Iron and Malaria: Absorption, Efficacy and Safety

2010 ◽  
Vol 80 (45) ◽  
pp. 279-292 ◽  
Author(s):  
Richard Hurrell
Keyword(s):  
Pathogenic Bacteria ◽  
Intestinal Barrier ◽  
Systemic Circulation ◽  
Malarial Parasite ◽  
Asymptomatic Malaria ◽  
Iron Supplements ◽  
Fortified Food ◽  
Care Giving ◽  
Single Meal ◽  
Women And Children

Febrile malaria and asymptomatic malaria parasitemia substantially decrease iron absorption in single-meal, stable isotope studies in women and children, but to date there is no evidence of decreased efficacy of iron-fortified foods in malaria-endemic regions. Without inadequate malarial surveillance or health care, giving iron supplements to children in areas of high transmission could increase morbidity and mortality. The most likely explanation is the appearance of non-transferrin-bound iron (NTBI) in the plasma. NTBI forms when the rate of iron influx into the plasma exceeds the rate of iron binding to transferrin. Two studies in women have reported substantially increased NTBI with the ingestion of iron supplements. Our studies confirm this, but found no significant increase in NTBI on consumption of iron-fortified food. It seems likely that the malarial parasite in hepatocytes can utilize NTBI, but it cannot do so in infected erythrocytes. NTBI however may increase the sequestration of parasite-infected erythrocytes in capillaries. Bacteremia is common in children with severe malaria and sequestration in villi capillaries could lead to a breaching of the intestinal barrier, allowing the passage of pathogenic bacteria into the systemic circulation. This is especially important as frequent high iron doses increase the number of pathogens in the intestine at the expense of the barrier bacteria.

scholarly journals Leaky Gut: Effect of Dietary Fiber and Fats on Microbiome and Intestinal Barrier

2021 ◽  
Vol 22 (14) ◽  
pp. 7613
Author(s):  
Haruki Usuda ◽  
Takayuki Okamoto ◽  
Koichiro Wada
Keyword(s):  
Intestinal Permeability ◽  
Intestinal Tract ◽  
Inflammatory Diseases ◽  
Intestinal Barrier ◽  
Short Chain Fatty Acids ◽  
Systemic Circulation ◽  
Mucosal Tissue ◽  
Leaky Gut ◽  
Exogenous Factors ◽  
Intestinal Barrier Integrity

Intestinal tract is the boundary that prevents harmful molecules from invading into the mucosal tissue, followed by systemic circulation. Intestinal permeability is an index for intestinal barrier integrity. Intestinal permeability has been shown to increase in various diseases—not only intestinal inflammatory diseases, but also systemic diseases, including diabetes, chronic kidney dysfunction, cancer, and cardiovascular diseases. Chronic increase of intestinal permeability is termed ‘leaky gut’ which is observed in the patients and animal models of these diseases. This state often correlates with the disease state. In addition, recent studies have revealed that gut microbiota affects intestinal and systemic heath conditions via their metabolite, especially short-chain fatty acids and lipopolysaccharides, which can trigger leaky gut. The etiology of leaky gut is still unknown; however, recent studies have uncovered exogenous factors that can modulate intestinal permeability. Nutrients are closely related to intestinal health and permeability that are actively investigated as a hot topic of scientific research. Here, we will review the effect of nutrients on intestinal permeability and microbiome for a better understanding of leaky gut and a possible mechanism of increase in intestinal permeability.

scholarly journals Procoagulatory State in Inflammatory Bowel Diseases Is Promoted by Impaired Intestinal Barrier Function

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Luca Pastorelli ◽  
Elena Dozio ◽  
Laura Francesca Pisani ◽  
Massimo Boscolo-Anzoletti ◽  
Elena Vianello ◽  
...  
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Intestinal Barrier ◽  
Systemic Circulation ◽  
Intestinal Barrier Function ◽  
Inflammatory Conditions ◽  
Immune Mediated ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Molecular Patterns ◽  
D Dimer

Inflammatory and immune mediated disorders are risk factors for arterial and venous thromboembolism. Inflammatory bowel diseases (IBD) confer an even greater risk of thromboembolic events than other inflammatory conditions. It has been shown that IBD patients display defective intestinal barrier functions. Thus, pathogen-associated molecular patterns (PAMPs) coming from the intestinal bacterial burden might reach systemic circulation and activate innate immunity receptors on endothelial cells and platelets, promoting a procoagulative state. Aim of the study was to test this hypothesis, correlating the presence of circulating PAMPs with the activation of innate immune system and the activation of the coagulatory cascade in IBD patients. Specifically, we studied lipopolysaccharide (LPS), Toll-like receptor (TLR) 2, TLR4, and markers of activated coagulation (i.e., D-Dimer and prothrombin fragmentF1+2) in the serum and plasma of IBD patients. We found that LPS levels are increased in IBD and correlate with TLR4 concentrations; although a mild correlation between LPS and CRP levels was detected, clinical disease activity does not appear to influence circulating LPS. Instead, serum LPS correlates with both D-Dimer andF1+2measurements. Taken together, our data support the role of an impairment of intestinal barrier in triggering the activation of the coagulatory cascade in IBD.

scholarly journals Emerging evidence for associations between periodontitis and the development of Alzheimer’s disease

2014 ◽  
Vol 5 (1) ◽  
pp. 38-42 ◽  
Author(s):  
Sophie Poole ◽  
Sim K Singhrao ◽  
St John Crean
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Immune Responses ◽  
Periodontal Disease ◽  
Potential Risk ◽  
Inflammatory Disease ◽  
Pathogenic Bacteria ◽  
Late Onset ◽  
Systemic Circulation

Periodontal disease (PD) is an inflammatory disease affecting tooth-supporting tissues in which interaction of specific bacteria and the host’s immune responses play a pivotal role. The pathogenic bacteria associated with PD are a source of systemic inflammation as they have the ability to enter systemic circulation during everyday tasks such as brushing teeth and chewing food. Alzheimer’s disease (AD) is a form of dementia whereby inflammation is thought to play a key role in its pathogenesis and the risk of developing the disease increasing with age. The exact aetiology of the late-onset AD is unknown but peripheral infections are being considered as a potential risk factor.

scholarly journals Microbial Signature in Adipose Tissue of Crohn’s Disease Patients

2020 ◽  
Vol 9 (8) ◽  
pp. 2448
Author(s):  
Carolina Serena ◽  
Maribel Queipo-Ortuño ◽  
Monica Millan ◽  
Lidia Sanchez-Alcoholado ◽  
Aleidis Caro ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Pathogenic Bacteria ◽  
Sulfur Metabolism ◽  
Clinical Status ◽  
Subcutaneous Fat ◽  
Intestinal Barrier ◽  
Fecal Calprotectin ◽  
Inactive Disease

Crohn’s disease (CD) is characterized by compromised immune tolerance to the intestinal commensal microbiota, intestinal barrier inflammation, and hyperplasia of creeping fat (CF) and mesenteric adipose tissue (AT), which seems to be directly related to disease activity. Gut microbiota dysbiosis might be a determining factor in CD etiology, manifesting as a low microbial diversity and a high abundance of potentially pathogenic bacteria. We tested the hypothesis that CF is a reservoir of bacteria through 16S-rRNA sequencing of several AT depots of patients with active and inactive disease and controls. We found a microbiome signature within CF and mesenteric AT from patients, but not in subcutaneous fat. We failed to detect bacterial DNA in any fat depot of controls. Proteobacteria was the most abundant phylum in both CF and mesenteric AT, and positively correlated with fecal calprotectin/C-reactive protein. Notably, the clinical status of patients seemed to be related to the microbiome signature, as those with the inactive disease showed a reduction in the abundance of pathogenic bacteria. Predictive functional profiling revealed many metabolic pathways including lipopolysaccharide biosynthesis and sulfur metabolism overrepresented in active CD relative to that in inactive CD. Our findings demonstrate that microbiota dysbiosis associated with CD pathophysiology is reflected in AT and might contribute to disease severity.

scholarly journals Gut Microbial Translocation in Critically Ill Children and Effects of Supplementation with Pre- and Pro Biotics

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Paola Papoff ◽  
Giancarlo Ceccarelli ◽  
Gabriella d'Ettorre ◽  
Carla Cerasaro ◽  
Elena Caresta ◽  
...  
Keyword(s):  
Critical Illness ◽  
Critically Ill ◽  
Bacterial Translocation ◽  
Ischemia Reperfusion ◽  
Intestinal Barrier ◽  
Systemic Circulation ◽  
Critically Ill Children ◽  
Positive Effects ◽  
Increased Risk ◽  
Abdominal Hypertension

Bacterial translocation as a direct cause of sepsis is an attractive hypothesis that presupposes that in specific situations bacteria cross the intestinal barrier, enter the systemic circulation, and cause a systemic inflammatory response syndrome. Critically ill children are at increased risk for bacterial translocation, particularly in the early postnatal age. Predisposing factors include intestinal obstruction, obstructive jaundice, intra-abdominal hypertension, intestinal ischemia/reperfusion injury and secondary ileus, and immaturity of the intestinal barrier per se. Despite good evidence from experimental studies to support the theory of bacterial translocation as a cause of sepsis, there is little evidence in human studies to confirm that translocation is directly correlated to bloodstream infections in critically ill children. This paper provides an overview of the gut microflora and its significance, a focus on the mechanisms employed by bacteria to gain access to the systemic circulation, and how critical illness creates a hostile environment in the gut and alters the microflora favoring the growth of pathogens that promote bacterial translocation. It also covers treatment with pre- and pro biotics during critical illness to restore the balance of microbial communities in a beneficial way with positive effects on intestinal permeability and bacterial translocation.

scholarly journals Contributions of microbiome and mechanical deformation to intestinal bacterial overgrowth and inflammation in a human gut-on-a-chip

2015 ◽  
Vol 113 (1) ◽  
pp. E7-E15 ◽  
Author(s):  
Hyun Jung Kim ◽  
Hu Li ◽  
James J. Collins ◽  
Donald E. Ingber
Keyword(s):  
Epithelial Cells ◽  
Pathogenic Bacteria ◽  
Intestinal Inflammation ◽  
Bacterial Overgrowth ◽  
Intestinal Barrier ◽  
Inflammatory Cells ◽  
Intestinal Barrier Function ◽  
Human Gut ◽  
Intestinal Bacterial Overgrowth

A human gut-on-a-chip microdevice was used to coculture multiple commensal microbes in contact with living human intestinal epithelial cells for more than a week in vitro and to analyze how gut microbiome, inflammatory cells, and peristalsis-associated mechanical deformations independently contribute to intestinal bacterial overgrowth and inflammation. This in vitro model replicated results from past animal and human studies, including demonstration that probiotic and antibiotic therapies can suppress villus injury induced by pathogenic bacteria. By ceasing peristalsis-like motions while maintaining luminal flow, lack of epithelial deformation was shown to trigger bacterial overgrowth similar to that observed in patients with ileus and inflammatory bowel disease. Analysis of intestinal inflammation on-chip revealed that immune cells and lipopolysaccharide endotoxin together stimulate epithelial cells to produce four proinflammatory cytokines (IL-8, IL-6, IL-1β, and TNF-α) that are necessary and sufficient to induce villus injury and compromise intestinal barrier function. Thus, this human gut-on-a-chip can be used to analyze contributions of microbiome to intestinal pathophysiology and dissect disease mechanisms in a controlled manner that is not possible using existing in vitro systems or animal models.

scholarly journals Intestinal Barrier Dysfunction, LPS Translocation, and Disease Development

2020 ◽  
Vol 4 (2) ◽  
Author(s):  
Siddhartha S Ghosh ◽  
Jing Wang ◽  
Paul J Yannie ◽  
Shobha Ghosh
Keyword(s):  
Barrier Function ◽  
Current Knowledge ◽  
Intestinal Barrier ◽  
Systemic Circulation ◽  
Intestinal Barrier Function ◽  
Disease Development ◽  
Barrier Dysfunction ◽  
Intestinal Alkaline Phosphatase ◽  
Targeted Interventions ◽  
Associated Diseases

Abstract The intestinal barrier is complex and consists of multiple layers, and it provides a physical and functional barrier to the transport of luminal contents to systemic circulation. While the epithelial cell layer and the outer/inner mucin layer constitute the physical barrier and are often referred to as the intestinal barrier, intestinal alkaline phosphatase (IAP) produced by epithelial cells and antibacterial proteins secreted by Panneth cells represent the functional barrier. While antibacterial proteins play an important role in the host defense against gut microbes, IAP detoxifies bacterial endotoxin lipopolysaccharide (LPS) by catalyzing the dephosphorylation of the active/toxic Lipid A moiety, preventing local inflammation as well as the translocation of active LPS into systemic circulation. The causal relationship between circulating LPS levels and the development of multiple diseases underscores the importance of detailed examination of changes in the “layers” of the intestinal barrier associated with disease development and how this dysfunction can be attenuated by targeted interventions. To develop targeted therapies for improving intestinal barrier function, it is imperative to have a deeper understanding of the intestinal barrier itself, the mechanisms underlying the development of diseases due to barrier dysfunction (eg, high circulating LPS levels), the assessment of intestinal barrier function under diseased conditions, and of how individual layers of the intestinal barrier can be beneficially modulated to potentially attenuate the development of associated diseases. This review summarizes the current knowledge of the composition of the intestinal barrier and its assessment and modulation for the development of potential therapies for barrier dysfunction-associated diseases.

Selective enrichment of commensal gut bacteria protects againstCitrobacter rodentium-induced colitis

2015 ◽  
Vol 309 (3) ◽  
pp. G181-G192 ◽  
Author(s):  
Linda Vong ◽  
Lee J. Pinnell ◽  
Pekka Määttänen ◽  
C. William Yeung ◽  
Eberhard Lurz ◽  
...  
Keyword(s):  
Pathogenic Bacteria ◽  
Intestinal Barrier ◽  
Gut Bacteria ◽  
Enterohemorrhagic Escherichia Coli ◽  
Host Immune System ◽  
Citrobacter Rodentium ◽  
Bacterial Strains ◽  
Microbial Composition ◽  
Selective Enrichment ◽  
Intestinal Pathogens

The intestinal microbiota plays a key role in shaping the host immune system. Perturbation of gut microbial composition, termed dysbiosis, is associated with an increased susceptibility to intestinal pathogens and is a hallmark of a number of inflammatory, metabolic, and infectious diseases. The prospect of mining the commensal gut microbiota for bacterial strains that can impact immune function represents an attractive strategy to counteract dysbiosis and resulting disease. In this study, we show that selective enrichment of commensal gut lactobacilli protects against the murine pathogen Citrobacter rodentium, a well-characterized model of enteropathogenic and enterohemorrhagic Escherichia coli infection. The lactobacilli-enriched bacterial culture prevented the expansion of Gammaproteobacteria and Actinobacteria and was associated with improved indexes of epithelial barrier function (dextran flux), transmissible crypt hyperplasia, and tissue inflammatory cytokine levels. Moreover, cultivation of gut bacteria from Citrobacter rodentium-infected mice reveals the differential capacity of bacterial subsets to mobilize neutrophil oxidative burst and initiate the formation of weblike neutrophil extracellular traps. Our findings highlight the beneficial effects of a lactobacilli -enriched commensal gut microenvironment and, in the context of an intestinal barrier breach, the ability of neutrophils to immobilize both commensal and pathogenic bacteria.

scholarly journals Prevalence of β-Lactamase Production among Pathogenic Bacteria Isolated from Surgical Site and Wound Infection amoung Patients Admitted in some selected Hospitals in Sokoto Metropolis, Nigeria

2014 ◽  
Vol 3 (3) ◽  
pp. 104-112
Author(s):  
UK Muhammad ◽  
TM Adamu ◽  
Z Binji ◽  
MA Isa
Keyword(s):  
Staphylococcus Aureus ◽  
Antimicrobial Resistance ◽  
Wound Infection ◽  
Proteus Mirabilis ◽  
Pathogenic Bacteria ◽  
Resistant Bacteria ◽  
Beta Lactamase ◽  
Penicillin Binding Proteins ◽  
Lactam Ring ◽  
Women And Children

Antimicrobial resistance among pathogenic bacteria is increasing worldwide especially against ß-lactam drugs, due to the production of ß-lactamase enzymes which destroy the ß-lactam ring of these antibiotics, thus preventing the action of penicillin binding proteins (PBPs). The prevalence of β-lactamase producing bacteria among patients admitted in three different hospitals were carried out in this study. The results of this study shows that out of one hundred and fifty one isolates obtained in three different hospitals in Sokoto metropolis, only 82 (54.0%) were resistant to the antibiotics tested. These include 42 (51.2%) were isolated in Usmanu Danfodiyo Teaching Hospital (UDUT), 26 (31.7%) were isolated from Specialist Hospital Sokoto (S.H.S) and 14 (17.1%) were isolated from Maryam Abatcha Women and Children Hospital (MAWCH) which has the least number of occurrence of the resistant isolates. β-lactamase test was carried out on the resistant isolates show s that out of the 82 isolates found resistant to the antibiotics tested, about 60 (73.2%) were β- lactamase positive and the remaining 22 (26.8%) were β-lactamase negative. Staphylococcus aureus has the highest resistant bacteria producing β-lactamase enzyme with 22 isolates, followed by Proteus mirabilis with 10 isolates. DOI: http://dx.doi.org/10.3126/ije.v3i3.11067 International Journal of Environment Vol.3(3) 2014: 89-112

scholarly journals Phenazines Modulate Gastrointestinal Metabolism and Microbiota

2021 ◽  
Author(s):  
Wenjing Peng ◽  
Hui Li ◽  
Xiaole Zhao ◽  
Bing Shao ◽  
Kui Zhu
Keyword(s):  
Gut Microbiota ◽  
Digestive Tract ◽  
Metabolic Disorder ◽  
Rational Design ◽  
Pathogenic Bacteria ◽  
Intestinal Barrier ◽  
Swine Model ◽  
Structural Skeleton ◽  
Gut Microbiota Dysbiosis

Abstract Background: Natural and synthetic phenazines are ubiquitously occurred in environment and have been used for various therapeutic purposes in human, animals and agriculture, and the widespread use makes residue problem in environment and foods increasingly serious. However, the metabolic and comprehensive impacts of phenazines on the digestive tract are poorly understood, particularly the microbial pyocyanin (PYO), the most representative phenazines produced by Pseudomonas . Here, we utilized PYO as the representative of phenazines to study the effects on digestive tract. Results: Metabolic kinetic analysis showed that PYO exhibited low oral bioavailability in both rats and swine model, revealing a restriction of PYO in gut and might cause impacts on digestive tract. PYO was subsequently found to induce intestinal barrier destruction including inflammation and reactive oxygen species (ROS) accumulation in duodenum. Microbiome analysis showed that PYO caused gut microbiota dysbiosis by decreasing the symbiotic bacteria and increasing the opportunistic pathogenic bacteria. Additionally, the integral and dysfunctional assessment of liver demonstrated that PYO induced liver inflammation and metabolic disorder. Metabolism analysis further confirmed that PYO could be metabolized by both gut microbiota and liver, and all metabolites retained the nitrogen-containing tricyclic structural skeleton of phenazines, which was the core bioactivity of phenazine compounds, indicating all the outcomes were due to the intrinsic characteristic of phenazine structure. Conclusions: PYO were low oral bioavailable and all the metabolites retained the nitrogen-containing tricyclic structural skeleton, final resulting in the damages to digestive tract including intestinal barrier destruction, gut microbiota dysbiosis, liver damages and metabolic disorder. These findings elucidated the effect of phenazines on digestive tract in vivo and shed light on the rational design of phenazines for the development and application of such compounds in future.

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