scholarly journals Exposure of the Host-Associated Microbiome to Nutrient-Rich Conditions May Lead to Dysbiosis and Disease Development—an Evolutionary Perspective

mBio ◽  
2019 ◽  
Vol 10 (3) ◽  
Author(s):  
Tim Lachnit ◽  
Thomas C. G. Bosch ◽  
Peter Deines
Keyword(s):  
Inflammatory Diseases ◽  
Developed Countries ◽  
Disease Development ◽  
Inflammatory Reactions ◽  
Bowel Diseases ◽  
Microbe Interactions ◽  
Inflammatory Bowel ◽  
Host Microbe Interactions ◽  
Increased Activity ◽  
Human Specific

ABSTRACTInflammatory diseases, such as inflammatory bowel diseases, are dramatically increasing worldwide, but an understanding of the underlying factors is lacking. We here present an ecoevolutionary perspective on the emergence of inflammatory diseases. We propose that adaptation has led to fine-tuned host-microbe interactions, which are maintained by secreted host metabolites nourishing the associated microbes. A constant elevation of nutrients in the gut environment leads to an increased activity and changed functionality of the microbiota, thus severely disturbing host-microbe interactions and leading to dysbiosis and disease development. In the past, starvation and pathogen infections, causing diarrhea, were common incidences that reset the gut bacterial community to its “human-specific-baseline.” However, these natural clearing mechanisms have been virtually eradicated in developed countries, allowing a constant uncontrolled growth of bacteria. This leads to an increase of bacterial products that stimulate the immune system and ultimately might initiate inflammatory reactions.

The Gut Microbiome and Inflammatory Bowel Diseases

2021 ◽  
Vol 73 (1) ◽  
Author(s):  
Yue Shan ◽  
Mirae Lee ◽  
Eugene B. Chang
Keyword(s):  
Gut Microbiota ◽  
Inflammatory Bowel Diseases ◽  
Gut Microbiome ◽  
Annual Review ◽  
Publication Date ◽  
Bowel Diseases ◽  
Microbe Interactions ◽  
Inflammatory Bowel ◽  
Host Microbe Interactions ◽  
And Function

Inflammatory bowel diseases (IBD) arise from a convergence of genetic risk, environmental factors, and gut microbiota, where each is necessary but not sufficient to cause disease. Emerging evidence supports a bidirectional relationship between disease progression and changes in microbiota membership and function. Thus, the study of the gut microbiome and host–microbe interactions should provide critical insights into disease pathogenesis as well as leads for developing microbiome-based diagnostics and interventions for IBD. In this article, we review the most recent advances in understanding the relationship between the gut microbiota and IBD and highlight the importance of going beyond establishing description and association to gain mechanistic insights into causes and consequences of IBD. The review aims to contextualize recent findings to form conceptional frameworks for understanding the etiopathogenesis of IBD and for the future development of microbiome-based diagnostics and interventions. Expected final online publication date for the Annual Review of Medicine, Volume 73 is January 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

scholarly journals The Role of Gut Microbiota Biomodulators on Mucosal Immunity and Intestinal Inflammation

Cells ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 1234 ◽  
Author(s):  
Chiara Amoroso ◽  
Federica Perillo ◽  
Francesco Strati ◽  
Massimo Fantini ◽  
Flavio Caprioli ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Immune Responses ◽  
Targeted Therapies ◽  
Intestinal Inflammation ◽  
Cost Effective ◽  
Bowel Diseases ◽  
Current Therapies ◽  
Microbe Interactions ◽  
Inflammatory Bowel ◽  
Host Microbe Interactions

Alterations of the gut microbiota may cause dysregulated mucosal immune responses leading to the onset of inflammatory bowel diseases (IBD) in genetically susceptible hosts. Restoring immune homeostasis through the normalization of the gut microbiota is now considered a valuable therapeutic approach to treat IBD patients. The customization of microbe-targeted therapies, including antibiotics, prebiotics, live biotherapeutics and faecal microbiota transplantation, is therefore considered to support current therapies in IBD management. In this review, we will discuss recent advancements in the understanding of host−microbe interactions in IBD and the basis to promote homeostatic immune responses through microbe-targeted therapies. By considering gut microbiota dysbiosis as a key feature for the establishment of chronic inflammatory events, in the near future it will be suitable to design new cost-effective, physiologic, and patient-oriented therapeutic strategies for the treatment of IBD that can be applied in a personalized manner.

scholarly journals Host–microbe interactions in the gut: lessons learned from models of inflammatory bowel diseases

2014 ◽  
Vol 1 (2) ◽  
pp. 61-76
Author(s):  
Eytan Wine
Keyword(s):  
Immune System ◽  
Animal Models ◽  
Patient Care ◽  
Inflammatory Bowel Diseases ◽  
Gut Microbes ◽  
Bowel Diseases ◽  
Microbe Interactions ◽  
Inflammatory Bowel ◽  
Host Microbe Interactions

The mammalian gut is the richest immune organ in the body and serves as a central location for immune system development, processing, and education. Inflammatory bowel diseases (IBD) provide excellent models for studying both innate and adaptive responses to gut microbes and the host-immune system – microbe interactions in the gut. Microbes are linked to almost all of the known disease-associated genetic polymorphisms in IBD and are critical mediators of environmental effects (through food, hygiene, and infection). Human and animal-based research supports the central role of microbes in IBD pathogenesis at multiple levels. Animal models of IBD only develop in the presence of microbes, and co-housing mice that are genetically susceptible to gut inflammation with normal mice can lead to the development of bowel injury. Recent advances in research technologies, such as deep-sequencing that enables detailed compositional analyses, have revolutionized the study of host–microbe interactions in the gut; however, knowing which bacteria are present in the bowel is likely not sufficient. The function of the microbiota as a community is recognized as a critical factor for gut homeostasis. Animal models of IBD have provided critical insight into basic biology and disease pathogenesis, especially regarding the role of microbes in IBD pathogenesis. Although many of these recent discoveries on host–microbe interactions are not yet applied to patient care, these basic observations will certainly revolutionize patient care in the future. Using such data, we may be able to predict risk of disease, define biological subtypes, establish tools for prevention, and even cure IBD using microbes or their products. A broad spectrum of therapeutic tools spanning from fecal transplantation, probiotics, prebiotics, and microbial products to microbe-tailored diets may supplement current IBD treatments.

scholarly journals The Role of Enterobacteriaceae in Gut Microbiota Dysbiosis in Inflammatory Bowel Diseases

2021 ◽  
Vol 9 (4) ◽  
pp. 697
Author(s):  
Valerio Baldelli ◽  
Franco Scaldaferri ◽  
Lorenza Putignani ◽  
Federica Del Chierico
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Inflammatory Diseases ◽  
Species Level ◽  
Unknown Etiology ◽  
Gut Dysbiosis ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Symbiotic Microbiota ◽  
Gut Microbiota Dysbiosis

Inflammatory bowel diseases (IBDs) are a group of chronic gastrointestinal inflammatory diseases with unknown etiology. There is a combination of well documented factors in their pathogenesis, including intestinal microbiota dysbiosis. The symbiotic microbiota plays important functions in the host, and the loss of beneficial microbes could favor the expansion of microbial pathobionts. In particular, the bloom of potentially harmful Proteobacteria, especially Enterobacteriaceae, has been described as enhancing the inflammatory response, as observed in IBDs. Herein, we seek to investigate the contribution of Enterobacteriaceae to IBD pathogenesis whilst considering the continuous expansion of the literature and data. Despite the mechanism of their expansion still remaining unclear, their expansion could be correlated with the increase in nitrate and oxygen levels in the inflamed gut and with the bile acid dysmetabolism described in IBD patients. Furthermore, in several Enterobacteriaceae studies conducted at a species level, it has been suggested that some adherent-invasive Escherichia coli (AIEC) play an important role in IBD pathogenesis. Overall, this review highlights the pivotal role played by Enterobacteriaceae in gut dysbiosis associated with IBD pathogenesis and progression.

Clinical Comparison of 99Tcm-Hmpao Labelled Leucocytes and 99Tcm-Nanocolloid in the Detection of Inflammation

1989 ◽  
Vol 30 (6) ◽  
pp. 633-637 ◽  
Author(s):  
M. Vorne ◽  
T. Lantto ◽  
S. Paakkinen ◽  
S. Salo ◽  
I. Soini
Keyword(s):  
Soft Tissue ◽  
Inflammatory Bowel Diseases ◽  
Vascular Graft ◽  
Inflammatory Diseases ◽  
Reliable Information ◽  
Imaging Method ◽  
Joint Diseases ◽  
Labelled Leucocytes ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Forty-five patients with various inflammatory diseases were imaged with 99Tcm-HMPAO labelled leucocytes and 99Tcm-nanocolloid within 7 days. The overall sensitivity of 99Tcm-leucocytes was 97% and that of 99Tcm-nanocolloid 59% and both agents had a 100% specificity. The 99Tcm-leucocyte method showed reliable results in various inflammatory and infectious conditions, and seems suitable as a primary imaging method. On the contrary, 99Tcm-nanocolloid cannot be recommended for use in inflammatory bowel diseases, soft tissue abscesses or prosthetic vascular graft infections. However, 99Tcm-nanocolloid gave reliable information in inflammatory and infectious bone and joint diseases in which it had a 90% sensitivity and 100% specificity. In those lesions the 99Tcm-nanocolloid method may be useful, because it is simple, fast and cheap. Yet, further evaluation is needed.

Increased serum nesfatin-1 levels in patients with inflammatory bowel diseases

2021 ◽  
pp. postgradmedj-2020-139227
Author(s):  
Şengül Beyaz ◽  
Erdem Akbal
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Inflammatory Diseases ◽  
Inflammatory Marker ◽  
White Cell Count ◽  
Characteristic Curve ◽  
Diagnostic Value ◽  
Healthy Individuals ◽  
Altered Expression ◽  
Bowel Diseases ◽  
Inflammatory Bowel

BackgroundAdipokines are adipose tissue–derived secreted molecules that can exert anti-inflammatory or proinflammatory activities. Altered expression of adipokines has been described in various inflammatory diseases, including inflammatory bowel diseases (IBDs) such as Crohn’s disease (CD) and ulcerative colitis (UC). Little is known about nesfatin-1, a recently identified adipokine, in IBD. The aim of this study was to investigate serum nesfatin-1 levels in patients with IBD.MethodsThis study included a total of 52 adult individuals (17 patients with CD, 18 patients with UC and 17 healthy volunteers) with similar age and body mass index. Serum nesfatin-1 levels were measured by ELISA in healthy individuals and patients with IBD in their active and remission periods. Blood inflammation markers including C reactive protein (CRP), erythrocyte sedimentation (ESR) and white cell count (WCC) were also measured in patients.ResultsWe found significantly elevated levels of serum nesfatin-1 in the active disease period in both patients with CD (p=0.00003) and patients with UC (p=0.00001), compared with healthy individuals. Serum nesfatin-1 levels moderately decreased in the remission period; however, they were still significantly higher than that of healthy individuals. Receiver operating characteristic curve analyses indicated serum nesfatin-1 with an excellent diagnostic value for IBD. Finally, patients had significantly high CRP, ESR and WCC in the active IBD; however, we found the nesfatin-1 strongly correlated only with ESR in the active CD.ConclusionThis is the first study investigating the circulating levels of nesfatin-1 in patients with IBD. Serum nesfatin-1 may serve as an additional inflammatory marker for diagnosis of IBD in affected individuals.

Can We Extrapolate Data from One Immune-Mediated Inflammatory Disease to Another One?

2019 ◽  
Vol 26 (2) ◽  
pp. 248-258 ◽  
Author(s):  
Fernando Magro ◽  
Rosa Coelho ◽  
Armando Peixoto
Keyword(s):  
Rheumatoid Arthritis ◽  
Inflammatory Diseases ◽  
Analytical Techniques ◽  
Approval Process ◽  
Homogeneous Population ◽  
Post Translational Modifications ◽  
Innovator Product ◽  
Immune Mediated ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Immune-mediated inflammatory diseases share several pathogenic pathways and this pushes sometimes to extrapolate from one disease or indication to others. A biosimilar can be defined as a biotherapeutic product which is similar in terms of quality, safety, and efficacy to an already licensed reference biotherapeutic product. We review the substrate for extrapolation, the current approval process for biosimilars and the pioneering studies on biosimilars performed in rheumatoid arthritis patients. A biosimilar has the same amino acid sequence as its innovator product. However, post-translational modifications can occur and the current analytical techniques do not allow the final structure. To test the efficacy in one indication, a homogeneous population should be chosen and immunogenicity features are essential in switching and interchangeability. CT-P13 (Remsima™; Inflectra™) is a biosimilar of reference infliximab (Remicade®). It meets most of the requirements for extrapolation. Nevertheless, in inflammatory bowel diseases (IBD) we need more studies to confirm the postulates of extrapolation from rheumatoid arthritis and ankylosing spondylitis to IBD. Furthermore, an effective pharmacovigilance schedule is mandatory to look for immunogenicity and side effects.

scholarly journals A circadian clock is essential for homeostasis of group 3 innate lymphoid cells in the gut

2019 ◽  
Vol 4 (40) ◽  
pp. eaax1215 ◽  
Author(s):  
Fei Teng ◽  
Jeremy Goc ◽  
Lei Zhou ◽  
Coco Chu ◽  
Manish A. Shah ◽  
...  
Keyword(s):  
Circadian Clock ◽  
Target Genes ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Expression Of Genes ◽  
Microbe Interactions ◽  
Inflammatory Bowel ◽  
Group 3 ◽  
Host Microbe Interactions ◽  
Specific Deletion

Group 3 innate lymphoid cells (ILC3s) critically orchestrate host-microbe interactions in the healthy mammalian intestine and become substantially impaired in the context of inflammatory bowel disease (IBD). However, the molecular pathways controlling the homeostasis of ILC3s remain incompletely defined. Here, we identify that intestinal ILC3s are highly enriched in expression of genes involved in the circadian clock and exhibit diurnal oscillations of these pathways in response to light cues. Classical ILC3 effector functions also exhibited diurnal oscillations, and lineage-specific deletion of BMAL1, a master regulator of the circadian clock, resulted in markedly reduced ILC3s selectively in the intestine. BMAL1-deficient ILC3s exhibit impaired expression of Nr1d1 and Per3, hyperactivation of RORγt-dependent target genes, and elevated proapoptotic pathways. Depletion of the microbiota with antibiotics partially reduced the hyperactivation of BMAL1-deficient ILC3s and restored cellular homeostasis in the intestine. Last, ILC3s isolated from the inflamed intestine of patients with IBD exhibit substantial alterations in expression of several circadian-related genes. Our results collectively define that circadian regulation is essential for the homeostasis of ILC3s in the presence of a complex intestinal microbiota and that this pathway is disrupted in the context of IBD.

scholarly journals Blockade of PLD2 Ameliorates Intestinal Mucosal Inflammation of Inflammatory Bowel Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Guangxi Zhou ◽  
Lin Yu ◽  
Wenjing Yang ◽  
Wei Wu ◽  
Leilei Fang ◽  
...  
Keyword(s):  
Peripheral Blood ◽  
Blood Cells ◽  
Inflammatory Diseases ◽  
Critical Role ◽  
Neutrophil Migration ◽  
Mucosal Inflammation ◽  
Peripheral Blood Cells ◽  
Before And After ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Background. Inflammatory bowel diseases (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), are chronically remittent and progressive inflammatory disorders. Phospholipase D2 (PLD2) is reported to be involved in the pathogenesis of several inflammatory diseases. However, the exact role of PLD2 in IBD is obscure.Methods. PLD2 expression was determined in peripheral blood cells and inflamed mucosa from patients with IBD by qRT-PCR. Colonic biopsies were also obtained from CD patients before and after infliximab (IFX) treatment to examine PLD2 expression. PLD2 selective inhibitor (CAY10594) was administrated daily by oral gavage in DSS-induced colitis mice. Bone marrow neutrophils from colitis mice were harvested to examine the migration using Transwell plate.Results. PLD2 was found to be significantly increased in peripheral blood cells and inflamed mucosa in patients with active IBD. Treatment with IFX could significantly decrease PLD2 expression in intestinal mucosa in patients with CD. Moreover, blockade of PLD2 with CAY10594 could markedly ameliorate DSS-induced colitis in mice and promote neutrophil migration.Conclusions. PLD2 plays a critical role in the pathogenesis of IBD. Blockade of PLD2 may serve as a new therapeutic approach for treatment of IBD.

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