Impact of the Gut Microbiota on Intestinal Immunity Mediated by Tryptophan Metabolism

Gao, Jing; Xu, Kang; Liu, Hongnan; Liu, Gang; Bai, Miaomiao; Peng, Can; Li, Tiejun; Yin, Yulong

doi:10.3389/fcimb.2018.00013

Cited by 864 publications

(783 citation statements)

References 212 publications

(305 reference statements)

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“…Trp is an essential amino acid involved in several important functions, mostly connected with the host-microbiome interaction. As a fraction of Trp is known to be metabolised into indole by the gut microbiota 37 , our results show that this process mainly happens in TI and TC ( Figure 4C).…”

Section: Intrigued By the High Bacteroides Enrichment In All Biopsy Mmentioning

confidence: 65%

Compositional and functional differences of the mucosal microbiota along the intestine of healthy individuals

Vaga

Lee

et al. 2019

Preprint

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Gut mucosal microbes evolved closest to the host, developing specialized local communities. There is, however, insufficient knowledge of these communities as most studies have employed sequencing technologies to investigate faecal microbiota. This work used shotgun metagenomics of mucosal biopsies to explore the microbial communities compositions of terminal ileum and large intestine in 5 healthy individuals. Functional annotations and genome-scale metabolic modelling of selected species were then employed to identify local functional enrichments. While faecal metagenomics provided a good approximation of the average gut microbiome composition, mucosal biopsies allowed detecting the subtle variations of local microbial communities. Given their significant enrichment in the mucosal microbiota, we highlight the roles of Bacteroides species and describe the antimicrobial resistance biogeography along the intestine. We also detail which species, at which locations, are involved with the tryptophan/indole pathway, whose malfunctioning has been linked to pathologies including inflammatory bowel disease. Our study thus provides invaluable resources for investigating mechanisms connecting gut microbiota and host pathophysiology.

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Section: Intrigued By the High Bacteroides Enrichment In All Biopsy Mmentioning

confidence: 65%

Compositional and functional differences of the mucosal microbiota along the intestine of healthy individuals

Vaga

Lee

et al. 2019

Preprint

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“…As a nutrient enhancer, Trp and its metabolites play crucial roles in gut microbiota maintenance, microbial metabolism, the host's immune system, the host-microbiome interface, and host immune system-intestinal microbiota interactions. [58]. Thus, supplementation with Trp or nicotinamide may regulate the gut microbiome and increase antimicrobial peptides to convert SARS-CoV-2-induced lesions in the intestine and further improve systemic conditions.…”

Section: Supplementation Of Essential Amino Acidsmentioning

confidence: 99%

ACE2: The key Molecule for Understanding the Pathophysiology of Severe and Critical Conditions of COVID-19: Demon or Angel?

Xiao

Sakagami

Miwa

2020

Viruses

166

177

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Recently, the SARS-CoV-2 induced disease COVID-19 has spread all over the world. Nearly 20% of the patients have severe or critical conditions. SARS-CoV-2 exploits ACE2 for host cell entry. ACE2 plays an essential role in the renin-angiotensin-aldosterone system (RAAS), which regulates blood pressure and fluid balance. ACE2 also protects organs from inflammatory injuries and regulates intestinal functions. ACE2 can be shed by two proteases, ADAM17 and TMPRSS2. TMPRSS2-cleaved ACE2 allows SARS-CoV-2 cell entry, whereas ADAM17-cleaved ACE2 offers protection to organs. SARS-CoV-2 infection-caused ACE2 dysfunction worsens COVID-19 and could initiate multi-organ failure. Here, we will explain the role of ACE2 in the pathogenesis of severe and critical conditions of COVID-19 and discuss auspicious strategies for controlling the disease.Viruses 2020, 12, 491 2 of 10 Profile of ACE2Human angiotensin-converting enzyme-related carboxypeptidase ACE2 is encoded by the ACE2 gene which maps to chromosome Xp22 [6]. ACE2 is a type I transmembrane protein, comprised of an extracellular heavily N-glycosylated N-terminal domain containing the carboxypeptidase site and a short intracellular C-terminal cytoplasmic tail [7]. The N-terminal peptidase domain is also the SARS-CoV binding site [8]. There are two forms of ACE2 protein: cellular (membrane-bound) form and circulating (soluble) form. Cellular ACE2 protein is the full-length protein which is expressed abundantly in pneumocytes and enterocytes of the small intestine [9]. ACE2 is also expressed in vascular endothelial cells of the heart, the kidneys, and other organs, such as the brain. However, ACE2 is absent in the spleen, thymus, lymph nodes, bone marrow, and cells of the immune system (including B and T lymphocytes, and macrophages) [10,11].Circulating ACE2 (with the N-terminal peptidase domain) is cleaved from the full-length ACE2 on the cell membrane by the metalloprotease ADAM17 and then released into the extracellular environment [7]. The type II transmembrane serine protease, TMPRSS2 was found to compete with ADAM17 for ACE2 shedding but cleaves ACE2 differently. Both ADAM17 and TMPRSS2 remove a short C-terminal fragment from ACE2. Arginine and lysine residues within amino acids 652 to 659 are critical for ADAM17 shedding, whereas arginine and lysine residues within amino acids 697 to 716 are essential for TMPRSS2 shedding. Only cleavage by TMPRSS2 results in augmented SARS-CoV cell entry [12][13][14][15]. There are two ways for SARS-CoV to enter the target cell: endocytosis, and fusion of the viral membrane with a membrane of the target cell, which is 100 times more efficient than endocytosis for viral replication [16]. With the help of TMPRSS2, ADAM17-regulated ectodomain shedding of ACE2 could induce SARS-CoV cell entry through endocytosis [7,12]; however, ADAM17 activity is not required for SARS-CoV cell entry through fusion [12]. As the N-terminal domain is the coronavirus binding site, circulating ACE2 also binds to the virus. Iwata-Yoshikawa et al. infected both ...

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“…Microbiota can also produce specific neurotransmitter and neuromodulator compounds (Holzer & Farzi, 2014). Serotonin or 5-hydroxytryptamine (5-HT) can be produced by several genera of bacteria including Streptococcus, Escherichia, and Enterococcus (Cryan & Dinan, 2012;Yano et al, 2015) or generated through the precursor tryptophan (Gao et al, 2018). Brain 5-HT is involved in the serotonergic neurotransmission pathways regulating mood and cognition (Wrase, Reimold, Puls, Kienast, & Heinz, 2006).…”

Section: Potential Mechanistic Pathwaysmentioning

confidence: 99%

Connection between gut microbiome and brain development in preterm infants

Lü

Claud

2018

Developmental Psychobiology

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Dysbiosis of the gut microbiome in preterm infants predisposes the neonate to various major morbidities including neonatal necrotizing enterocolitis and sepsis in the neonatal intensive care unit, and adverse neurological outcomes later in life. There are parallel early developmental windows for the gut microbiota and the nervous system during prenatal to postnatal of life. Therefore, preterm infants represent a unique population in which optimization of initial colonization and microbiota development can affect brain development and enhance neurological outcomes. In this review, we will first discuss the factors affecting the assembly of neonatal gut microbiota and the contribution of dysbiosis in preterm infants to neuroinflammation and neurodevelopmental disorders. We then will discuss the emerging pathways connecting the gut microbiome and brain development. Further we will discuss the significance of current models for alteration of the gut microbiome (including humanized gnotobiotic models and exposure to antibiotics) to brain development and functions. Understanding the role of early optimization of the microbiome in brain development is of paramount importance for developing microbiome‐targeted therapies and protecting infants from prematurity‐related neurodevelopmental diseases.

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Impact of the Gut Microbiota on Intestinal Immunity Mediated by Tryptophan Metabolism

Cited by 864 publications

References 212 publications

Compositional and functional differences of the mucosal microbiota along the intestine of healthy individuals

Compositional and functional differences of the mucosal microbiota along the intestine of healthy individuals

ACE2: The key Molecule for Understanding the Pathophysiology of Severe and Critical Conditions of COVID-19: Demon or Angel?

Connection between gut microbiome and brain development in preterm infants

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