interleukin-8 and Enterocolitis

An increase in absolute neutrophil count (ANC) is seen after oral food challenge test (OFC) in patients with food protein-induced enterocolitis syndrome (FPIES). Although it has been suggested that interleukin (IL)-8 is involved in this phenomenon, a possible role for cortisol has not yet been studied.. Six positive OFC in five patients with FPIES due to cows' milk (CM) proteins, and two negative OFC in two patients with suspected FPIES were analyzed. Absolute neutrophil count, serum IL-8, and serum cortisol were measured before OFC, 6 and 24 h after the ingestion of CM formula.. For the positive OFC, ANC measured 6 h after the ingestion of CM formula was significantly higher than that measured before the OFC (median, 8,761 versus 2,297/μL; P < 0.05). Significant increases in serum cortisol and IL-8 were observed 6 h after OFC (cortisol, median 1,119 pg/mL before versus 2,141 pg/mL after, P < 0.05; IL-8, median 15.5 pg/mL before versus 165.3 pg/mL after, P < 0.05). The change ratio (i.e. ratio of that after OFC to that before OFC) of ANC was significantly correlated not only with that of serum IL-8 (r = 0.90, P < 0.01) but also with that of serum cortisol (r = 0.76, P < 0.05). Moreover, the serum cortisol change ratio was significantly higher in subjects with vomiting than in those without (median, 2.5 versus 1.0, P < 0.05).. Serum cortisol, in combination with IL-8, affects the increase in ANC after OFC.

Topics: Biomarkers; Case-Control Studies; Enterocolitis; Female; Humans; Hydrocortisone; Infant; Infant, Newborn; Interleukin-8; Male; Milk Hypersensitivity; Milk Proteins; Neutrophils; Syndrome

Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE-mediated food allergy manifesting within 1 to 4 hours of food ingestion with repetitive emesis and lethargy.. We sought to characterize immune responses to casein in children with FPIES caused by cow's milk (CM).. We found low levels of CM and casein-specific IgG and casein-specific IgG. We confirm the paucity of humoral response in patients with CM-FPIES. IL-10 might play a key role in acquisition of tolerance in patients with CM-FPIES. Increased serum IL-8 levels in patients with active FPIES suggest neutrophil involvement. Elevated baseline serum tryptase levels in patients with active FPIES suggest low-grade intestinal mast cell activation or increased mast cell load.

Topics: Allergens; Animals; Caseins; Cattle; Cells, Cultured; Child; Enterocolitis; Female; Humans; Immune Tolerance; Immunity, Cellular; Immunity, Humoral; Interleukin-10; Interleukin-8; Male; Milk Hypersensitivity; Tryptases

Enterocolitis in oncology patients remains an important complication, but there is a lack of insight into its likely severity from microbial, pathological and inflammatory aspects. Paediatric oncology patients admitted with neutropenic fever, who developed abdominal pain and diarrhoea, were monitored by the takers of rectal biopsies, cultures, and inflammatory marker measurements. Twenty-five patients were included (mean age 7.1 years). 8 patients (32%) needed intensive care treatment, 3 (12%) patients died. Gram-positive bacteraemia was diagnosed in 4 patients (16%). Most patients had negative blood and stool cultures. Predictors of a severe clinical course of the enterocolitis were an increased serum interleukin-8 (IL-8) (>1000 pg/ml) level and an increased serum C-reactive protein level (CRP) (>150 mg/l) level, both measured on the first day of clinical illness. Relative risks (RR) for admission to an Intensive Care Unit (ICU) were 11.3 (95% Confidence Interval (CI) 1.6-77.9) for elevated IL-8 levels and 6.4 (95% (CI) 0.92-45.1) for increased CRP levels. Rectal biopsies and pathology could not predict outcome (P=0.22). IL-8 analysis at the onset of enterocolitis symptoms can identify high-risk patients, which might be used clinically to design future intervention trials.

Topics: Abdominal Pain; Biopsy; C-Reactive Protein; Child; Diarrhea; Enterocolitis; Female; Fever; Humans; Interleukin-8; Male; Neoplasms; Neutropenia; Physical Examination; Prognosis; Prospective Studies; Rectum

It is difficult to distinguish clinically between bacterial and viral causes of enterocolitis. The aim of the study was to investigate if serum cytokines can distinguish bacterial from viral enterocolitis. We prospectively enrolled 147 paediatric in-patients with acute enterocolitis. Blood was taken for leucocyte count, CRP, ESR, IL-6, IL-8, IFN-alpha and TNF-alpha on the day of admission. A pathogen was identified in 115 of the 147 children, 72 of whom had a bacterial pathogen (bacterial group) and 43 rotavirus (viral group). Mean values of the serum markers IL-6, IL-8 and CRP were significantly higher in the bacterial group. Receiver-operating characteristic curves demonstrated that a cut-off of 15 pg/ml for IL-6 had a sensitivity of 0.75 and a specificity of 0.91 for bacterial diarrhoea. Comparable values for CRP at a cut-off of 13 mg/L demonstrated a sensitivity of 0.54 and a specificity of 0.72. Values for IL-8 at a cut-off of 80 pg/ml had a sensitivity of 0.46 and a specificity of 0.71. Despite the small sample size, our data suggest that serum IL-6, IL-8 and CRP are significantly elevated in children with bacterial enterocolitis. IL-6 has a higher sensitivity, specificity and positive predictive value than IL-8 and CRP. Determination of serum cytokines might be a useful way of differentiating viral from bacterial gastro-enteritis.

Topics: Bacterial Infections; Biomarkers; C-Reactive Protein; Child, Preschool; Cytokines; Diagnosis, Differential; Enterocolitis; Female; Humans; Infant; Infant, Newborn; Interferon-gamma; Interleukin-6; Interleukin-8; Leukocyte Count; Male; Sensitivity and Specificity; Tumor Necrosis Factor-alpha; Virus Diseases

Campylobacter jejuni is a food-borne pathogen responsible for infectious enterocolitis. The early-response transcription factor NF-kappa B triggers the expression of genes associated with cellular immune and inflammatory responses. Co-incubation of HeLa cells with viable C. jejuni leads to the activation of the transcription factor NF-kappa B as determined by specific induction of a cellular luciferase-based reporter. Boiled cell-free extracts of C. jejuni are also potent dose-dependent stimulators of NF-kappa B-dependent transcription, the levels of which can reach up to 1000-fold as compared with independent controls. Using both cultured HeLa cells and human colonic epithelial (HCA-7) cells, the activation of NF-kappa B by C. jejuni boiled extract has been monitored through the degradation of IKB alpha and DNA binding of the nuclear translocated p50/p65 heterodimer of NF-kappa B. These events are co-ordinated with elaboration of the pro-inflammatory cytokine interleukin-8. Fractionation of the boiled C. jejuni extract suggests that the majority of the bioactive component has a molecular mass of 3 kDa or less, which is insensitive to proteinase K treatment.

Topics: Blotting, Western; Campylobacter Infections; Campylobacter jejuni; Cell Line; Enterocolitis; Gene Expression Regulation, Bacterial; HeLa Cells; Hot Temperature; Humans; Interleukin-8; NF-kappa B; Transcriptional Activation

Intestinal epithelial cells (IECs) respond to lipopolysaccharide (LPS) from gram-negative bacteria in the presence of the soluble form of CD14 (sCD14), a major endotoxin receptor. Since sCD14 is also known to interact with gram-positive bacteria and their components, we looked at whether sCD14 could mediate their effects on human IECs. To this end, we examined the production of proinflammatory cytokines following exposure of the IECs to specific gram-positive bacteria or their lipoteichoic acids (LTAs) in the absence and presence of human milk as a source of sCD14. In contrast to LPS from Escherichia coli or Salmonella enteritidis, neither the gram-positive bacteria Lactobacillus johnsonii strain La1 and Lactobacillus acidophilus strain La10 nor their LTAs stimulated IECs, even in the presence of sCD14. However, both LTAs inhibited the sCD14-mediated LPS responsiveness of IECs. We have previously hypothesized that sCD14 in human milk is a means by which the neonate gauges the bacterial load in the intestinal lumen and liberates protective proinflammatory cytokines from IECs. The present observations suggest that gram-positive organisms, via their LTAs, temper this response and prevent an exaggerated inflammatory response.

Topics: Chemokine CXCL5; Chemokines, CXC; Enterocolitis; Gram-Negative Bacteria; HT29 Cells; Humans; Interleukin-8; Intestinal Mucosa; Lactobacillus; Lactobacillus acidophilus; Lipopolysaccharide Receptors; Lipopolysaccharides; Teichoic Acids; Tumor Necrosis Factor-alpha

Topics: Biomarkers; Cystic Fibrosis; Enterocolitis; Humans; Interleukin-8; Intestines; Reproducibility of Results; Sputum; Therapeutic Irrigation

There is controversy about whether the inflammatory response observed in the cystic fibrosis (CF) lung occurs secondary to bacterial infection or is caused by a dysregulation of the inflammatory response associated with the basic cellular defect of CF.. To study the inflammatory response in the gastrointestinal tract of children with CF; and to investigate whether there is increased inflammation in the gastrointestinal tract of CF children with fibrosing colonopathy.. Whole gut lavage was performed on 21 pancreatic insufficient children with CF, who were clinically well, five children with CF and fibrosing colonopathy, and 12 controls. Intestinal outputs of plasma derived proteins (albumin, alpha(1) antitrypsin, IgG), secretory immunoglobulins (IgA and IgM), cellular constituents (eosinophil cationic protein and neutrophil elastase), and cytokines (interleukin 8 and interleukin 1beta) were measured.. Compared to controls, the 21 CF patients, with no intestinal complications, had increased intestinal outputs of albumin, IgG, IgM, eosinophil cationic protein, neutrophil elastase, interleukin 1beta, and interleukin 8. Similar values were obtained for the CF patients with fibrosing colonopathy.. These data suggest that there is immune activation in the gastrointestinal mucosa of children with cystic fibrosis, which may result from the basic cellular defect. Fibrosing colonopathy does not appear to be associated with increased inflammation.

Topics: Adolescent; Albumins; Case-Control Studies; Child; Child, Preschool; Cystic Fibrosis; Enterocolitis; Eosinophils; Humans; Immunoglobulin A; Immunoglobulin G; Immunoglobulin M; Infant; Interleukin-1; Interleukin-8; Intestinal Mucosa; Leukocyte Elastase; Trypsin Inhibitors