Early Marker Of Inflammation Research Articles

Correlation between Interleukin-17, High Sensitivity C-Reactive Protein and Pepsinogen in Helicobacter pylori Infected Gastritis

Gastritis is an inflammatory process in the gastric mucosa and submucosa caused by Helicobacter pylori (H. pylori). The infection modulates immune components, such as interleukin (IL) 17, high sensitivity C-reactive protein (hsCRP) and pepsinogen. This study aimed to determine the relationship between IL-17, hsCRP and pepsinogen in H. pylori infected gastritis. This observational cross-sectional study was conducted at Prof. Dr. R. D. Kandou General Hospital Manado from May-July 2022. Measurement of blood sample levels of IL-17, hsCRP, pepsinogen I, pepsinogen II and pepsinogen I/II ratio. Spearman’s statistical test was used to determine correlations between these variables. This study involved 48 patients aged 21–64, with a majority of females (67%). IL-7 had a positive correlation with pepsinogen I (r = 0.292; p = 0.044) and pepsinogen II (r = 0.288; p = 0.047) in H. pylori infected gastritis. Meanwhile, IL-17 with pepsinogen I/II ratio, hsCRP with pepsinogen I, pepsinogen II, pepsinogen I/II ratio and IL-17 with hsCRP did not show a significant correlation (p > 0.05). There was a correlation between IL 17 to pepsinogen I and pepsinogen II in gastritis infected with H. pylori, suggesting the importance of these early markers of inflammation in determining the severity of gastric mucosal inflammation in pylori-infected patients.

Detrimental Actions of Chlorinated Nucleosides on the Function and Viability of Insulin-Producing Cells.

Neutrophils are innate immune cells that play a key role in pathogen clearance. They contribute to inflammatory diseases, including diabetes, by releasing pro-inflammatory cytokines, reactive oxygen species, and extracellular traps (NETs). NETs contain a DNA backbone and catalytically active myeloperoxidase (MPO), which produces hypochlorous acid (HOCl). Chlorination of the DNA nucleoside 8-chloro-deoxyguanosine has been reported as an early marker of inflammation in diabetes. In this study, we examined the reactivity of different chlorinated nucleosides, including 5-chloro-(deoxy)cytidine (5ClC, 5CldC), 8-chloro-(deoxy)adenosine (8ClA, 8CldA) and 8-chloro-(deoxy)guanosine (8ClG, 8CldG), with the INS-1E β-cell line. Exposure of INS-1E cells to 5CldC, 8CldA, 8ClA, and 8CldG decreased metabolic activity and intracellular ATP, and, together with 8ClG, induced apoptotic cell death. Exposure to 8ClA, but not the other nucleosides, resulted in sustained endoplasmic reticulum stress, activation of the unfolded protein response, and increased expression of thioredoxin-interacting protein (TXNIP) and heme oxygenase 1 (HO-1). Exposure of INS-1E cells to 5CldC also increased TXNIP and NAD(P)H dehydrogenase quinone 1 (NQO1) expression. In addition, a significant increase in the mRNA expression of NQO1 and GPx4 was seen in INS-1E cells exposed to 8ClG and 8CldA, respectively. However, a significant decrease in intracellular thiols was only observed in INS-1E cells exposed to 8ClG and 8CldG. Finally, a significant decrease in the insulin stimulation index was observed in experiments with all the chlorinated nucleosides, except for 8ClA and 8ClG. Together, these results suggest that increased formation of chlorinated nucleosides during inflammation in diabetes could influence β-cell function and may contribute to disease progression.

Peri-Implant Sulcular Fluid (PISF) Nitric Oxide (NO) as an Early Marker of Inflammation

Peri-Implant Sulcular Fluid (PISF) Nitric Oxide (NO) as an Early Marker of Inflammation

Relationship between Body Mask Index (BMI) and Titer C-Reactive Protein in Women

Abstract
 Background:
 The prevalence of metabolic syndrome is certainly likely to increase with the increasing prevalence of obesity. A reliable indicator and easy-to-use for measuring body fat is body mass index (BMI), in the state of obesity there is a disruption of adiposity balance that is released and as an early marker of inflammation and triggers the formation of C-Reactive protein in the liver.
 Objectives:
 The goal of the study was to analyze the relationship between BMI and Titer C-Reactive Protein in women..
 Research Metodes: 
 This study is an observational analytical study with a cross sectional approach. The population in this study was women aged 25-65 years. A total of 39 samples were conducted in quota sampling. The data was analyzed with Kendal's tau non parametric test.
 Findings: 
 The results of the study obtained a value of significance or Sig. (2-tailed) 0.908 > 0.05, This result states that there is no relationship between body mass index and titer C-Reactive protein. Correlation coefficient value is -0.015, express a very weak linear relationship. Negative values indicate the opposite direction of the relationship, where the higher the BMI, the lower the C-Reactive protein titer.
 Conclusion: 
 Statistical test results obtained a value of p (0.908) > α (0.05), it states that no significant association between BMI and Titer C-Reactive Protein in women 

Telomere length and outcome of treatment for pulmonary tuberculosis in a gold mining community

Telomere length (TL) is a marker of ageing and mitochondrial DNA (mtDNA) is an early marker of inflammation caused by oxidative stress. We determined TL and mtDNA content among active pulmonary tuberculosis (PTB) patients to assess if these cellular biomarkers differed between artisanal miners and non-miners, and to assess if they were predictive of treatment outcome. We conducted a prospective cohort study from August 2018 to May 2019 involving newly diagnosed PTB patients at three outpatient TB clinics in a rural Democratic Republic of Congo. We measured relative TL and mtDNA content in peripheral blood leukocytes (at inclusion) via qPCR and assessed their association with PTB treatment outcome. We included 129 patients (85 miners and 44 non-miners) with PTB (median age 40 years; range 5–71 years, 22% HIV-coinfected). For each increase in year and HIV-coinfection, TL shortened by − 0.85% (− 0.19 to − 0.52) (p ≤ 0.0001) and − 14% (− 28.22 to − 1.79) (p = 0.02) respectively. Independent of these covariates, patients with longer TL were more likely to have successful TB treatment [adjusted hazard ratio; 95% CI 1.27 for a doubling of leucocyte telomere length at baseline; 1.05–1.44] than patients with a shorter TL. Blood mtDNA content was not predictive for PTB outcome. For a given chronological age, PTB patients with longer telomeres at time of diagnosis were more likely to have successful PTB treatment outcome.

Maternal C-reactive protein and in vitro fertilization (IVF) cycles.

Embryo implantation is accompanied by a potent inflammatory response, and a gradient of cytokines and chemokines produced by endometrial cells supports the embryo-endometrial interaction. C-reactive protein (CRP) serves as an early marker of inflammation and recent studies have illustrated that controlled ovarian hyperstimulation (COH) could increase its levels. Interestingly, a high chance of pregnancy has been reported in women who had an elevated CRP level on the day of embryo transfer. It seems an elevated systemic inflammation in the in vitro fertilization (IVF) cycle can increase the implantation and pregnancy rates. However, the results regarding the association of CRP with ART outcomes are controversial. Therefore, in this review, we aimed to describe how CRP levels change during a cycle of IVF treatment and which factors can potentially affect this pattern of change. Furthermore, the association of CRP with ART outcomes has been discussed.

Acute Phase Proteins in Marine Mammals: State of Art, Perspectives and Challenges.

The term “acute phase response” (APR) is referred to a nonspecific and complex reaction of an organism that occurs shortly after any tissue damage, such as infection, trauma, neoplasia, inflammation, and stress. The APR can be identified and monitored with some laboratory tests, such as the concentration of several plasma proteins, the acute phase proteins (APPs). The APPs are components of the non-specific innate immune response, and their plasma concentration is proportional to the severity and/or the extent of tissue damage. The evaluation of health status of marine mammals is difficult because the classical clinical signs of illness used for human and domestic animals are difficult to recognize and understand. For this reason, in the past years, several efforts were done to identify laboratory markers of disease in these animals. The APPs have demonstrated their role as early markers of inflammation in veterinary medicine, thus several APPs were tested in marine mammals, such as C-reactive protein (CRP), serum amyloid-A (SAA), and Haptoglobin (Hp). However, the difficulty to extrapolate the knowledge about APPs in one species to another, the lack of specie-specific reagents, the absence of data about negative APPs have hampered their extent use in marine mammals. Herein, the state of art of APPs in marine mammals is reviewed, with particular attention to pre-analytical and analytical factors that should be taken into account in validation and interpretation of APPs assays. Moreover, the current application, potential utility and the future developments of APPs in marine mammals is highlighted and discussed.

Poststroke Depression Biomarkers: A Narrative Review.

Poststroke depression (PSD) is the most prevalent psychiatric disorder after stroke, which is independently correlated with negative clinical outcome. The identification of specific biomarkers could help to increase the sensitivity of PSD diagnosis and elucidate its pathophysiological mechanisms. The aim of current study was to review and summarize literature exploring potential biomarkers for PSD diagnosis. The PubMed database was searched for papers published in English from October 1977 to December 2017, 90 of which met inclusion criteria for clinical studies related to PSD biomarkers. PSD biomarkers were subdivided into neuroimaging, molecular, and neurophysiological. Some of them could be recommended to support PSD diagnosing. According to the data, lesions affecting the frontal-subcortical circles of mood regulation (prefrontal cortex, basal nuclei, and thalamus) predominantly in the left hemisphere can be considered as neuroimaging markers and predictors for PSD for at least 1 year after stroke. Additional pontine and lobar cerebral microbleeds in acute stroke patients, as well as severe microvascular lesions of the brain, increase the likelihood of PSD. The following molecular candidates can help to differentiate PSD patients from non-depressed stroke subjects: decreased serum BDNF concentrations; increased early markers of inflammation (high-sensitivity C-reactive protein, ferritin, neopterin, and glutamate), serum pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-18, IFN-γ), as well as pro-inflammatory/anti-inflammatory ratios (TNF-α/IL-10, IL-1β/IL-10, IL-6/IL-10, IL-18/IL-10, IFN-γ/IL-10); lowered complement expression; decreased serum vitamin D levels; hypercortisolemia and blunted cortisol awakening response; S/S 5-HTTLPR, STin2 9/12, and 12/12 genotypes of the serotonin transporter gene SLC6A4, 5-HTR2a 1438 A/A, and BDNF met/met genotypes; higher SLC6A4 promoter and BDNF promoter methylation status. Neurophysiological markers of PSD, that reflect a violation of perception and cognitive processing, are the elongation of the latency of N200, P300, and N400, as well as the decrease in the P300 and N400 amplitude of the event-related potentials. The selected panel of biomarkers may be useful for paraclinical underpinning of PSD diagnosis, clarifying various aspects of its multifactorial pathogenesis, optimizing therapeutic interventions, and assessing treatment effectiveness.

Complement activation in acute myocardial infarction: An early marker of inflammation and tissue injury?

BackgroundAcute myocardial infarction (AMI) is a potentially fatal condition, being a major cause of death worldwide. Ischemia suffered during AMI causes tissue damage, leading to an inflammatory process. Moreover, myocardial injury can generate damage-associated molecular patterns that activate pattern recognition molecules including some complement proteins. MethodsHere we investigated products of complement activation, C3d and soluble C5b9 (sC5b9), as potential biomarkers for myocardial injury and inflammation, as well as serum cytokines (IL-6 and TNF-alpha), alpha-1-acid glycoprotein (AGP), and classical markers of myocardial necrosis (creatine kinase, creatine kinase-MB isoform, myoglobin and troponin-I) in a longitudinal study of patients with AMI (from admission, 6 h and 12 h post admission, and at discharge from hospital). Individuals undergoing cardiac catheterization (CC) with normal coronary arteries and asymptomatics with no history of cardiovascular disease or invasive procedures were included as controls. ResultsPlasma C3d was higher in AMI at admission, 6 h, 12 h, and discharge vs CC (p < 0.0001; p = 0.0061; p = 0.0081; p = 0.044) and asymptomatic (p = 0.0001 for admission, 6 h and 12 h; p = 0.0002 for discharge). Moreover, sC5b9 was higher only at admission and 6 h vs asymptomatic (p = 0.0031 and p = 0.0019). Additionally, AGP levels were elevated at admission, 6 h, 12 h, and discharge vs asymptomatic (p = 0.0003; p = 0.0289; p = 0.0009, p = 0.0017). IL-6 concentration was low at admission and 6 h and reached a peak at 12 h (p < 0.0001 for all groups). All classical markers of myocardial necrosis presented higher concentration at 6 h. ConclusionsOur results showed that complement activation is an early event in AMI occurring before the elevation of classical markers of myocardial necrosis such as creatine kinase, creatine kinase-MB isoform, myoglobin and troponin-I. These findings indicated C3d and sC5b9 as possible biomarkers for inflammation and tissue damage in AMI.

Abstract TP331: Plasma IL-6 Levels are Independently Associated With Functional Outcome and Markers of Secondary Injury in Spontaneous Intracerebral Hemorrhage

Introduction: The impact of the inflammatory response after intracerebral hemorrhage (ICH) has not been well characterized in patients and little is known about the relationship between early markers of inflammation and functional outcome. It is hypothesized that cytokine levels may be associated with three-month functional outcome and radiologic markers of secondary injury. Methods: Fifty-four patients with spontaneous ICH were prospectively enrolled at Yale-New Haven Hospital. Blood samples were collected at 24 (n=44) and 72 (n = 33) hours post-ICH. Plasma cytokine levels were measured using commercially available multiplex ELISA kits (Millipore). Modified Rankin Scale (mRS) was collected at three months by telephone interview. Associations between cytokines and outcome were assessed using ordinal logistics regression. Linear regression was used to evaluate the association between cytokine levels and markers of secondary injury. Results: IL-6 was correlated with ICH volume (p = 0.003) and PHE volume (p = 0.009) in univariable analysis. In multivariable analysis, IL-6 was associated with midline shift after adjustment for ICH volume (p=0.027). 24h IL-6 (p &lt; 0.001), IL-10 (p &lt; 0.001), IL-15 (p = 0.001), admission Glasgow Coma Score (GCS), ICH volume, ICH Score, and external ventricular drain (EVD) placement were associated with higher (worse) mRS in univariable ordinal regression. After adjustment for the ICH score, 24h IL-6 (OR 2.00, 95% CI 1.2-3.3, p = 0.003) and IL-15 (OR 2.7, 95% CI 1.4-5.0, p = 0.007) were significantly associated with worse mRS. Conclusions: Plasma IL-6 is independently associated with 24h midline shift, a measure of global hemispheric swelling, and with functional outcome after spontaneous ICH. These data are consistent with the early robust increase in brain IL-6 in experimental models of ICH. These data warrant further investigation of IL-6 levels as a biomarker for secondary injury and poor outcome in ICH.

Carboxylated and undercarboxylated osteocalcin in metabolic complications of human obesity and prediabetes.

BackgroundCarboxylated osteocalcin (Gla‐OC) participates in bone remodeling, whereas the undercarboxylated form (Glu‐OC) takes part in energy metabolism. This study was undertaken to compare the blood levels of Glu‐OC and Gla‐OC in nonobese, healthy obese, and prediabetic volunteers and correlate it with the metabolic markers of insulin resistance and early markers of inflammation.MethodsNonobese (body mass index [BMI] <30 kg/m2; n = 34) and obese subjects (30 <BMI <40 kg/m2; n = 98), both sexes, aged 25 to 65 years, were divided into healthy control, normal weight subjects, healthy obese, and obese with biochemical markers of prediabetes. The subgroups with obesity and low or high Gla‐OC or Glu‐OC were also considered for statistical analysis. After 2 weeks of diet standardization, venous blood was sampled for the determination of Gla‐OC, Glu‐OC, lipid profile, parameters of inflammation (hsCRP, interleukin 6, sE‐selectin, sPECAM‐1, and monocyte chemoattractant protein 1), and adipokines (leptin, adiponectin, visfatin, and resistin).ResultsGla‐OC in obese patients was significantly lower compared to nonobese ones (11.36 ± 0.39 vs 12.69 ± 0.90 ng/mL, P = .048) and weakly correlated with hsCRP (r = −0.18, P = .042), visfatin concentration (r = −0.19, P = .033), and BMI (r = −0.17, P = .047). Glu‐OC was negatively associated with fasting insulin levels (r = −0.18, P = .049) and reduced in prediabetic individuals compared with healthy obese volunteers (3.04 ± 0.28 vs 4.48 ± 0.57, P = .025).ConclusionsDecreased blood concentration of Glu‐OC may be a selective early symptom of insulin resistance in obesity, whereas the decreased level of Gla‐OC seems to be associated with the appearance of early markers of low grade inflammation accompanying obesity.

The association of serum gamma-glutamyl transpeptidase level and other laboratory parameters with blood pressure in hypertensive patients under ambulatory blood pressure monitoring.

BackgroundHypertension is a very important cause of morbidity and mortality. Serum gamma-glutamyl transpeptidase (GGT) is a biomarker of oxidative stress and associated with increased risk of hypertension and diabetes. The aim of this study was to evaluate the association of serum GGT level, which is an early marker of inflammation and endothelial dysfunction, with the deterioration of the diurnal rhythm of the blood pressure.MethodsA total of 171 patients with hypertension were included in this study. Patients whose nighttime mean blood pressure, measured via ambulatory blood pressure monitoring, decreased between 10% and 20% compared with the daytime mean blood pressure were defined as “dippers”, whereas patients with a nighttime blood pressure decrease lower than 10% were defined as “non-dippers”.ResultsA total of 99 hypertensive patients (65 females/34 males) were classified as dippers and 72 patients (48 females/24 males) as non-dippers. The mean age of the non-dipper group was significantly greater than the dipper group. Serum GGT, C-reactive protein and uric acid levels were significantly higher among patients in the non-dipper group. Negative correlations were detected between GGT levels and diurnal systolic and diastolic blood pressure decreases.ConclusionOur findings revealed that GGT level was higher in the non-dipper group, and was negatively correlated with the nighttime decrease of diurnal blood pressure. C-reactive protein and uric acid levels were also higher in the non-dipper group. However, future randomized controlled prospective studies with larger patient populations are necessary to confirm our findings.

Lipopolysaccharide-binding protein is efficient in biodosimetry during radiotherapy of lung cancer.

The aim of the present study was to determine if the serum levels of early markers of inflammation, such as interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), C-reactive protein (CRP), and lipopolysaccharide-binding protein (LBP) were correlated with the radiation dose received by the pulmonary and mediastinal structures of patients with non-small cell lung cancer (NSCLC). This pilot study included 26 patients with NSCLC who received total radiation doses ranging from 54 to 74 Gy (2.0 Gy/fraction). Cytokines were measured at baseline by enzyme-linked immunosorbant assay, and following administration of total doses of 20 and 40 Gy. A control group of 26 participants was sampled for comparisons with patient baseline cytokine levels. Only data from the 40-Gy cytokine blood levels of patients with NSCLC were identified to be correlated with histograms of the parameters of each patient's radiotherapy protocol. The IL-6, TNF-α and CRP median baseline levels of the patients with NSCLC were significantly higher than those of the controls (all P≤0.01). No differences were observed between the LBP levels of the patients and controls [median, 36.34 (25-75%; 31.35-39.27) vs. 36.92 (30.20-44.05) µg/ml, respectively; P=0.42]. No significant differences in the levels of the four cytokines between baseline, and at 20 and 40 Gy were observed [IL-6 (P=0.19); TNF-α (P=0.68); CRP (P=0.44) and LBP (P=0.29)]. LBP was significantly and positively correlated with the mean radiation dose to the lung (r=0.409; P=0.038), and showed a positive correlation with the percentage of lung volume exposed to at least 20 Gy of the planned radiation dose (r=0.3536; P=0.0764). CRP levels were positively correlated with the mean radiation dose to the esophagus (r=0.404; P=0.041); however, IL-6, TNF-α and CRP were not significantly associated with other lung dosimetry parameters. Thus, LBP levels were correlated with radiation exposure of pulmonary tissues, and LBP may be a marker that warrants further investigation on radiotoxicity in NSCLC patients.

Opioid treatment of experimental pain activates nuclear factor-κB.

To determine the independent and combined effects of pain and opioids on the activation of an early marker of inflammation, nuclear factor-κB (NF-κB). NF-κB activation was compared within-subjects following four randomly ordered experimental sessions of opioid-only (intravenous fentanyl 1 μg/kg), painonly (cold-pressor), opioid + pain, and a resting condition. University General Clinical Research Center. Twenty-one (11 female) healthy controls. Following exposure to treatment (fentanyl administration and/or cold-pressor pain), blood samples for NF-κB analysis were obtained. Intracellular levels of activated NF-κB, in unstimulated and stimulated peripheral blood mononuclear cells at 15 and 30 minutes. Neither pain nor opioid administration alone effected NF-κB levels in cell populations; however, the combination of treatments induced significant increases of NF-κB in stimulated peripheral blood mononuclear cell, lymphocytes, and monocytes. The combination of acute pain with opioids, as occurs in clinical situations, activates a key transcription factor involved in proinflammatory responses.

Significance of bone marrow edema in pathogenesis of rheumatoid arthritis

SummaryAssessing the pathology of the synovium, its thickening and increased vascularity through ultrasound and magnetic resonance examinations (more often an ultrasound study alone) is still considered a sensitive parameter in the diagnosis of rheumatoid arthritis and in monitoring of treatment efficacy. Magnetic resonance studies showed that, aside from the joint pannus, the subchondral bone tissue constitutes an essential element in the development of rheumatoid arthritis. Bone marrow edema correlates with inflammation severity, joint destruction, clinical signs and symptoms of rheumatoid arthritis, and thus is considered a predictor of rapid radiological progression of the disease. The newest studies reveal that bone marrow edema may be a more sensitive indicator of the response to therapy than appearance of the synovium. Bone marrow edema presents with increased signal in T2-weighted images, being most visible in fat saturation or IR sequences (STIR, TIRM). On the other hand, it is hypointense and less evident in T1-weighted images. It becomes enhanced (hyperintense) after contrast administration. Histopathological studies confirmed that it is a result of bone inflammation (osteitis/osteomyelitis), i.e. replacememt of bone marrow fat by inflammatory infiltrates containing macrophages, T lymphocytes, B lymphocytes, plasma cells and osteoclasts. Bone marrow edema appears after a few weeks from occurrence of symptoms and therefore is considered an early marker of inflammation. It correlates with clinical assessment of disease activity and elevated markers of acute inflammatory phase, i.e. ESR and CRP. It is a reversible phenomenon and may become attenuated due to biological treatment. It is considered a “herald” of erosions, as the risk of their formation is 6-fold higher in sites where BME was previously noted

Early markers of inflammation

AbstractAbstract not provided

Adiponectin-deficiency exaggerates sepsis-induced microvascular dysfunction in the mouse brain.

Obesity increases circulating cell-endothelial cell interactions; an early marker of inflammation in laboratory model of sepsis, but little is known about the effect of different adipokines. Adiponectin is an anti-inflammatory adipokine secreted by adipocytes. Adiponectin deficiency is implicated in exaggerated proinflammatory phenotype in both obesity and sepsis via increased proinflammatory cytokine expression. However the effect of adiponectin deficiency on circulating cell-endothelial cell interactions in polymicrobial sepsis is unknown. Furthermore although brain dysfunction in septic patients is a known predictor of death, the pathophysiology involved is unknown. In the current study, we examined the effects of adiponectin deficiency on leukocyte (LA) and platelet adhesion (PA) in cerebral microcirculation of septic mice. Adiponectin deficient (Adipoq(-/-): Adko) and background strain C57Bl/6 (wild type (WT)) mice were used. Sepsis was induced using cecal ligation and puncture (CLP). We studied LA and PA in the cerebral microcirculation using intravital fluorescent video microscopy (IVM), blood brain barrier (BBB) dysfunction using Evans Blue (EB) leakage method and E-selectin expression using dual radiolabeling technique in different WT and Adko mice with CLP. Adiponectin deficiency significantly exaggerated LA (WT-CLP:201 ± 17; Adko-CLP: ± 53 cells/mm(2); P < 0.05) and PA (WT-CLP:125 ± 17; Adko-CLP:188 ± 20 cells/mm(2); P < 0.05) in cerebral microcirculation, EB leakage (WT-CLP:10 ± 3.7; Adko-CLP:24 ± 4.3 ng/g × µl plasma; P < 0.05) and E-selectin expression (WT-CLP:0.06 ± 0.11; Adko-CLP:0.44 ± 0.053 ng/g; P < 0.05) in the brain tissue of the mice with CLP. Furthermore, E-selectin monoclonal antibody (mAb) treatment attenuated cell adhesion and BBB dysfunction of Adko-CLP mice. Adiponectin deficiency is associated with exaggerated leukocyte and PA in cerebral microcirculation of mice with CLP via modulation of E-selectin expression.

Exhaled nitric oxide and urinary EPX levels in infants: a pilot study

BackgroundObjective markers of early airway inflammation in infants are not established but are of great interest in a scientific setting. Exhaled nitric oxide (FeNO) and urinary eosinophilic protein X (uEPX) are a two such interesting markers.ObjectiveTo investigate the feasibility of measuring FeNO and uEPX in infants and their mothers and to determine if any relations between these two variables and environmental factors can be seen in a small sample size. This was conducted as a pilot study for the ongoing Swedish Environmental Longitudinal Mother and child Asthma and allergy study (SELMA).MethodsConsecutive infants between two and six months old and their mothers at children's health care centres were invited, and 110 mother-infant pairs participated. FeNO and uEPX were analysed in both mothers and infants. FeNO was analyzed in the mothers online by the use of the handheld Niox Mino device and in the infants offline from exhaled air sampled during tidal breathing. A 33-question multiple-choice questionnaire that dealt with symptoms of allergic disease, heredity, and housing characteristics was used.ResultsFeNO levels were reduced in infants with a history of upper respiratory symptoms during the previous two weeks (p < 0.002). There was a trend towards higher FeNO levels in infants with windowpane condensation in the home (p < 0.05). There was no association between uEPX in the infants and the other studied variables.ConclusionThe use of uEPX as a marker of early inflammation was not supported. FeNO levels in infants were associated to windowpane condensation. Measuring FeNO by the present method may be an interesting way of evaluating early airway inflammation. In a major population study, however, the method is difficult to use, for practical reasons.

Assessment of an in vitro model of human cells to evaluate the toxic and irritating potential of chemical compounds

We attempted to induce differentation in unidifferentiated NCTC2544 human keratinocyte line, by exposure to ZnSO4 and CaCl2. Analysis of specific markers, transglutaminase I, involucrin and loricrin, show that basal NCTC2544 (BL) reached spinous- (SL) and granular-like (GL) phenotypes. BL-, SI- and GL- NCTC were exposed to SDS, as irritant stimulus and Neutral red uptake (NRU) and MTT cytoxicity tests evidenced a relatively higher toxicity in SL- and GL cells on lysosomes respect to mitochondria. ILIα cytokine was monitored as early inflammation marker. The complex of data provides evidence for the suitability of our in vitro model to the analysis of cytotoxic/biological effects of topically applied exogenous compounds.

Usefulness of Assessing Circulating Levels of Resistin, Ghrelin, and IL-18 in Alcoholic Acute Pancreatitis

Acute pancreatitis (AP) is a severe inflammatory disease with high mortality and morbidity rates. We have previously demonstrated that resistin may represent an early marker of inflammation in AP. It was also revealed that ghrelin may have anti-inflammatory potential. However, the role of adipohormones in AP-resistin and ghrelin as well as the proinflammatory cytokine interleukin (IL)-18-has not yet been fully elucidated. The study group comprised 32 patients with alcoholic AP and 30 controls matched for age, sex, and body mass index (BMI). In all cases AP was classified as grade C according to Balthazar's computed tomography (CT) score and as severe (3 points) according to Ranson's criteria. Serum levels of resistin, ghrelin, and IL-18 were measured on first, third, and fifth day of hospitalization by enzyme-linked immunosorbent assay (ELISA). On first day of hospitalization the mean serum resistin concentration in AP patients was significantly higher than in controls (P < 0.05) and further increased on third and fifth day of hospitalization (17.4 ± 4.23 ng/ml and 25.8 ± 8.14 ng/ml, respectively). On first day of hospitalization the mean serum IL-18 concentration in AP patients was significantly higher than in controls (P < 0.05), on third day its level further increased, and on fifth day it decreased to a level similar to that observed on admission. The serum ghrelin concentrations on first, third, and fifth day of hospitalization were comparable, and significantly higher than in controls (P < 0.01). Significant correlation between C-reactive protein (CRP) and resistin levels (r = 0.43; P < 0.05) and between CRP and IL-18 (r = 0.58; P <0.05) on day of admission was found. Serum concentration of IL-18 and resistin may contribute to inflammatory response and may be useful as an early marker of inflammation in AP. We also suspect that ghrelin affects the course of AP and plays an important role in inflammatory response.