RESUMO
OBJECTIVES: To test the utility of various biomarkers as indicators of gut dysfunction in cystic fibrosis (CF) and determine whether intraindividual variations in these measures are repeatable over short intervals and whether interindividual variations correlate with clinical outcomes. STUDY DESIGN: We performed a cross-sectional, limited longitudinal study of children with CF aged 1-21 years who provided blood and stool samples at 2 or 3 visits, 2 weeks and 3 months apart, which were assayed for markers of intestinal inflammation (fecal calprotectin [fCal], lipocalin-2 [fLcn2], neopterin), and permeability (plasma lipopolysaccharide [LPS] antibodies, LPS-binding protein) by enzyme immunoassays. Control specimens were obtained from children without CF who had undergone esophagogastroduodenoscopy and had no evidence of gut inflammation. RESULTS: Twenty-six of 29 participants with CF completed the study. Sixty-nine stools (57 case/12 control) and 76 plasmas (60 case/16 control) were analyzed. LPS antibody had reliable intraindividual stability. fCal, fLcn2, and neopterin were significantly greater in CF than in control samples. fCal was negatively correlated with 3-month interval change (Δ) in weight-for-age z-score, body mass index/weight-for-length z-score, and forced expiratory volume in 1 second. fLcn2 was negatively correlated with FEV1 but not with anthropometrics. No marker correlated with Δbody mass index/weight-for-length z-score or ΔFEV1. CONCLUSIONS: fLcn2 is elevated in people with CF and might predict worse interval pulmonary function. Expanded studies are warranted to test if fLcn2 correlates with changes in additional outcomes.
Assuntos
Fibrose Cística , Criança , Humanos , Fibrose Cística/complicações , Fibrose Cística/metabolismo , Estudos Longitudinais , Neopterina , Estudos Transversais , Lipopolissacarídeos , Inflamação/metabolismo , AnticorposRESUMO
INTRODUCTION: Celiac disease (CD) is an autoimmune enteropathy triggered by gluten ingestion in genetically susceptible individuals. In CD, activation of the immune response causes damage of the intestinal mucosa, and a gluten-free diet (GFD) is the only available therapy. Intestinal damage can lead to an increase in the circulation of components of bacteria from the intestinal lumen, such as lipopolysaccharide (LPS). Soluble CD14 (sCD14) and lipopolysaccharide-binding protein (LBP) participate in the recognition of LPS, and their levels are altered in different pathologies. In the present study, the circulating levels of sCD14 and LBP from untreated CD patients were evaluated and compared to CD patients on a GFD and controls. MATERIAL AND METHODS: In total seventy-two adult patients with CD, twenty-three untreated CD patients and forty-nine on a GFD were included. In addition, fifty-five healthy individuals were included as controls. Additionally, the effect of LPS on sCD14 production by both normal and inflamed intestinal tissue culture was explored. RESULTS: Serum levels of sCD14 were found to be significantly increased in untreated CD patients compared to patients on a GFD and controls. In addition, we found that LPS induced the production of sCD14 by biopsies of intestinal tissue from untreated CD patients. CONCLUSIONS: The data from this study show that circulating levels of sCD14 are increased in the untreated CD patients compared to patients on a GFD. Our data show that LPS induces the production of sCD14 by the intestinal tissue from untreated CD patients.
RESUMO
INTRODUCTION: Systemic exposure to bacterial components like lipopolysaccharide (LPS) is among the non-genetic factors that could be involved in the onset or progression of systemic lupus erythematosus (SLE). Lipopolysaccharide-binding protein (LBP) participates in the recognition of LPS and in the inflammatory response. Here, we investigated LBP in SLE patients and its relationship with disease activity and SLE phenotypes. METHODS: Eighty-one adult patients with SLE from IMID-PY biobank (Paraguay) were included in the study. The clinical and laboratory variables were used to determine SLE activity. LBP levels were determined by ELISA in SLE patients and age- and sex-matched population-based controls. RESULTS: Patients with SLE have lower levels of circulating LBP compared to healthy controls (p = 0.0007). No significant correlation was found between serum LBP levels and disease activity. A significant difference was observed in LBP levels with regard to the presence of arthritis (p = 0.026). No other relation was found with clinical parameters. CONCLUSIONS: We found low levels of LBP in SLE patients compared to the control group. No correlation was detected between LBP levels and disease activity. It would be interesting for future studies to evaluate the impact of low levels of LBP on lupus immunopathogenesis.