dysbiosis/phosphatase

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Intestinal alkaline phosphatase deficiency leads to dysbiosis and bacterial translocation in the newborn intestine.

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BACKGROUND Intestinal alkaline phosphatase (IAP) has been shown to help maintain intestinal homeostasis. Decreased expression of IAP has been linked with pediatric intestinal diseases associated with bacterial overgrowth and subsequent inflammation. We hypothesize that the absence of IAP leads to

Intestinal alkaline phosphatase prevents antibiotic-induced susceptibility to enteric pathogens.

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OBJECTIVE To determine the efficacy of oral supplementation of the gut enzyme intestinal alkaline phosphatase (IAP) in preventing antibiotic-associated infections from Salmonella enterica serovar Typhimurium (S. Typhimurium) and Clostridium difficile. BACKGROUND The intestinal microbiota plays a

Supplementation with brush border enzyme alkaline phosphatase slows aging.

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Diminished integrity of the intestinal epithelial barrier with advanced age is believed to contribute to aging-associated dysfunction and pathologies in animals. In mammals, diminished gut integrity contributes to inflammaging, the increase in inflammatory processes observed in old age. Recent work

Alternative therapy in prevention of experimental and clinical inflammatory bowel disease. Impact of regular physical activity, intestinal alkaline phosphatase and herbal products.

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Inflammatory bowel diseases (IBD), such as ulcerative colitis and Crohn's disease, are multifactorial, chronic, disabling, and progressive diseases characterised by cyclical nature, alternating between active and quiescent states. While the aetiology of IBD is not fully understood, this complex of

Tissue hypoxia and intestinal dysbiosis in children with tuberculosis.

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We studied the role of autochthonous microflora from body cavities in the development of tissue hypoxia and instability of cell membranes. In children with tuberculosis dysbiosis manifested in nonspecific quantitative changes in the intestinal microflora and the presence of coxsackievirus antigens

[Biological properties of opportunistic enterobacteria isolated from healthy persons and from patients with intestinal dysbacteriosis].

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The comparative study of the signs of pathogenicity in 724 enterobacterial strains and in some species of nonfermenting microorganisms isolated from the feces of 115 somatic patients with intestinal dysbacteriosis and 80 healthy persons (565 strains) has revealed that microorganisms belonging to the

SHP-2 Phosphatase Prevents Colonic Inflammation by Controlling Secretory Cell Differentiation and Maintaining Host-Microbiota Homeostasis.

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Polymorphisms in the PTPN11 gene encoding for the tyrosine phosphatase SHP-2 were described in patients with ulcerative colitis. We have recently demonstrated that mice with an intestinal epithelial cell-specific deletion of SHP-2 (SHP-2(IEC-KO) ) develop severe colitis 1 month after birth. However,

Protein tyrosine phosphatase non-receptor type 22 modulates colitis in a microbiota-dependent manner.

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The gut microbiota is crucial for our health, and well-balanced interactions between the host's immune system and the microbiota are essential to prevent chronic intestinal inflammation, as observed in inflammatory bowel diseases (IBD). A variant in protein tyrosine phosphatase non-receptor type 22

Porphyromonas gingivalis lipid A phosphatase activity is critical for colonization and increasing the commensal load in the rabbit ligature model.

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Periodontitis is a disease of polymicrobial etiology characterized by inflammation, degradation of host tissue, and bone that irreversibly destroys the supporting apparatus of teeth. Porphyromonas gingivalis contains lipid A with structural heterogeneity that has been postulated to contribute to the

Influence of different probiotic lactic Acid bacteria on microbiota and metabolism of rats with dysbiosis.

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Lactic acid bacteria (LAB) are often used for prevention and treatment of dysbiosis. However, the action of various strains of LAB on metabolism and digestion under these conditions are poorly understood. The purpose of this study was to investigate the influence of probiotic LAB on metabolism,

Intestinal alkaline phosphatase preserves the normal homeostasis of gut microbiota.

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OBJECTIVE The intestinal microbiota plays a critical role in maintaining human health; however, the mechanisms governing the normal homeostatic number and composition of these microbes are largely unknown. Previously it was shown that intestinal alkaline phosphatase (IAP), a small intestinal brush

Loss of Intestinal Alkaline Phosphatase Leads to Distinct Chronic Changes in Bone Phenotype.

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BACKGROUND The gut is becoming increasingly recognized as the source of various systemic diseases, and recently, it has been linked to bone metabolism via the so-called gut-bone axis. The microbiome and gut-derived mediators are thought to impact upon bone metabolism, and administration of

Multisystemic functions of alkaline phosphatases.

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Human and mouse alkaline phosphatases (AP) are encoded by a multigene family expressed ubiquitously in multiple tissues. Gene knockout (KO) findings have helped define some of the precise exocytic functions of individual isozymes in bone, teeth, the central nervous system, and in the gut. For

PTPN2 controls differentiation of CD4⁺ T cells and limits intestinal inflammation and intestinal dysbiosis.

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Loss-of-function variants within the gene locus encoding protein tyrosine phosphatase non-receptor type 2 (PTPN2) are associated with increased risk for Crohn's disease (CD). A disturbed regulation of T helper (Th) cell responses causing loss of tolerance against self- or commensal-derived antigens

Intestinal alkaline phosphatase promotes gut bacterial growth by reducing the concentration of luminal nucleotide triphosphates.

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The intestinal microbiota plays a pivotal role in maintaining human health and well-being. Previously, we have shown that mice deficient in the brush-border enzyme intestinal alkaline phosphatase (IAP) suffer from dysbiosis and that oral IAP supplementation normalizes the gut flora. Here we aimed to

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