Adherent‐invasive <i>Escherichia coli</i> (AIEC): Cause or consequence of inflammation, dysbiosis, and rupture of cellular joints in patients with IBD?

Perna, Angelica; Hay, Eleonora; Contieri, Marcella; Luca, Antonio De; Guerra, Germano; Lucariello, Angela

doi:10.1002/jcp.29430

Cited by 28 publications

(23 citation statements)

References 106 publications

(144 reference statements)

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“…Since serine peptidases were often studied as virulence factors, pathogen‐derived proteases have been most investigated for their potential effects in the GI tract 105 . One example of such bacterial species is illustrated by the eminent Escherichia coli 106 . E coli has been widely recognized to be associated with IBD and was highly enriched in patient samples 107‐110 .…”

Section: Gut Microbial Serine Proteasesmentioning

confidence: 99%

Serine proteases at the cutting edge of IBD: Focus on gastrointestinal inflammation

et al. 2020

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Serine proteases have been long recognized to coordinate many physiological processes and play key roles in regulating the inflammatory response. Accordingly, their dysregulation has been regularly associated with several inflammatory disorders and suggested as a central mechanism in the pathophysiology of digestive inflammation. So far, studies addressing the proteolytic homeostasis in the gut have mainly focused on host serine proteases as candidates of interest, while largely ignoring the potential contribution of their bacterial counterparts. The human gut microbiota comprises a complex ecosystem that contributes to host health and disease. Yet, our understanding of microbially produced serine proteases and investigation of whether they are causally linked to IBD is still in its infancy. In this review, we highlight recent advances in the emerging roles of host and bacterial serine proteases in digestive inflammation. We also discuss the application of available tools in the gut to monitor disease‐related serine proteases. An exhaustive representation and understanding of such functional potential would help in closing existing gaps in mechanistic knowledge.

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Section: Gut Microbial Serine Proteasesmentioning

confidence: 99%

Serine proteases at the cutting edge of IBD: Focus on gastrointestinal inflammation

et al. 2020

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“…AIEC has been postulated as a cause of inflammatory bowel disease. However, at present, there is no consensus on this issue (Palmela et al, 2018 ; Perna et al, 2020 ), and the putative virulence factors described as involved in AIEC pathogenesis are common to strains isolated from extraintestinal infections (Martinez-Medina et al, 2009 ; Yang et al, 2017 ). Furthermore, although DAEC is a recognized enteric pathogen and the presence of genes encoding afimbrial adhesins are occasionally used for screening this pathotype, these genes are also present in other intestinal and extraintestinal pathogenic E. coli as well as in commensal strains, limiting their usefulness in defining the DAEC pathotype (Croxen et al, 2013 ).…”

Section: Introductionmentioning

confidence: 99%

Diversity of Hybrid- and Hetero-Pathogenic Escherichia coli and Their Potential Implication in More Severe Diseases

Santos¹,

Santos²,

Silva³

et al. 2020

Front. Cell. Infect. Microbiol.

112

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Although extraintestinal pathogenic Escherichia coli (ExPEC) are designated by their isolation site and grouped based on the type of host and the disease they cause, most diarrheagenic E. coli (DEC) are subdivided into several pathotypes based on the presence of specific virulence traits directly related to disease development. This scenario of a well-categorized E. coli collapsed after the German outbreak of 2011, caused by one strain bearing the virulence factors of two different DEC pathotypes (enteroaggregative E. coli and Shiga toxin-producing E. coli ). Since the outbreak, many studies have shown that this phenomenon is more frequent than previously realized. Therefore, the terms hybrid- and hetero-pathogenic E. coli have been coined to describe new combinations of virulence factors among the classic E. coli pathotypes. In this review, we provide an overview of these classifications and highlight the E. coli genomic plasticity that results in some mixed E. coli pathotypes displaying novel pathogenic strategies, which lead to a new symptomatology related to E. coli diseases. In addition, as the capacity for genome interrogation has grown in the last few years, it is clear that genes encoding some virulence factors, such as Shiga toxin, are found among different E. coli pathotypes to which they have not traditionally been associated, perhaps foreshowing their emergence in new and severe outbreaks caused by such hybrid strains. Therefore, further studies regarding hetero-pathogenic and hybrid-pathogenic E. coli isolates are necessary to better understand and control the spread of these pathogens.

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“…The improvement of anti-inflammatory status has been reported to be followed by the increase in the abundance of Prevotella [26]. Intestinal barrier injury is closely associated with numerous factors, such as bacterial infection, inflammation, and mechanical damage; all of which can be caused by Helicobacter and Escherichia_Shigella infection [27,28]. Thus, picroside II treatment may ameliorate intestinal barrier injury by improving the proportion of gut microbiota.…”

mentioning

confidence: 99%

Picroside II Improves Severe Acute Pancreatitis-Induced Intestinal Barrier Injury by Inactivating Oxidative and Inflammatory TLR4-Dependent PI3K/AKT/NF-κB Signaling and Improving Gut Microbiota

Piao¹,

Liu

Sui

et al. 2020

Oxidative Medicine and Cellular Longevity

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Background. Picroside II exerts anti-inflammatory and antidiarrheal effects for treating the diseases associated with oxidative injury. However, its function on pancreatitis-induced intestinal barrier injury remains unclear. Hypothesis/Purpose. We hypothesized that picroside II will have protective effects against pancreatitis-induced intestinal barrier injury by affecting oxidative and inflammatory signaling (Toll-like receptor 4- (TLR4-) dependent phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT), and nuclear factor kappa B (NF-κB)). Study Design and Methods. A Sprague-Dawley (SD) rat model with severe acute pancreatitis (SAP) was induced via the injection of sodium taurocholate (4% wt/vol; 1 mL/kg). All rats were divided into 3 groups: sham (CG), SAP-induced intestinal barrier injury (MG), and picroside II (PG) groups. Intestinal barrier injury was assessed by scanning electron microscopy (SEM), hematoxylin and eosin staining, and pathological scores. We measured the levels of pancreatitis biomarkers (amylase and lipase), oxidative and inflammatory signaling (TLR4-dependent PI3K/AKT/NF-κB), oxidative stress marker (superoxidase dismutase (SOD), catalase (CAT), glutathione peroxidases (GPx), and malondialdehyde), and inflammatory markers (tumor necrosis factor α (TNFα), interleukin- (IL-) 1, IL-6, and IL-10) in serum and/or gut tissues. Gut microbiota composition in feces was measured by using 16S rRNA sequencing. Results. SEM showed that intestinal barrier injury was caused with the loss of intestinal villi and mitochondria destruction, and pathological scores were increased in the MG group. The levels of amylase, lipase, malondialdehyde, TNFα, IL-1, IL-6, TLR4, PI3K, AKT, and NF-κB were increased, and the levels of SOD, GPx, CAT, and IL-10 was reduced in the MG group when compared with CG group (P<0.05). Picroside II treatment inhibited the symptoms in the MG group and showed antioxidant and anti-inflammatory activities. The serum levels of picroside II had strong correlation with the levels of inflammatory and oxidative stress biomarkers (P<0.05). Picroside II treatment increased the proportion of Lactobacillus and Prevotella and decreased the proportion of Helicobacter and Escherichia_Shigella in the model. Conclusions. Picroside II improved the SAP-induced intestinal barrier injury in the rat model by inactivating oxidant and inflammatory signaling and improving gut microbiota.

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Adherent‐invasive Escherichia coli (AIEC): Cause or consequence of inflammation, dysbiosis, and rupture of cellular joints in patients with IBD?

Cited by 28 publications

References 106 publications

Serine proteases at the cutting edge of IBD: Focus on gastrointestinal inflammation

Serine proteases at the cutting edge of IBD: Focus on gastrointestinal inflammation

Diversity of Hybrid- and Hetero-Pathogenic Escherichia coli and Their Potential Implication in More Severe Diseases

Picroside II Improves Severe Acute Pancreatitis-Induced Intestinal Barrier Injury by Inactivating Oxidative and Inflammatory TLR4-Dependent PI3K/AKT/NF-κB Signaling and Improving Gut Microbiota

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