Serum Myeloperoxidase Concentrations Research Articles

The role of paraoxonase and myeloperoxidase as oxidative stress markers in pregnant women with hypothyroidism

Objective: This study aims to measure paraoxonase 1 (PON 1) and myeloperoxidase (MPO) levels in patients diagnosed with hypothyroidism during pregnancy by spectrophotometric method and to compare the results with healthy controls. Methods: For the study, the blood samples of 45 hypothyroid pregnant patients and 45 healthy control pregnant individuals who were compatible with the patient group in terms of age were taken. PON 1 and MPO levels in both groups were measured using spectrophotometric methods and statistical analysis was performed. Results: Serum PON 1 activity levels were significantly lower in hypothyroid pregnant patients than in the control group (p=.020). The patients group had significantly higher serum MPO concentrations than in control group (p=.020). MPO/PON-1 ratio was higher in pregnant patients with hypothyroidism than in the control group (p=.030). Conclusion: Decreased levels of PON1 with increased levels of MPO in hypothyroid pregnant patients suggest the critical role of oxidative stress in hypothyroidism during pregnancy.

Myeloperoxidase and Advanced Oxidation Protein Products in the Cerebrospinal Fluid in Women and Men with Parkinson's Disease.

Background: Myeloperoxidase (MPO) and advanced oxidation protein products, or AOPP (a type of MPO-derived chlorinated adducts), have been implicated in Parkinson´s disease (PD). Human MPO also show sex-based differences in PD. The objective was to study the relationship of MPO and AOPP in the cerebrospinal fluid (CSF) with motor features of idiopathic PD in male and female patients. Methods: MPO concentration and activity and AOPP content were measured in the CSF and serum in 34 patients and 30 controls. CSF leukocytes and the integrity of the blood-brain barrier were evaluated. Correlations of MPO and AOPP with clinical variables were examined. Results: The blood-brain barrier was intact and CSF leukocyte count was normal in all patients. CSF MPO concentration and activity were similar in the cohort of patients and controls, but CSF MPO content was significantly higher in male patients than in PD women (p = 0.0084). CSF MPO concentration correlated with disease duration in male and female patients (p < 0.01). CSF MPO concentration was significantly higher in men with disease duration ≥12 years versus the remainder of the male subjects (p < 0.01). Changes in CSF MPO in women were not significant. Serum MPO concentration and activity were significantly higher in all PD patients relative to controls (p < 0.0001). CSF MPO was not correlated with serum MPO. Serum AOPP were detected in all patients, but CSF AOPP was undetectable in 53% of patients. AOPP were not quantifiable in controls. Conclusions: CSF MPO is not a good biomarker for PD because mean CSF MPO concentration and activity are not different between the cohort of patients and controls. CSF MPO concentration positively correlated with disease duration in men and women, but CSF MPO is significantly enhanced only in male patients with disease duration longer than 12 years. It can be hypothesized that the MPO-related immune response in early-stage PD might be weak in all patients, but then the MPO-related immune response is progressively enhanced in men, not women. Since the blood-brain barrier is intact, and CSF MPO is not correlated with serum MPO, CSF myeloperoxidase would reflect MPO content in brain cells, not blood-derived cells. Finally, serum AOPP was detected in all patients, but not controls, which is consistent with the occurrence of chlorinative stress in blood serum in PD. The study of CSF AOPP as biomarker could not be assessed because the ELISA assay was hampered by its detection limit in the CSF.

El aumento de la mieloperoxidasa sérica se correlaciona con datos clínicos de la enfermedad de Parkinson

Objectives. Myeloperoxidase (MPO) has been implicated in Parkinson´s disease (PD). The objective was to look at the relationship of MPO concentration in serum and cerebrospinal fluid (CSF) with clinical variables of PD. Methods. In this prospective, observational, and cross-sectional study, MPO concentration in serum and the CSF was analyzed in 36 patients with idiopathic PD and 30 controls, who were enrolled from 2012 to 2017. In the group of patients, correlation of MPO content with demographic, clinical and tomographic variables was examined. The extent and degree of nigrostriatal dopaminergic cell loss was evaluated by using SPECT and 123I-Ioflupane, radioligand that has binding affinity for dopamine-transporter (DAT). Results. Serum MPO concentration, not CSF MPO content, was significantly higher in the patients (p&lt;.0001). Significant correlation values were found between serum MPO concentration and rating scales of motor severity (Hoehn-Yahr, MDS-UPDRS part-III), and percentage reduction of DAT binding on basal ganglia (p&lt;.0001). Patients with moderate-advanced disease (Hoehn-Yahr stage 3) showed significantly higher serum MPO content relative to patients with early disease (Hoehn-Yahr stages 1-2, p&lt;.0001). DAT binding was reduced on all striatal regions, and signal reduction was higher in the putamen relative to the caudate nucleus (p&lt;.0001). Percentage reduction of DAT binding on the striatum and putamen significantly correlated with rating scales of motor severity. Conclusions. Myeloperoxidase content in serum is increased in PD patients and correlates with motor severity degree and loss of dopamine-transporter binding on basal ganglia. The results allow proposing that the measurement of MPO level in serum could be useful for PD diagnosis, and that the inhibition of serum MPO would be a promising therapeutic tool. The study also confirms that the putamen shows higher reduction of DAT binding than the caudate nucleus, and degree of nigrostriatal dopaminergic cell loss is well quantified with rating scales of motor severity.

Increased concentrations of myeloperoxidase in serum and serum extracellular vesicles are associated with type 2 diabetes mellitus

BackgroundInflammatory response plays a critical role in the initiation and progression of type 2 diabetes mellitus (T2DM). Myeloperoxidase (MPO), a leukocyte-derived protagonist, exerts its proinflammatory properties in many complications. We explored the associations between serum extracellular vesicle (EV)-derived MPO as well as serum MPO and T2DM. MethodsWe performed a cross-sectional study in 151 individuals, including 93 patients with T2DM and 58 non-T2DM controls. The concentrations of serum EV-derived MPO and serum MPO were measured by Luminex Assay. ResultsOur data showed that serum EV-derived MPO concentrations and serum MPO concentrations were significantly higher in T2DM patients compared with non-T2DM subjects. In addition, multivariate logistic regression analysis revealed that serum EV-derived MPO as well as serum MPO was independently associated with the presence of T2DM even after adjusting for confounding factors (OR = 1.836 /1 ng EV-derived MPO, 95% CI = 1.395–2.417, P < 0.001; OR = 4.135 /10 ng serum MPO, 95% CI = 2.285–7.483, P < 0.001). Furthermore, serum MPO showed marginally higher discriminatory accuracy than serum EV-derived MPO in screening T2DM (AUC = 0.858; AUC = 0.779). ConclusionIncreased concentrations of the inflammatory marker MPO either in serum or in serum EVs were independently associated with T2DM.

Linking myeloperoxidase with subclinical atherosclerosis in adults with metabolic syndrome.

Myeloperoxidase (MPO) is aleukocyte-derived enzyme that has been associated with cardiovascular diseases in many studies. Together with hydrogen peroxide and ahalogen, MPO forms avery strong antimicrobial system and there is evidence of links between MPO and inflammation in cardiovascular diseases. Brachial flow-mediated dilation (FMD) refers to aphysiologic measure, and carotid intima-media thickness (IMT) is an anatomic structural measure of subclinical atherosclerosis. This research aimed to assess the correlation of MPO serum levels with subclinical atherosclerosis in patients with metabolic syndrome (MS) using the parameters FMD and IMT. Atotal of 88patients with metabolic syndrome defined according to the International Diabetes Criteria (IDF) criteria were recruited in the study. Doppler ultrasound was used to determine the left and right common carotid artery thickness (left and right CCA IMT) and FMD of brachial artery. The MPO concentrations were measured using the Immundiagnostik MPO ELISA kit. Asignificant inverse correlation between MPO and brachial FMD (r = -0.354, p < 0.001), asignificant positive correlation between MPO and right CCA IMT (r = 0.327, p < 0.001), and asignificant positive correlation between MPO and left CCA IMT (r = 0.301, p < 0.001) in patients with MS were obtained in this research study. Serum MPO concentration is correlated with subclinical atherosclerosis in patients with MS. The MPO may be apotential therapeutic goal in patients with MS. This finding suggests that new biological markers for MS and subclinical atherosclerosis are helpful for understanding the mechanisms of the risk factors and their role as a considerable burden on the population.

Therapeutic Myeloperoxidase Inhibition Attenuates Neutrophil Activation, ANCA-Mediated Endothelial Damage, and Crescentic GN.

Myeloperoxidase released after neutrophil and monocyte activation can generate reactive oxygen species, leading to host tissue damage. Extracellular glomerular myeloperoxidase deposition, seen in ANCA-associated vasculitis, may enhance crescentic GN through antigen-specific T and B cell activation. Myeloperoxidase-deficient animals have attenuated GN early on, but augmented T cell responses. We investigated the effect of myeloperoxidase inhibition, using the myeloperoxidase inhibitor AZM198, to understand its potential role in treating crescentic GN. We evaluated renal biopsy samples from patients with various forms of crescentic GN for myeloperoxidase and neutrophils, measured serum myeloperoxidase concentration in patients with ANCA-associated vasculitis and controls, and assessed neutrophil extracellular trap formation, reactive oxygen species production, and neutrophil degranulation in ANCA-stimulated neutrophils in the absence and presence of AZM198. We also tested the effect of AZM198 on ANCA-stimulated neutrophil-mediated endothelial cell damage in vitro, as well as on crescentic GN severity and antigen-specific T cell reactivity in the murine model of nephrotoxic nephritis. All biopsy specimens with crescentic GN had extracellular glomerular myeloperoxidase deposition that correlated significantly with eGFR and crescent formation. In vitro, AZM198 led to a significant reduction in neutrophil extracellular trap formation, reactive oxygen species production, and released human neutrophil peptide levels, and attenuated neutrophil-mediated endothelial cell damage. In vivo, delayed AZM198 treatment significantly reduced proteinuria, glomerular thrombosis, serum creatinine, and glomerular macrophage infiltration, without increasing adaptive T cell responses. Myeloperoxidase inhibition reduced neutrophil degranulation and neutrophil-mediated endothelial cell damage in patients with ANCA-associated vasculitis. In preclinical crescentic GN, delayed myeloperoxidase inhibition suppressed kidney damage without augmenting adaptive immune responses, suggesting it might offer a novel adjunctive therapeutic approach in crescentic GN.

Serum myeloperoxidase concentrations for outcome prediction in acute intracerebral hemorrhage

BackgroundOxidative stress is related to brain injury after spontaneous intracerebral hemorrhage (ICH). Myeloperoxidase (MPO) is a potent oxidizing enzyme. We tested the hypothesis that serum MPO concentrations are increased after ICH and they correlate with stroke severity and outcome. MethodsSerum MPO concentrations were measured in 128 ICH patients and 128 controls. Odds ratios of dependent variables, including early neurological deterioration, hematoma growth, 1-week mortality, 6-month mortality, 6-month unfavorable outcome (modified Rankin Scale score > 2) and 6-month overall survival, were calculated and adjusted for age, sex, hematoma volume, National Institutes of Health Stroke Scale (NIHSS) score and vascular risk factors. ResultsAs compared to the controls, the patients had significantly increased serum MPO concentrations. MPO concentrations of the ICH patients were strongly correlated with hematoma volume and NIHSS scores. Serum MPO were independently associated with the above-mentioned study points. Its area under receiver operating characteristic curve was equivalent to those of hematoma volume and NIHSS score. Moreover, serum MPO significantly improved the discriminatory ability of hematoma and NIHSS in predicting 6-month mortality and unfavorable outcome. ConclusionsSerum MPO concentrations rise in ICH patients and there is a correlation between MPO concentrations and severity or prognosis.

The Relation of Serum Myeloperoxidase to Disease Progression and Mortality in Patients with Chronic Obstructive Pulmonary Disease (COPD)

Myeloperoxidase is a strong oxidant stored in primary granules of neutrophils with potent antibacterial and proatherogenic properties. Myeloperoxidase has been implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD). However, the relationship of myeloperoxidase to health outcomes in COPD is not well known. We measured serum myeloperoxidase levels from 4,677 subjects with mild to moderate airflow limitation in the Lung Health Study. Using a Cox proportional hazards model, we determined the relationship of serum myeloperoxidase concentration to the risk of all-cause and disease specific causes of mortality. We found that serum myeloperoxidase concentrations were significantly related to accelerated decline in forced expiratory volume in 1 second (FEV1) over 11 years of follow-up (p<0.0001), and this association persisted after adjustments for age, sex, race, baseline FEV1, and smoking status (p = 0.048). Serum myeloperoxidase concentrations were also associated with increased risk of cardiovascular mortality (p = 0.036). Individuals in the highest quintile of myeloperoxidase had a hazard ratio of cardiovascular mortality of 1.90 (95% confidence interval 1.00–3.58; p = 0.049) compared with those in the lowest quintile, which was particularly notable in patients who continued to smoke (adjusted p-value of 0.0396). However, serum myeloperoxidase concentration was not related to total mortality, respiratory mortality, or deaths from malignancies. In conclusion, increased serum myeloperoxidase levels are associated with rapid lung function decline and poor cardiovascular outcomes in COPD patients, which support the emerging role of myeloperoxidase in the pathogenesis of COPD progression and cardiovascular disease.

The Association of Serum Neutrophil Markers and Acute Coronary Syndrome

An association exists between chronic infection-induced inflammation, such as periodontitis, and acute coronary syndrome (ACS). We studied the association of serum neutrophil markers, myeloperoxidase (MPO), matrix metalloproteinase (MMP)-8, tissue inhibitor of metalloproteinase (TIMP)-1 concentrations and MMP-8/TIMP-1 ratio, with the risk of recurrent ACS. Radiographic periodontal status was recorded from 141 patients with acute non-Q-wave infarction or unstable angina pectoris, who participated in a double-blind, placebo-controlled study with clarithromycin for 3 months. Serum samples were collected within arrival to the hospital, at 1 week, 3 months and 1 year. Recurrent ACS events were registered during the 1-year follow-up. In the whole population, high serum MPO concentrations at 1 week (fourth quartile versus quartiles 1-3) were associated with the risk of recurrent ACS with a relative risk (RR) of 2.52 (95% CI, 1.277-4.980; P = 0.008). In patients without periodontal disease, high MPO concentration at 1 week and 1 year predicted recurrent ACS with RRs of 3.54 (1.600-7.831; P = 0.002) and 2.87 (1.171-7.038; P = 0.021), respectively. In the placebo group, but not in the clarithromycin group, high serum MMP-8/TIMP-1 ratio at 1 week predicted recurrent ACS with an RR of 3.23 (1.295-8.063; P = 0.012). Our results suggest that high serum neutrophil markers reflect increased risk of recurrent ACS, especially in patients without periodontal disease and not receiving antimicrobial medication.

Serum myeloperoxidase levels and platelet activation parameters as diagnostic and prognostic markers in the course of coronary disease

Early prediction of coronary artery disease complications is vital for the prevention and effective treatment of patients with coronary cardiac disease. It has been reported that inflammatory markers play a key role in the progression of cardiovascular diseases. Platelet count and platelet morphological parameters were analyzed on a fully-automated hematological analyzer ADVIA 2120 (Siemens). Serum myeloperoxidase (MPO) level was determined with an enzyme immunoassay (BioCheck). The measuring range of this assay is between 0 and 40 ng/ml. We demonstrate that serum MPO concentration and platelet activation increase systematically with the advancement of coronary artery disease. Moreover, MPO level is significantly higher in patients with unstable coronary artery disease and myocardial infarction compared with healthy subjects and patients with stable angina. The diagnostic sensitivity of these parameters was higher than of TnI (cardiac troponin I), CK-MB (creatine kinase-heart type), CRP (C-reactive protein), and fibrinogen and DD (D-dimers). MPO, L-PLT (large platelet), MPV (mean platelet volume), and MPC (mean platelet component concentration) may serve as attractive diagnostic and prognostic markers in the assessment of the risk for unstable atheroma in the course of coronary artery disease.

Low serum myeloperoxidase in autistic children with gastrointestinal disease

To assess serum myeloperoxidase (MPO) levels in autistic children with severe gastrointestinal (GI) disease and to test the hypothesis that there is an association between serum MPO concentration and inflammatory GI disease, including antineutrophil cytoplasmic antibodies (ANCA), previously seen in a subgroup of autistic children. Serum from 40 autistic children with chronic digestive disease (most with ileo-colonic lymphoid nodular hyperplasia (LNH) and inflammation of the colorectum, small bowel and/or stomach), and 48 controls (12 age-matched autistic children with no GI disease, 20 age-matched children without autism or GI disease, and 16 nonautistic individuals with no family history of autism) were tested using enzyme-linked immunosorbent assays designed to quantitate serum MPO levels. MPO serum concentration of autistic children with GI disease was compared to GI disease severity (including LNH and erythema) and presence of ANCA. We found that a significant number of autistic children with chronic digestive disease had low serum levels of MPO. However, there was no significant relationship between these levels and severity of GI disease, including the presence of ANCA. These results suggest a relationship between low MPO levels and GI disease seen in a subpopulation of autism spectrum disorders individuals. MPO concentration may therefore be a useful biomarker for GI disease in this group of autistic children.

Myeloperoxidase and paraoxonase-1 in type 2 diabetic patients

Background and aims Reduced high density lipoproteins (HDL) and increased oxidative stress are features of type 2 diabetes. Myeloperoxidase is an oxidative enzyme partly associated with HDL and causing HDL dysfunction. It is an independent risk factor for cardiovascular disease. Paraoxonase-1 is an HDL-associated enzyme that protects against cardiovascular disease and is reduced in diabetes. The present study examined if serum myeloperoxidase was (i) increased in type 2 diabetes, (ii) correlated with paraoxonase-1 activity. Methods and results The study was based on cross-sectional analyses of serum myeloperoxidase and paraoxonase-1 in type 2 diabetic patients and non-diabetic participants, with and without cardiovascular disease. Serum myeloperoxidase concentrations were not increased in type 2 diabetic patients without cardiovascular disease compared to non-diabetic controls. They were significantly higher in type 2 patients and non-diabetic patients with angiographically confirmed coronary disease. HDL-associated myeloperoxidase was correlated with serum myeloperoxidase ( r = 0.80, p < 0.001) but not HDL-cholesterol ( r = 0.08) or apolipoprotein AI ( r = 0.08). Multivariate analyses showed serum myeloperoxidase to be an independent determinant of paraoxonase activities (arylesterase, p = 0.024; paraoxonase, p = 0.026). Conclusions Myeloperoxidase is an independent, negative determinant of paraoxonase-1 activity, which may be one mechanism by which it promotes HDL dysfunction and increases cardiovascular risk. Increased serum myeloperoxidase is not a feature of type 2 diabetes in the absence of overt cardiovascular disease. The level of HDL-associated myeloperoxidase is determined by the serum concentration of the enzyme suggesting that, in the context of reduced HDL concentrations in diabetic patients, myeloperoxidase may have a greater impact on HDL function.

The effect of atorvastatin on serum myeloperoxidase and CRP levels in patients with acute coronary syndrome

Background Inflammation is involved in the atherogenesis and pathogenesis of acute coronary syndrome (ACS). As the acute-phase reaction proteins in ACS, myeloperoxidase (MPO) and C-reactive protein (CRP) may play critical roles. Anti-inflammation may be one of benefits of statin drugs in ACS. Studies have showed that statins can suppress serum CRP concentrations. However, whether statins also reduce serum MPO concentrations in patients with ACS is unknown. Methods Seventy-eight patients with ACS were randomly separated into Group A and Group B, the patients in Group A receiving conventional therapy, which include no cholesterol-lowering drugs, + atorvastatin (10 mg/day, n = 40), the patients in Group B receiving conventional therapy ( n = 38). The serum concentrations of MPO were measured by enzyme-linked immunosorbent assay (ELISA) and CRP were measured by turbidimetric immunoassay. Results Serum concentrations of MPO were significantly lower after 1-week therapy in both groups of patients [Group A from 590 ± 168 to 496 ± 154 μg/l, Group B from 570 ± 165 to 521 ± 153 μg/l; P < 0.01, respectively]. Serum concentrations of CRP also were markedly lower than pretreatment [Group A from 6.56 ± 1.87 to 5.14 ± 2.07 mg/l; Group B from 6.36 ± 1.94 to 5.45 ± 1.90 mg/l, P < 0.05, respectively]. Compared with conventional therapy alone, atorvastatin significantly further reduced serum MPO [ P = 0.014] and CRP concentrations [ P = 0.032]. There were no correlations detected between the reduction of MPO and CRP ( r = 0.124, P = 0.068). Conclusions Atorvastatin reduced serum MPO and CRP concentrations in patients with ACS. These effects may explain some clinical benefits of statins in the treatment of these patients.

Beta-carotene supplementation decreases leukocyte superoxide dismutase activity and serum glutathione peroxidase concentration in humans

The effects of a 30 mg/day beta-carotene supplement for 60 days on blood cell and serum antioxidant enzymes and selenium concentrations were examined in healthy adults. Serum beta-carotene concentrations increased significantly ( P < 0.05) in response to supplementation. Forty percent of subjects exhibited hypercarotenemia of the skin after 30 days. There were no changes in the activity of red blood cell or leukocyte catalase activity, red blood cell copper,zinc-dependent superoxide dismutase activity or serum myeloperoxidase concentration in response to beta-carotene supplementation. Leukocyte superoxide dismutase activity decreased significantly ( P < 0.05) at 30 and 60 days compared to baseline. Serum glutathione peroxidase concentration decreased significantly ( P < 0.05) between baseline and days 45 and 60 of supplementation. Serum selenium and blood hemoglobin concentrations did not change during the study. Supplemental beta-carotene may alter the antioxidant capacity of plasma and/or blood cells in vivo.

Serum myeloperoxidase concentration in a healthy population: biological variations, familial resemblance and new genetic polymorphisms.

Myeloperoxidase (MPO) has been involved in the pathogenesis of several diseases through excessive production of reactive oxygen species (ROS) as well as through its genetic polymorphism. The aims of this study were to identify the factors affecting MPO serum concentration, to study the familial resemblance of MPO levels and to investigate the association between newly described MPO polymorphisms as well as the G-463A one and MPO levels in a healthy population. MPO serum concentrations were measured by an enzymatic immuno-assay (EIA) in 82 healthy families of the STANISLAS Cohort and MPO genotype, determination was performed using PCR-restriction fragment length polymorphism or allele specific oligonucleotide assay. MPO concentrations were significantly higher in parents than in offspring. The factors affecting MPO levels were age, the number of white cells, smoking in fathers and oral contraceptive intake in mothers. They explain from 12.4% up to 35.9% of MPO variability in men and women, respectively. Family correlations of MPO concentrations were of similar magnitude. The -129A allele of a newly described G-129A substitution was significantly associated with decreased MPO levels, whereas the -463A allele was suggested to be associated with increased levels of lipid variables. In this study, we identified factors affecting MPO serum concentrations and showed that molecular variations of the gene have only a weak influence on MPO variability. In contrast, the association between the G-463A polymorphism and lipid levels would suggest a possible implication of MPO in the risk of cardiovascular diseases. These results have to be confirmed and further investigations will be conducted in that way.

Vincristine degradation by serum from leukemic patients: role of myeloperoxidase.

Myeloperoxidase (MPO) has been shown to catalyze the in vitro degradation of vincristine (VCR). Given that MPO is a lysosomal enzyme that can be released into the circulation by both normal activated and leukemic myeloid cells, we investigated the possibility that sera from patients with acute myeloblastic leukemia (AML) might exhibit an increased capacity to degrade VCR. 31 serum samples (23 from patients with acute myeloblastic leukemia and 8 from patients with other conditions) were analyzed after incubation with ((3)H)VCR by using HPLC. Sera from patients with AML demonstrated an increased ability to breakdown VCR when compared to either normal sera or to sera from patients with lymphoid leukemias. VCR degradation was significantly increased by adding hydrogen peroxide, an electron donor for MPO, to the sera and was almost completely inhibited by adding 1 mM acetaminophen, an inhibitor of MPO. VCR peroxidation in the presence of hydrogen peroxide correlated both with the number of leukemic blasts in the circulation at the time the sera were obtained and with serum MPO concentrations determined by an immunoassay. These data suggest that the inactivity of VCR in AML may be due in part to its rapid peroxidation to inactive species by the MPO of leukemic myeloblasts.

Myeloperoxidase and eosinophil cationic protein in serum and sputum during antibiotic treatment in cystic fibrosis patients with Pseudomonas aeruginosa infection

I order to study the time-course of myeloperoxidase (MPO) and eosinophil cationic protein (ECP) as parameters for monitoring inflammation in cystic fibrosis (CF), we investigated ten patients during both a 14-day intravenous antibiotic treatment and a corresponding self control. Modified Shwachman-Kulczycki score improved significantly (p < 0.008), C-reactive protein (CRP) levels decreased significantly (p < 0.05) during antibiotic treatment, while in the control phase there were no significant differences. Lung function parameters did not change significantly during antibiotic treatment or control phase. Serum MPO concentration (p < 0.006) and peripheral blood neutrophil granulocyte counts (p < 0.04) decreased significantly during antibiotic treatment, but not during the control phase. Sentm ECP concentration showed a tendency to decrease during antibiotic treatment, but this failed to reach significance. In general, sputum concentrations of MPO and ECP Were 500- to 1000-fold higher than in serum. However, neither MPO nor ECP in sputum showed a significan variation over time during antibiotic treatment or control phase. From our data we conclude that: (1) measurements of MPO, neutrophils and CRP in peripheral blood do correlate with clinical parameters such as the modified Shwachman-Kulczycki score; (2) neutrophils and MPO seem to reflect inflammatory changes induced by antibiotic treatment; (3) eosinophils may play a role in CF by an enhanced ‘releasability’ and (4) Sputum measurements of mediators of inflammation cannot be recommended.