Serum Intestinal Fatty Acid Binding Protein Research Articles

Indirect Markers of Intestinal Damage in IgA Nephropathy

Introduction: Presence of subclinical intestinal inflammation has repeatedly been shown in IgA nephropathy (IgAN) and the degree of histological inflammation has correlated with abnormal urinary findings. There is lack of noninvasive biomarkers evaluating the presence of subclinical intestinal damage in IgAN. We conducted this study hypothesizing that selected biomarkers regarded as indirect markers of intestinal damage could be elevated in IgAN. Methods: Eighty-five primary IgAN patients (median age 55 years, 54% men) participated in this single-center study in Tampere, Finland. None had end-stage kidney disease or previously diagnosed enteropathies. Celiac disease was excluded with serum transglutaminase 2 antibody (TG2Ab) and endomysial antibody tests and inflammatory bowel disease with fecal calprotectin. Intestinal damage was evaluated from sera with analyses of intestinal fatty-acid binding protein (I-FABP), soluble cluster of differentiation molecule 14 (sCD14), and lipopolysaccharide binding protein. Fourteen people suffering from dyspepsia and 15 healthy people served as controls. Results: I-FABP levels among IgAN patients were higher than in the healthy controls (median 830 pg/mL vs. 289 pg/mL, p < 0.001). Also, sCD14 was increased in IgAN patients compared to dyspepsia controls. Although TG2Ab levels were within the normal range among IgAN patients, they were higher than in the healthy controls (median 1.3 U/mL vs. 0.6 U/mL, p < 0.001). Conclusions: Elevated serum levels of I-FABP were present in primary IgAN patients without known enteropathies. Serum I-FABP may indicate the presence of subclinical intestinal damage. These findings encourage further investigation into the role of the intestine in the pathophysiology of IgAN.

Bergapten enhances mitophagy to regulate intestinal barrier and Th17/Treg balance in mice with Crohn's disease-like colitis via PPARγ/NF-κB signaling pathway.

This study aimed to investigate whether bergapten (BG), a furanocoumarin phytohormone, holds promise for Crohn's disease (CD)-like colitis treatment and to preliminarily explore its potential mechanisms. 2,4,6-Trinitrobenzenesufonic acid (TNBS)-treated mice were applied to establish an in vivo research model, and BG was administered with different concentrations. The status of mice in each group was evaluated by disease activity index (DAI), and the severity was evaluated by pathological sections. The intestinal barrier was assessed by measuring in vivo intestinal permeability, peripheral blood intestinal fatty acid-binding protein (I-FABP) levels, epithelial resistance values, and tight junction protein levels. Markers were then used to assess Th17/Treg levels, mitophagy, and the peroxisome proliferator-activated receptor (PPAR)γ/ nuclear factor kappa B (NF-κB) signaling pathway. BG significantly reduced colon tissue damage in a concentration-dependent manner. DAI scores showed that the loose feces, occult blood, and weight loss of mice in the BG treatment were significantly reduced, and pathological section results revealed reduced inflammatory infiltration and fibrosis. Reduced serum FITC-dextran and I-FABP and increased levels of epithelial resistance and tight junction proteins support that the intestinal barrier was protected upon BG. The proportion of Th17 in mesenteric lymph nodes increased while Treg decreased in the model group. BG treatment effectively reduced the conversion of Treg to Th17. Additionally, BG was found to enhance mitophagy and activate the PPARγ/NF-κB signaling. BG demonstrates promising effects in ameliorating intestinal barrier damage and Th17/Treg imbalance in a murine model of CD-like colitis, while also promoting intracellular mitophagy. The PPARγ/NF-κB signaling pathway may serve as a key mediator of BG's regulatory mechanisms.

Altered lactate/pyruvate ratio may be responsible for aging-associated intestinal barrier dysfunction in male rats

Some evidence points to a link between aging-related increased intestinal permeability and mitochondrial dysfunction in in-vivo models. Several studies have also demonstrated age-related accumulation of the of specific deletion 4834-bp of “common” mitochondrial DNA (mtDNA) in various rat tissues and suggest that this deletion may disrupt mitochondrial metabolism. The present study aimed to investigate possible associations among the mitochondrial DNA (mtDNA) common deletion, mitochondrial function, intestinal permeability, and aging in rats. The study was performed on the intestinal tissue from (24 months) and young (4 months) rats. mtDNA4834 deletion, mtDNA copy number, mitochondrial membrane potential, and ATP, lactate and pyruvate levels were analyzed in tissue samples. Zonulin and intestinal fatty acid-binding protein (I-FABP) levels were also evaluated in serum. Serum zonulin and I-FABP levels were significantly higher in 24-month-old rats than 4-month-old rats (p = 0.04, p = 0.026, respectively). There is not significant difference in mtDNA4834 copy levels was observed between the old and young intestinal tissues (p > 0.05). The intestinal mitochondrial DNA copy number was similar between the two age groups (p > 0.05). No significant difference was observed in ATP levels in the intestinal tissue lysates between old and young rats (p > 0.05). ATP levels in isolated mitochondria from both groups were also similar. Analysis of MMP using JC-10 in intestinal tissue mitochondria showed that mitochondrial membrane potentials (red/green ratios) were similar between the two age groups (p > 0.05). Pyruvate tended to be higher in the 24-month-old rat group and the L/P ratio was found to be approximately threefold lower in the intestinal tissue of the older rats compared to the younger rats (p < 0.002). The tissue lactate/pyruvate ratio (L/P) was three times lower in old rats than in young rats. Additionally, there were significant negative correlations between intestinal permeability parameters and L/P ratios. The intestinal tissues of aged rats are not prone to accumulate mtDNA common deletion, we suggest that this mutation does not explain the age-related increase in intestinal permeability. It seems to be more likely that altered glycolytic capacity could be a link to increased intestinal permeability with age. This observation strengthens assertions that the balance between glycolysis and mitochondrial metabolism may play a critical role in intestinal barrier functions.

Markers of intestinal barrier damage in patients with chronic insomnia disorder.

Insomnia disorder stands out as one of the prevalent clinical sleep and psychiatric disorders. Prior research has unequivocally demonstrated variations in the diversity and abundance of gut microbiota among individuals with insomnia disorder. These alterations may play a direct or indirect role in the onset and progression of insomnia disorder by compromising the integrity of the intestinal barrier. This study aims to evaluate the impairment of the intestinal barrier in individuals with insomnia disorder by scrutinizing the serum functionality of this barrier. 45 patients with chronic insomnia disorder and 30 matched healthy volunteers were meticulously selected based on inclusion criteria. ELISA technology was employed to measure serum levels of diamine oxidase (DAO), D-lactic acid (D-LA), intestinal fatty acid binding protein (I-FABP), and endothelin (ET). Spearman correlation analysis was used to explore the relationship between intestinal mucosal markers and clinical characteristics. Data were analyzed using SPSS 26.0. Compared to the healthy control group, the insomnia disorder group exhibited significantly elevated scores on subjective mood and sleep scales (GAD-7, PHQ-9, HAMA, HAMD, PSQI, and ISI) (P < 0.05). Overnight PSG indicated a notable increase in bed time, total wake time, sleep onset latency, and wake after sleep onset in individuals with insomnia disorder. Additionally, there was a decrease in sleep efficiency and alterations in sleep structure (increased proportion of N1 and N3 stages, prolonged N1 stage) (P < 0.05). The chronic insomnia disorder group displayed significantly reduced concentrations of serum DAO, D-LA, I-FABP, and ET (P < 0.05). Furthermore, significant positive correlations were identified between intestinal epithelial barrier markers and sleep efficiency, while negative correlations were found with wake after sleep onset, total wake time, PSQI, HAMA, and HAMD. Additionally, D-LA levels were significantly positively correlated with ET concentrations. Individuals with chronic insomnia disorder manifest disruptions in sleep structure, heightened susceptibility to anxiety and depressive moods, and impaired intestinal barrier function. These findings suggest that the occurrence and development of insomnia disorder may be linked to the impairment of the intestinal barrier.

Values of serum intestinal fatty acid-binding protein, fecal calprotectin, and fecal human β-defensin 2 for predicting necrotizing enterocolitis

BackgroundThis study aimed to assess the diagnostic potential of serum intestinal fatty acid-binding protein (I-FABP), fecal calprotectin (FC), and fecal human β-defensin 2 (hBD2) in predicting necrotizing enterocolitis (NEC) in preterm infants.MethodsA prospective cohort of neonates with a gestational age < 32 weeks, suspected of NEC, was enrolled between June 2021 and December 2022. Serum I-FABP, FC, and fecal hBD2 levels were measured upon NEC suspicion, and diagnosis was confirmed through radiological examination or surgical intervention. Diagnostic precision of serum I-FABP, FC, and fecal hBD2 was assessed using a logistic regression model with multiple variables.ResultsThe study included 70 neonates (45 males, 25 females), with 30 developing NEC (40% Stage III, n = 12; 60% Stage II, n = 18) and 40 in the control group. NEC patients exhibited significantly higher serum I-FABP and FC levels (4.76 ng/mL and 521.56 µg/g feces, respectively) than those with other diagnoses (1.38 ng/mL and 213.34 µg/g feces, respectively; p ˂ 0.05 for both biomarkers). Stage II NEC neonates showed elevated fecal hBD2 levels (376.44 ng/g feces) than Stage III NEC neonates and controls (336.87 ng/g and 339.86 ng/g feces, respectively; p ˂ 0.05). No such increase was observed in infants progressing to Stage III NEC. Using a serum I-FABP threshold of > 2.54 ng/mL yielded 76.7% sensitivity, 87.5% specificity, 82.1% positive predictive value (PPV), and 83.3% negative predictive value (NPV). For FC (cutoff > 428.99 µg/g feces), corresponding values were 76.7% sensitivity, 67.5% specificity, 63.9% PPV, and 79.4% NPV.ConclusionSerum I-FABP and FC levels are valuable for early NEC detection and provide insights into disease severity. Low fecal hBD2 levels suggest an inadequate response to luminal bacteria, potentially rendering these infants more susceptible to NEC development or exacerbation.

PSVI-13 Dietary Milk Fat Globule Membrane Improves Neonatal Piglet Intestinal Architecture and Enhances Mucosal Diamine Oxidase Activity Following Lipopolysaccharide Challenge

Abstract Early life stressors alter the trajectory of gut development and impair nutrient utilization, barrier function, and animal performance throughout life. Gastrointestinal (GI) maladies increase morbidity and mortality in neonates, and dietary nutrients are essential in supporting GI function. Although maternal milk is the gold-standard for yielding developmental benefits to offspring, genetic selection in the modern sow has resulted in large litter size and milk yield potentially insufficient to achieve the high biological growth potential in sow-reared piglets. Research into milk quality has led to the identification of many bioactive nutrients important in neonatal development. Components of the milk fat globule membrane (MFGM) contribute immensely to neonatal nutrition and gut health. However, mechanisms of actions are still being defined. The objective is to define the effect of MFGM supplementation on neonatal piglet intestinal health. We hypothesize dietary MFGM will enhance piglet intestinal architecture and tight junction (TJ) protein abundance, attenuating systemic lipopolysaccharide (LPS)-induced intestinal barrier disruption. One-day-old piglets (n = 32) were assigned to soy (CON) or MFGM phospholipid supplemented diet (0.75% wt/wt) ± LPS (100 µg/kg body weight) challenge in a 2 × 2 factorial design (n = 8/diet/challenge). Piglets were fed for 21 d and 8 animals/diet received saline or LPS injections 4 h before euthanasia. Piglet weights and feed intake were recorded daily to calculate performance. Intestinal tissues were collected to assess villus height (VH) and crypt depth (CD) by hematoxylin and eosin staining. Two biomarkers of intestinal integrity, intestinal fatty acid-binding protein (I-FABP) and diamine oxidase (DAO), were measured in serum or tissue. Protein abundance of claudin-1 and occludin in ileal and colonic mucosa were detected by Western blot. Data were analyzed by 2 × 2 factorial arrangement of traetments using the PROC MIXED. Dietary MFGM had no adverse impact on growth performance or TJ proteins (P &amp;gt; 0.05). Dietary MFGM increased VH (CON: 348.8 and MFGM: 427.0 ± 26.79 µm) and decreased CD (CON: 166.3 and MFGM: 147.4 ± 8.42 µm) in ileum, thereby increasing the VH: CD ratio (CON: 2.2; MFGM: 3.1 ± 0.13; P &amp;lt; 0.05). Further, LPS treatment increased serum I-FABP by 4.4-fold and decreased jejunal mucosal DAO by 0.5-fold compared with saline treatment (P &amp;lt; 0.05). Additionally, there was a 93.1 % increase in colon DAO activity with MFGM diet compared with soy-fed pigs, regardless of LPS challenge (P &amp;lt; 0.05). Dietary MFGM improved neonatal piglet ileum architecture and increased colon DAO activity, potentially attenuating the intestinal barrier disruption following LPS challenge.

Intestinal injury and vasculitis biomarkers in cats with feline enteric coronavirus and effusive feline infectious peritonitis.

To investigate intestinal injury, repair and vasculitis biomarkers that may illuminate the progression and/or pathogenesis of feline infectious peritonitis (FIP) or feline enteric coronavirus (FECV) infection. A total of 40 cats with effusive FIP (30 with abdominal effusion, AE group; 10 with thoracic effusion, TE group) and 10 asymptomatic but FECV positive cats (FECV group), all were confirmed by reverse transcription polymerase chain reaction either in faeces or effusion samples. Physical examinations and effusion tests were performed. Trefoil factor-3 (TFF-3), intestinal alkaline phosphatase (IAP), intestinal fatty acid binding protein (I-FABP), myeloperoxidase-anti-neutrophilic cytoplasmic antibody (MPO-ANCA) and proteinase 3-ANCA (PR3-ANCA) concentrations were measured both in serum and effusion samples. Rectal temperature and respiratory rate were highest in the TE group (p<0.000). Effusion white blood cell count was higher in the AE group than TE group (p<0.042). Serum TFF-3, IAP and I-FABP concentrations were higher in cats with effusive FIP than the cats with FECV (p<0.05). Compared with the AE group, TE group had lower effusion MPO-ANCA (p<0.036), higher IAP (p<0.050) and higher TFF-3 (p<0.016) concentrations. Markers of intestinal and epithelial surface injury were higher in cats with effusive FIP than those with FECV. Compared to cats with abdominal effusions, markers of apoptosis inhibition and immunostimulation to the injured epithelium were more potent in cats with thoracic effusion, suggesting the possibility of a poorer prognosis or more advanced disease in these patients.

Intestinal disturbances associated with mortality of children with complicated severe malnutrition

BackgroundChildren admitted to hospital with complicated severe malnutrition (CSM) have high mortality despite compliance with standard WHO management guidelines. Limited data suggests a relationship between intestinal dysfunction and poor prognosis in CSM, but this has not been explicitly studied. This study aimed to evaluate the role of intestinal disturbances in CSM mortality.MethodsA case-control study nested within a randomized control trial was conducted among children hospitalized with CSM in Kenya and Malawi. Children who died (cases, n = 68) were compared with those who were discharged, propensity matched to the cases on age, HIV and nutritional status (controls, n = 68) on fecal metabolomics that targeted about 70 commonly measured metabolites, and enteropathy markers: fecal myeloperoxidase (MPO), fecal calprotectin, and circulating intestinal fatty acid binding protein (I-FABP).ResultsThe fecal metabolomes of cases show specific reductions in amino acids, monosaccharides, and microbial fermentation products, when compared to controls. SCFA levels did not differ between groups. The overall fecal metabolomics signature moderately differentiates cases from controls (AUC = 0.72). Enteropathy markers do not differ between groups overall, although serum I-FABP is elevated in cases in a sensitivity analysis among non-edematous children. Integrative analysis with systemic data suggests an indirect role of intestinal inflammation in the causal path of mortality.ConclusionsIntestinal disturbances appear to have an indirect association with acute mortality. Findings of the study improve our understanding of pathophysiological pathways underlying mortality of children with CSM.

Impaired intestinal permeability in patients with multiple sclerosis.

A number of recent studies have shown that the intestinal microbiome, part of the brain-gut axis, is implicated in the pathophysiology of multiple sclerosis. An essential part of this axis, is the intestinal barrier and gastrointestinal disorders with intestinal barrier dysregulation appear to be linked to CNS demyelination, and hence involved in the etiopathogenesis of multiple sclerosis (MS). The aim of this study was to evaluate the integrity of the intestinal barrier in patients with clinically definite multiple sclerosis (CDMS) and clinically isolated syndrome (CIS) using two serum biomarkers, claudin-3 (CLDN3), a component of tight epithelial junctions, and intestinal fatty acid binding protein (I-FABP), a cytosolic protein in enterocytes. Serum levels of CLDN3 in 37 MS patients and 22 controls, and serum levels of I-FABP in 46 MS patients and 51 controls were measured using commercial ELISA kits. Complete laboratory tests excluded the presence of gluten-related disorders in all subjects. Thirty MS patients received either disease-modifying drugs (DMD), immunosuppression (IS) or corticosteroid treatment. CLDN3 levels were only significantly higher in the MS patients treated with DMD or IS compared to the control group (P=0.006). There were no differences in I-FABP serum levels between the groups. Serum CLDN3 levels did not correlate with serum I-FABP levels in CDMS, in CIS patients or controls. In multiple sclerosis patients, the intestinal epithelium may be impaired with increased permeability, but without significant enterocyte damage characterized by intracellular protein leakage. Based on our data, CLDN3 serum levels appear to assess intestinal dysfunction in MS patients but mainly in treated ones.

Evaluation of Some Intestinal Biomarkers in the Determination of Intestinal Damage in Calves with Coccidiosis

This study aimed to assess the usefulness of injury biomarkers specific to the intestines in identifying the presence and degree of intestinal epithelial damage in coccidiosis-infected calves. Forty calves of various breeds and sexes, aged 21 days to 60 days, were used in the study. Of these, 30 were in the experimental group, and 10 were healthy control. The McMaster Oocyte counting technique was used to diagnose Eimeria and confirm clinical coccidiosis. Cases with clinical signs and more than 5,000 oocysts in gram feces were included in the study. All calves had blood samples drawn at the 0 th hours and 72 nd hours. Blood gas measurements were performed with a blood gas analyzer. Hemogram was performed with an automated hematologic analyzer. Bovine-specific enzyme-linked immunosorbent analysis (ELISA) test kits were used to measure the intestinal fatty acid binding protein (I-FABP), trefoil factor-3 (TFF-3), intestinal alkaline phosphatase (IAP), claudin-3 (CLD-3), intestinal smooth muscle actin (ACTG2), and interleukin-8 (IL-8) biomarkers from serum samples. Calves with coccidiosis received a single dose of toltrazuril (15 mg/kg) and supportive care. Before treatment (0 th hours) in coccidiosis-infected calves, serum I-FABP and CLD-3 levels were greater than in healthy calves (p<0.05), and after treatment (72 nd hours), serum TFF-3 and ACTG2 levels were higher than in healthy calves. There was a significant decrease in serum IL-8 levels in coccidiosis-infected calves after treatment (72 nd hours) compared to pre-treatment (0 th hours) (p<0.05). I-FABP, TFF-3, CLD-3, ACTG2, and IL-8 are helpful and reliable biomarkers that can be utilized to assess the presence of intestinal epithelium injury in coccidiosis-infected calves.

Predictive value of serum markers in the operation evaluation of neonatal necrotizing enterocolitis.

Neonatal necrotizing enterocolitis (NEC) is a common gastrointestinal emergency in newborns. Currently, the pathogenesis of the disease remains unknown. This study aims to determine the application value of serum markers in the selection of operation opportunities for NEC. This study consisted of a retrospective analysis of the clinical data of 150 participants with NEC admitted to Maternal and Child Health Hospital of Hubei Province from March 2017 to March 2022. Participants were assigned to an operation group (n=58) and a nonoperation group (n=92) according to the presence or absence of surgical treatment. Serum sample data for serum C-reactive protein (CRP) and interleukin 6 (IL-6), serum amyloid A (SAA), procalcitonin (PCT), and intestinal fatty acid-binding protein (I-FABP) concentrations were estimated. To compare the differences in overall data and serum markers between the 2 groups, independent factors related to surgical treatment in pediatric patients with NEC were analyzed using logistic regression. The utility of serum markers in selecting surgical options in pediatric patients with NEC was analyzed by constructing a receiver operating characteristic (ROC) curve. CRP, I-FABP, IL-6, PCT, and SAA levels were higher in the operation group than in the nonoperation group (P<0.05). Multivariate logistic regression analysis confirmed that CRP, I-FABP, IL-6, PCT, and SAA were independent related factors of NEC surgical remedy (P<0.05). Meanwhile, ROC curve analysis yielded a serum CRP, PCT, IL-6, I-FABP, and SAA area under curve (AUC) of NEC operation timing of 0.805, 0.844, 0.635, 0.872, and 0.864, respectively; a sensitivity of 75.90%, 86.20%, 60.30%, 82.80%, and 84.50%, respectively; and a specificity of 80.40%, 79.30%, 68.35%, 80.40%, and 80.55%, respectively. The serum markers CRP, PCT, IL-6, I-FABP, and SAA have certain guiding values in the choice of operation opportunity for pediatric patients with NEC.

Brief report: Assessment of mucosal barrier integrity using serological biomarkers in preclinical stages of rheumatoid arthritis.

The pathogenesis of rheumatoid arthritis (RA) is believed to initiate at mucosal sites. The so-called 'mucosal origin hypothesis of RA' postulates an increased intestinal permeability before disease onset. Several biomarkers, including lipopolysaccharide binding protein (LBP) and intestinal fatty acid binding protein (I-FABP), have been proposed to reflect gut mucosa permeability and integrity, while serum calprotectin is a new inflammation marker proposed in RA. We analyzed serum samples of individuals genetically at increased risk of RA in a nested-case-control study. Participants from a longitudinal cohort of first-degree relatives of RA patients (SCREEN-RA cohort) were divided into three pre-clinical stages of RA, based on the presence of risk factors for subsequent RA onset: 1) low-risk healthy asymptomatic controls; 2) intermediate-risk individuals without symptoms, but with RA-associated auto-immunity; 3) high-risk individuals with clinically suspect arthralgias. Five patients with newly diagnosed RA were also sampled. Serum LBP, I-FABP and calprotectin were measured using commercially available ELISA kits. We included 180 individuals genetically at increased risk for RA: 84 asymptomatic controls, 53 individuals with RA-associated autoimmunity and 38 high risk individuals. Serum LBP, I-FAPB or calprotectin concentrations did not differ between individuals in different pre-clinical stages of RA. Based on the serum biomarkers LBP, I-FABP and calprotectin, we could not detect any evidence for intestinal injury in pre-clinical stages of RA.

Gastric ultrasound, citrulline, and intestinal fatty acid-binding protein as markers of gastrointestinal dysfunction in critically ill patients: A pilot prospective cohort study.

Gastrointestinal (GI) dysfunction is common in the intensive care unit (ICU), although there is no consensus on biomarkers of GI dysfunction. We aimed to evaluate ultrasound-based gastric antrum measurements and serum intestinal fatty acid-binding protein (IFABP) and citrulline levels in relation to GI dysfunction in critically ill patients. Adult critically ill patients receiving enteral nutrition and stayed for in the ICU for ≥48 h was included. GI dysfunction was described using Gastrointestinal Dysfunction Score (GIDS). Gastric antrum measurements, including craniocaudal (CC) diameter, anteroposterior diameter, and antral-cross sectional area (CSA), as well as serum levels for IFABP and citrulline, were prospectively recorded at baseline and on day 3 and day 5 of enteral nutrition. The receiver operating characteristic (ROC) analysis was performed to evaluate gastric ultrasound parameters, serum IFABP, and citrulline concentrations in predicting GI dysfunction. Thirty-nine participants with a median age of 60 years were recruited and 46.2% of participants had GI dysfunction. ROC analysis revealed that the cutoff value of CSA score to predict GI dysfunction was 4.48 cm2 , which provided 72.7% sensitivity and 77.2% specificity (area under the curve = 0.768, 95% CI: 0.555-0.980). At baseline, gastric residual volume was highly correlated with CC diameter and CSA (r = 0.764, P < 0.001 and r = 0.675, P < 0.001, respectively). Serum IFABP and citrulline levels had no correlation with GI dysfunction or gastric ultrasound parameters (P > 0.05). CSA was associated with GI dysfunction in critically ill patients. Serum IFABP and citrulline concentrations were poor in predicting GI dysfunction.

Intestinal Fatty Acid-binding Protein in Patients with Psoriasis: A Marker of Impaired Intestinal Permeability Barrier and its Relation to Demographic Data and Clinical Characteristics

Abstract Background: Alterations of intestinal microbiota may play a role in the pathogenesis of psoriasis. Dysbiosis may cause disruption of the intestinal barrier, which contributes to immune activation by translocation of microbial antigens and metabolites. Intestinal fatty acid-binding protein (I-FABP) serves as a biomarker of enterocyte damage. Purpose: The aim of this study was to investigate serum concentration of I-FABP in patients with psoriasis. Methods: A cross-sectional hospital-based study on fifty psoriatic patients and thirty-five age and sex-matched healthy volunteers as a control group were enrolled in the study, serum I-FABP concentration was measured using an enzyme-linked immunosorbent assay. Results: Concentration of serum I-FABP was higher in patients compared to controls (P = 0.04). The serum level of I-FABP was higher in patients with skin phototype IV than in those with skin phototype III (P = 0.040). There were significant positive statistical correlations between I-FABP with age and disease duration. Conclusion: I-FABP, a biomarker for gut permeability, is increased in psoriasis and correlates with disease duration and age. Further investigations are needed to determine whether reinforcing intestinal barrier may be a new therapeutic target in psoriasis.

Evaluation of galectin-3 and intestinal fatty acid binding protein as serum biomarkers in autosomal recessive polycystic kidney disease.

Autosomal recessive polycystic kidney disease (ARPKD) causes fibrocystic kidney disease, congenital hepatic fibrosis, and portal hypertension. Serum galectin-3 (Gal-3) and intestinal fatty acid binding protein (I-FABP) are potential biomarkers of kidney fibrosis and portal hypertension, respectively. We examined whether serum Gal-3 associates with kidney disease severity and serum I-FABP associates with liver disease severity in ARPKD. Cross-sectional study of 29 participants with ARPKD (0.2-21years old) and presence of native kidneys (Gal-3 analyses, n = 18) and/or native livers (I-FABP analyses, n = 21). Serum Gal-3 and I-FABP were analyzed using enzyme linked immunosorbent assay. Kidney disease severity variables included estimated glomerular filtration rate (eGFR) and height-adjusted total kidney volume (htTKV). Liver disease severity was characterized using ultrasound elastography to measure liver fibrosis, and spleen length and platelet count as markers of portal hypertension. Simple and multivariable linear regression examined associations between Gal-3 and kidney disease severity (adjusted for liver disease severity) and between I-FABP and liver disease severity (adjusted for eGFR). Serum Gal-3 was negatively associated with eGFR; 1 standard deviation (SD) lower eGFR was associated with 0.795 SD higher Gal-3 level (95% CI -1.116, -0.473; p < 0.001). This association remained significant when adjusted for liver disease severity. Serum Gal-3 was not associated with htTKV in adjusted analyses. Overall I-FABP levels were elevated, but there were no linear associations between I-FABP and liver disease severity in unadjusted or adjusted models. Serum Gal-3 is associated with eGFR in ARPKD, suggesting its value as a possible novel biomarker of kidney disease severity. We found no associations between serum I-FABP and ARPKD liver disease severity despite overall elevated I-FABP levels.

Intestinal fatty acid binding protein (I-FABP) and CXC3L1 evaluation as biomarkers for patients at high-risk for coeliac disease in Johannesburg, South Africa

Coeliac disease (CD) is an autoimmune disorder and one of the few gastroenteropathies with accurate serological testing. CD serology has decreased accuracy for patients on a gluten-free diet and for monitoring mucosal healing. New ancillary tests would, therefore, be useful. Intestinal Fatty Acid Binding Protein (I-FABP) and CX3CL1 (Fractalkine) are two promising biomarkers for CD but haven’t been examined in patients who are at a high-risk for CD such as patients with type one diabetes (TID). This study, therefore, aimed to investigate serum levels of I-FABP and CX3CL1 in a cohort of South African patients with TID at a high-risk of developing CD. The serum I-FABP levels were significantly higher in CD-positive patients compared to CD-negative individuals (p = 0.03). No significant differences in the serum CX3CL1 levels were detected although this may reflect the impact of the comorbid autoimmune diseases had on the serum CX3CL1 levels. In conclusion, this study is the first to assess the levels of these biomarkers in a multiethnic population with comorbid autoimmune disease and determined I-FABP to be the more promising biomarker in such clinical contexts. Future research should focus on a diverse biomarker panel and longitudinal follow-up of patients at a high-risk for CD.

Carbon monoxide-releasing molecule-2 protects intestinal mucosal barrier function by reducing epithelial tight-junction damage in rats undergoing cardiopulmonary resuscitation

BackgroundIschemia-reperfusion injury (IRI) to the small intestine is associated with the development of systemic inflammation and multiple organ failure after cardiopulmonary resuscitation (CPR). It has been reported that exogenous carbon monoxide (CO) reduces IRI. This study aimed to assess the effects of carbon monoxide-releasing molecule-2 (CORM-2) on intestinal mucosal barrier function in rats undergoing CPR. MethodsWe established a rat model of asphyxiation-induced cardiac arrest (CA) and resuscitation to study intestinal IRI, and measured the serum levels of intestinal fatty acid-binding protein. Morphological changes were investigated using light and electron microscopes. The expression levels of claudin 3 (CLDN3), occludin (OCLN), zonula occludens 1 (ZO-1), tumor necrosis factor-alpha (TNF-α), interleukin-10 (IL-10), and nuclear factor kappa B (NF-κB) p65 were detected by western blotting. ResultsCompared with the sham-operated group, histological changes and transmission electron microscopy revealed severe intestinal mucosal injury in the CPR and inactive CORM-2 (iCORM-2) groups. In contrast, CORM-2 alleviated intestinal IRI. CORM-2, unlike iCORM-2, markedly decreased the Chiu's scores (2.38 ± 0.38 vs. 4.59 ± 0.34; P < 0.05) and serum intestinal fatty acid-binding protein level (306.10 ± 19.22 vs. 585.64 ± 119.84 pg/mL; P < 0.05) compared with the CPR group. In addition, CORM-2 upregulated the expression levels of tight junction proteins (CLDN3, OCLN, and ZO-1) (P < 0.05) and downregulated those of IL-10, TNF-α, and NF-кB p65 (P < 0.05) in the ileum tissue of rats that received CPR. ConclusionsCORM-2 prevented intestinal mucosal damage as a result of IRI during CPR. The underlying protective mechanism was associated with inhibition of ischemia-reperfusion-induced changes in intestinal epithelial permeability and inflammation in intestinal tissue.

Serum Intestinal Fatty Acid-Binding Protein and Calprotectin Concentrations to Assess Clinical Severity and Prognosis of Canine Parvovirus Enteritis

Serum Intestinal Fatty Acid-Binding Protein and Calprotectin Concentrations to Assess Clinical Severity and Prognosis of Canine Parvovirus Enteritis

Intestinal Complication With Myxomatous Mitral Valve Diseases in Chihuahuas.

The effects of cardiac disease on the intestine have been reported in humans but not in dogs. We investigated the effects of myxomatous mitral valve disease (MMVD), which is capable of causing congestion and tissue hypoperfusion, on the intestine in Chihuahuas, a breed frequently encountered in clinical practice as the preferred breed for MMVD. In this study, 69 Chihuahuas were divided into four groups based on echocardiography and chest radiography: 19 healthy Chihuahuas (H) and 50 Chihuahuas with MMVD classified according to the ACVIM consensus (stage B1, B2, C/D). In all the cases, serum intestinal fatty acid-binding protein (I-FABP) and D/L-lactate concentrations, markers of intestinal mucosal injury, were measured. I-FABP was significantly higher in stage C/D Chihuahuas than in other groups (p < 0.05), and stage B2 was significantly higher than H (p < 0.05). D-lactate was significantly increased in stages B2 and C/D compared to H and stage B1 (p < 0.05). L-lactate was significantly higher in stage C/D Chihuahuas than in any other group (p < 0.05), and stage B2 was significantly higher than that in H and stage B1 (p < 0.05). Intestinal mucosal injury risk was significantly higher in Chihuahuas with heart failure due to MMVD, suggesting that the risk could increase with worsening heart disease. This is the first study to investigate the intestinal complications of MMVD, and further investigations a needed in the future.

Association between enterocyte injury and fluid balance in patients with septic shock: a post hoc exploratory analysis of a prospective observational study

BackgroundThe required fluid volume differs among patients with septic shock. Enterocyte injury caused by shock may increase the need for fluid by triggering a systematic inflammatory response or an ischemia-reperfusion injury in the presence of intestinal ischemia/necrosis. This study aimed to evaluate the association between enterocyte injury and positive fluid balance in patients with septic shock.MethodsThis study was a post hoc exploratory analysis of a prospective observational study that assessed the association between serum intestinal fatty acid-binding protein, a biomarker of enterocyte injury, and mortality in patients with septic shock. Intestinal fatty acid-binding protein levels were recorded on intensive care unit admission, and fluid balance was monitored from intensive care unit admission to Day 7. The association between intestinal fatty acid-binding protein levels at admission and the infusion balance during the early period after intensive care unit admission was evaluated. Multiple linear regression analysis, with adjustments for severity score and renal function, was performed.ResultsOverall, data of 57 patients were analyzed. Logarithmically transformed intestinal fatty acid-binding protein levels were significantly associated with cumulative fluid balance per body weight at 24 and 72 h post-intensive care unit admission both before (Pearson’s r = 0.490 [95% confidence interval: 0.263–0.666]; P < 0.001 and r = 0.479 [95% confidence interval: 0.240–0.664]; P < 0.001, respectively) and after (estimate, 14.4 [95% confidence interval: 4.1–24.7]; P = 0.007 and estimate, 26.9 [95% confidence interval: 11.0–42.7]; P = 0.001, respectively) adjusting for severity score and renal function.ConclusionsEnterocyte injury was significantly associated with cumulative fluid balance at 24 and 72 h post-intensive care unit admission. Enterocyte injury in patients with septic shock may be related to excessive fluid accumulation during the early period after intensive care unit admission.