammatory Bowel Disease (IBD) typically occurs between the second and fourth decades of life
Inflammatory bowel disease (IBD) symptoms are abdominal pain , Diarrhea / Diarrhoea , and weight loss
Its main symptoms include bloody diarrhea, abdominal cramps, weight loss, fatigue, anemia, hematochezia, and emesis; and extraintestinal symptoms (especially joint pain or arthritis; further: iridocyclitis, hepatosis, and eye and skin lesion
However, the exact cause of IBD has yet to be determined, which makes it difficult to develop targeted treatments
Most patients with IBD suffer from fecal incontinence and face the risk of a weakened immune system and bowel cancer
Inflammatory Bowel Disease (IBD) affects 0.3 to 0.5% of the world's population. It means a group of bowel diseases characterized by chronic inflammation of the gastrointestinal tract (GIT) with a sharply rising global prevalence, comprising Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic intermittent disorder characterized by intestinal inflammation
Furthermore, mouse studies indicate that changes in the microbiota composition can occur before colitis development, suggesting that microbial modifications might be involved in IBD development
However, whether dysbiosis is a cause or a consequence of IBD in humans remains solved.
Genetic predisposition, environmental factors, intestinal microbiome, and a dysregulated immune system.
Inflammatory bowel disease (IBD) affects 0.3 to 0.5% of the world's population. Even though the prevalence of IBD, especially in western countries such as the USA, is high (1.3%), and the resulting costs to the health systems are increasing (), the underlying cause of IBD is still unknown.
Nevertheless, barrier defects typically present in IBD seem to cause a dysregulated immune response against so far unknown components of the commensals.
Especially the adaptive immunity, more specifically CD4 + T cells, seems to be inappropriately activated in response to commensal microorganisms in IBD.
Intestinal fibrosis is a major problem. It is a big challenge in Inflammatory Bowel Disease (IBD). There is no known cause or cure. Treatments are not effective. Fibrosis affects Crohn's disease (CD) patients. It is irreversible. It causes thickening and stricturing of the intestines. This can lead to obstruction. Surgery may be needed. Scarring and stricturing often return after surgery. Something in the gut environment may drive fibrosis.
Inflammatory Bowel Disease (IBD) ranges from a milder disease course characterized by long periods of clinical remission to severe cases characterized by flares of inflammation despite intensive treatment () that require surgical intervention in 47% of patients with Crohn's disease (CD) and 16% of patients with Ulcerative colitis (UC) within 10 years of diagnosis
Biomarkers, such as C-reactive protein in blood and fecal Calprotectin (FCal) often do not accurately capture inflammatory activity in IBD
Genetic studies have identified over 200 host genetic loci associated with the risk of IBD and mostly related to immunological pathways
Environmental factors contributing to IBD risk are diet, smoking, stress, sleep patterns, hygiene, and antibiotic usage
Genetic studies have identified over 200 host genetic loci associated with the risk of Inflammatory Bowel Disease (IBD) and mostly related to immunological pathways
Additionally, several bacterial pathogens have been implicated in the onset or progression of the disease
Inflammatory Bowel Disease (IBD) is currently incurable and affects the quality of life of an increasing number of people
An estimated 1 million individuals in the United States and 2.5 million people in Europe suffer from inflammatory bowel disease (IBD)
And in addition immune regulation dysfunction, gut microbiota, nutrition, and lifestyle
Several studies describe a reduced diversity of commensal bacteria species in patients suffering from IBD
Initial studies have shown increased IL17A mRNA expression and increased numbers of Th17 cells in the inflamed tissue of IBD patients compared to healthy mucosa
There are over 240 identified genetic risk loci for Inflammatory Bowel Disease (IBD), and among these, genes related to mitochondrial function suggest its involvement in Inflammatory Bowel Disease (IBD)
The peak incidence of Inflammatory Bowel Disease (IBD) is between the second to fourth decades of life
Twin studies revealed that genetic predispositions to developing IBD exist; however, the concordance rate for IBD in monozygotic twins does not exceed 50%, highlighting the importance of environmental factors, referred to as Exposome, for disease development
Patients with inflammatory bowel disease (IBD) develop uncontrolled inflammatory CD4 + T-cell responses which can be caused by either by insufficient suppression of inflammatory CD4 + T-cell responses but also by insufficient host defense to pathogens, both resulting in tissue damage and chronic intestinal inflammation
see also:
Aging / Senescence & Inflammation / Inflammatory Diseases
Crohn's disease (CD)
Dysbiosis & Inflammatory Bowel Disease (IBD)
Gut microbiota & Inflammatory Bowel Disease (IBD)
Intestinal Homeostasis
Ulcerative colitis (UC)