interleukin-8 and Dyspnea

The respiratory system is the first line of defense against outside pollutants. Recently, respiratory health has been receiving increasing attention due to the increase in fine dust, which reduces respiratory function and increases incidence of chronic obstructive pulmonary disease, and in coronavirus pandemic, which can cause severe acute respiratory syndrome.. This clinical pilot trial was designed to secure evidence for a main clinical trial and to confirm the efficacy and safety of Liriope platyphylla (LP) extract for improving respiratory function. We conducted a double-blind randomized placebo-controlled trial with 22 participants from June 30, 2021, to August 25, 2021. The primary outcome was Breathlessness, Cough, and Sputum Scale score. Secondary outcomes included forced vital capacity, forced expiratory volume at 1 second (FEV1), forced expiratory volume at 1 s/forced vital capacity ratio, cough assessment test score, chronic obstructive pulmonary disease assessment test score, peripheral blood mononuclear cell counts (white blood cells, eosinophils, T cells, and B cells), high-sensitivity C-reactive protein level, erythrocyte sedimentation rate, cytokine (interleukin-1β, interleukin-4, tumor necrosis factor-α, interleukin-6, interleukin-8, interferon-γ, and immunoglobulin E) levels, antioxidant (glutathione peroxidase and superoxide dismutase) levels, and nitric oxide level.. A total of 22 participants were randomly assigned to 2 groups: the LP group (n = 11), who took 1000 mg of LP extract per day, and the placebo group, who took 1000 mg of dextrin per day. Participants took 1 capsule twice a day for 4 weeks. For the Breathlessness, Cough, and Sputum Scale, the interaction between group and visit was statistically significant in a blend of analyses of variance. interleukin-8, tumor necrosis factor-α, and interferon-γ levels decreased more in the LP group than in the placebo group. The sample size required for large-scale clinical trials in the future was 50. There were no side effects.. LP extract can enhance respiratory function. The detailed data we obtained support conducting the future main large-scale clinical trial.

Topics: Antioxidants; C-Reactive Protein; Cough; Dextrins; Dust; Dyspnea; Glutathione Peroxidase; Humans; Immunoglobulin E; Interferon-gamma; Interleukin-1beta; Interleukin-4; Interleukin-6; Interleukin-8; Leukocytes, Mononuclear; Nitric Oxide; Pilot Projects; Plant Extracts; Pulmonary Disease, Chronic Obstructive; Superoxide Dismutase; Tumor Necrosis Factor-alpha

Post-transfusion reactions with dyspnoea (PTR) are major causes of morbidity and death after blood transfusion. Transfusion-related acute lung injury (TRALI) and transfusion-associated circulatory overload (TACO) are most dangerous, while transfusion-associated dyspnoea (TAD) is a milder respiratory distress. We investigated blood components for immune and non-immune factors implicated in PTR.. We analysed 464 blood components (RBCs, PLTs, L-PLTs, FFP) transfused to 271 patients with PTR. Blood components were evaluated for 1/antileucocyte antibodies, 2/cytokines: IL-1β, IL-6, IL-8, TNF-α, sCD40L, 3/lysophosphatidylcholines (LysoPCs), 4/microparticles (MPs) shed from plateletes (PMPs), erythrocytes (EMPs) and leucocytes (LMPs).. Anti-HLA class I/II antibodies or granulocyte-reactive anti-HLA antibodies were detected in 18.2% of blood components (RBC and FFP) transfused to TRALI and in 0.5% of FFP transfused to TAD cases. Cytokines and LysoPCs concentrations in blood components transfused to PTR patients did not exceed those in blood components transfused to patients with no PTR. Only EMPs percentage in RBCs transfused to patients with TRALI was significantly higher (P < 0.05) than in RBCs transfused to patients with no PTR.. Immune character of PTR was confirmed mainly in 1/5 TRALI cases. Among non-immune factors, only MPs released from stored RBCs are suggested as potential mediators of TRALI. Our results require further observations in a more numerous and better defined group of patients.

Topics: Acute Lung Injury; Adult; Antibodies; Cell-Derived Microparticles; Dyspnea; Female; Humans; Interleukin-8; Male; Middle Aged; Platelet Transfusion; Transfusion Reaction

Interferon gamma-1b (IFN-gamma1b) is a pleiotropic cytokine with immunomodulatory activities that could decrease bacterial burden, inflammation, and obstruction in patients with CF. Patients with CF (> or =12 years old, FEV1 > or =40% predicted) were randomly assigned to sequential dose cohorts inhaling 500 microg IFN-gamma1b, 1,000 microg IFN-gamma1b, or placebo by Respirgard II nebulizer thrice weekly for 12 weeks. Sputum bacterial density and spirometry were measured. Safety, antibiotic use, hospitalization, and sputum neutrophils, elastase, DNA, IL-8, and myeloperoxidase were also evaluated. Sixty-six patients (mean age, 24 years, with mean baseline FEV1 of 74 +/- 20 (SD) percent predicted) were studied. One patient had bronchospasm after the first dose of IFN-gamma1b; the overall withdrawal rate was 15% (5 in the placebo group, 2 in the 500-microg IFN-gamma1b group, and 3 in the 1,000 microg IFN-gamma1b group). The 500-microg IFN-gamma1b dose was well-tolerated, but the 1,000-mug dose cohort, who had a higher baseline bacterial density than placebo patients (mean difference, 1.2 log(10) CFU/g sputum, 95% confidence interval (CI), 0.1,2.8, P=0.04), had 24% more hospitalizations for exacerbation than placebo patients (95% CI, 2,45%, P=0.05). There was a 0.12-l difference between the 500-microg IFN-gamma1b and placebo groups with respect to the 12-week change in FEV1 (active group minus placebo group, 95% CI, -0.03,0.26, P=0.11), as compared to a 0.01-l difference between the 1,000-microg IFN-gamma1b and placebo groups (95% CI, -0.16,0.17, P=0.96). No effects of IFN-gamma1b were seen in sputum bacterial density or inflammatory biomarkers at 12 weeks. Aerosolized IFN-gamma1b did not improve pulmonary function, reduce sputum bacterial density, or affect inflammatory sputum markers in patients with mild-moderate lung disease.

Topics: Administration, Inhalation; Adolescent; Adult; Anti-Bacterial Agents; Antineoplastic Agents; Colony Count, Microbial; Cystic Fibrosis; Dose-Response Relationship, Drug; Double-Blind Method; Drug Administration Schedule; Dyspnea; Female; Hemoptysis; Hospitalization; Humans; Interferon-gamma; Interleukin-8; Male; Neutrophils; Pancreatic Elastase; Peroxidase; Recombinant Proteins; Respiratory Tract Infections; Sputum; Treatment Outcome

To investigate the efficacy and safety of a fully human monoclonal antibody recognizing the chemokine interleukin (IL)-8 in patients with COPD.. Randomized, double-blind, parallel-group, placebo-controlled trial.. Eighteen clinics/hospitals in the United States.. One hundred nine patients with stable COPD.. Three IV infusions of either monoclonal antibody recognizing IL-8 (800-mg loading dose; 400-mg subsequent doses) or active buffer solution administered monthly over a 3-month period.. The differences in the transition dyspnea index (TDI) total score, the primary outcome measure, between fully human monoclonal IgG(2) antibody directed against IL-8 and placebo were 0.8, 1.0, 0.8, and 0.3 at week 2 (p = 0.046) and months 1 to 3, respectively. At all time points, the proportion of patients achieving >/= 1 point improvement in the TDI was greater for the monoclonal antibody group compared with the placebo group: 28% vs 11% at week 2 (p = 0.028). There were no significant differences observed for lung function, health status, 6-min walking distance, and adverse events between groups.. The results of this phase 2 study suggest that neutralization of IL-8 with monoclonal antibody therapy may improve dyspnea in patients with COPD. These results support the further investigation of monoclonal antibody therapy targeting IL-8 for the treatment of this disease.

Topics: Aged; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Dose-Response Relationship, Drug; Double-Blind Method; Dyspnea; Female; Humans; Infusions, Intravenous; Interleukin-8; Male; Middle Aged; Neutrophil Activation; Pilot Projects; Pulmonary Disease, Chronic Obstructive; Receptors, Interleukin-8A; Respiratory Function Tests

To explore the clinical benefits of azithromycin in the treatment of Pseudomonas aeruginosa induced bronchiectasis and to evaluate its effect on MUC5AC. From April 2018 to June 2020, 160 patients with bronchiectasis due to Pseudomonas aeruginosa infection were selected. The patients were divided into a control groupand an azithromycin group. Statistics of patients' general clinical data, lung function indexes, sputum volume, oxidative stress level, Bhalla score before and after treatment; Western blot analysis of MUC5AC expression; RT-PCR analysis of TNF-α, IL-8, IL- 1β mRNA expression. The mRNA expression of TNF-α, IL-8 and IL-1β in the azithromycin group was lower than that in the control group (P<0.05). After treatment, the protein expression of MUC5AC in the azithromycin group was lower than that in the control group (P<0.05). The improvement rate in the azithromycin group was significantly higher than that in the control group (P<0.05). The azithromycin group had a lower lung infection rate than the control group (P<0.05). The azithromycin group had a lower dyspnea rate than the control group (P<0.05). Azithromycin treatment has certain clinical benefits for patients with bronchiectasis induced by Pseudomonas aeruginosa and inhibits the MUC5AC expression.

Topics: Adult; Anti-Bacterial Agents; Azithromycin; Bronchiectasis; Dyspnea; Female; Humans; Interleukin-1beta; Interleukin-8; Male; Middle Aged; Mucin 5AC; Pseudomonas aeruginosa; Pseudomonas Infections; RNA, Messenger; Tumor Necrosis Factor-alpha

The Global Initiative classification (GOLD) for chronic obstructive pulmonary disease (COPD), which relies on the practical issues of treatment of this complex and heterogeneous disease, may not be reliable in predicting disease severity and prognosis as the term of inflammation is excluded from the definition.. The aim of this study was to determine systemic inflammatory markers in GOLD ABCD groups and to compare these parameters according to clinical and functional features.. The study included 60 COPD patients and 59 healthy subjects. Comparisons were made with the pulmonary function test, transthoracic echocardiography and the six-minute walk test (6MWT). The COPD assessment test (CAT), modified Medical Research Council (mMRC), and index scores of body mass index, airflow obstruction, dyspnea, and exercise capacity (BODE) were recorded. The systemic inflammatory state was assessed using C-reactive protein, fibrinogen, tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, IL-8 and IL-18.. The levels of all serum inflammatory markers were higher in the COPD group than in the control group. TNF-α and IL-6 were significantly higher in the symptomatic groups (B and D) than in the less symptomatic groups (A and C) (P < 0.05). Spirometric parameters were more severe in Group D, followed by groups C, B and A, respectively. The 6MWT and the BODE scores were worst in Group D, followed by groups B, C and A.. The results suggest that bronchodilator treatment alone might be insufficient in Group B patients, as the systemic inflammatory markers in addition to exercise capacity and mortality predictors were at the worst level in Groups D and B.

Topics: Aged; Biomarkers; Body Mass Index; C-Reactive Protein; Case-Control Studies; Cross-Sectional Studies; Dyspnea; Echocardiography; Exercise Tolerance; Female; Humans; Inflammation; Inflammation Mediators; Interleukin-6; Interleukin-8; Lung; Male; Middle Aged; Pulmonary Disease, Chronic Obstructive; Respiratory Function Tests; Severity of Illness Index; Spirometry; Tumor Necrosis Factor-alpha; Walk Test

Various biomarkers have emerged as potential surrogates to represent various subgroups of chronic obstructive pulmonary disease (COPD), which manifest with different phenotypes. However, the biomarkers representing never-smokers with COPD have not yet been well elucidated. The aim of this study was to evaluate the associations of certain serum and radiological biomarkers with the presence of COPD in never-smokers. To explore the associations of serum and radiological biomarkers with the presence of COPD in never-smokers, we conducted a cross-sectional patient cohort study composed of never-smokers from the COPD in Dusty Areas (CODA) cohort, consisting of subjects living in dusty areas near cement plants in South Korea. Of the 131 never-smokers in the cohort, 77 (58.8%) had COPD. There were no significant differences in the number of subjects with high levels of inflammatory biomarkers (>90th percentile of never-smokers without COPD), including white blood cell count, total bilirubin, interleukin (IL)-6, IL-8, and C-reactive protein, or radiologic measurements (including emphysema index and mean wall area percentage) between never-smokers with COPD and those without COPD. However, the number of subjects with high uric acid was significantly higher in never-smokers with COPD than never-smokers without COPD (31.2% (24/77) vs. 11.1% (6/54); p = 0.013). In addition, multivariate analysis revealed that high uric acid was significantly associated with the presence of COPD in never-smokers (adjusted relative risk: 1.63; 95% confidence interval: 1.21, 2.18; p = 0.001). Our study suggests that high serum levels of uric acid might be a potential biomarker for assessing the presence of COPD in never-smokers.

Topics: Aged; Bilirubin; C-Reactive Protein; Case-Control Studies; Cohort Studies; Cross-Sectional Studies; Dust; Dyspnea; Female; Forced Expiratory Volume; Humans; Inflammation; Interleukin-6; Interleukin-8; Lung; Male; Manufacturing and Industrial Facilities; Non-Smokers; Pulmonary Disease, Chronic Obstructive; Quality of Life; Republic of Korea; Residence Characteristics; Tomography, X-Ray Computed; Uric Acid; Vital Capacity

The objective was to identify inflammatory biomarkers that predict risk of 90-day mortality in patients with acute dyspnea.. We analyzed 25 inflammatory biomarkers, in plasma, in 407 adult patients admitted to the emergency department (ED) with acute dyspnea and related them to risk of 90-day mortality using Cox proportional hazard models adjusted for age, sex, oxygen saturation, respiratory rate, C-reactive protein, and Medical Emergency Triage and Treatment System-Adult score.. Fifty patients (12%) died within 90 day from admission. Two strong and independent biomarker signals were detected: The hazard ratio (95% confidence interval) for 90-day mortality per 1-SD increment of interleukin-8 (IL-8) was 2.20 (1.67-2.90) (P = 2.5 × 10(-8)) and for growth differentiation factor-15 (GDF-15) was 3.45 (2.18-5.45) (P = 1.3 × 10(-7)) A Biomarker Mortality Risk Score (BMRS) summing standardized and weighted values of IL-8 and GDF-15 revealed that of patients belonging to quartile 1 (Q1) of the BMRS, only 1 patient died, whereas 32 patients died among those belonging to quartile 4. Each 1-SD increment of the BMRS was associated with a hazard ratio of 3.79 (2.50-5.73) (P = 2 × 10(-10)) for 90-day mortality, and the point estimate was 13 times higher in Q4 as compared with Q1 of the BMRS (P(trend) over quartiles = 2 × 10(-6)).. Interleukin-8 and GDF-15 are strongly and independently related to risk of 90-day mortality in unselected patients admitted to the ED because of acute dyspnea, suggesting that they may guide first-line physicians at the ED in risk assessment which in turn could lead to more accurate level of care and treatment intensity.

Topics: Age Factors; Aged; Biomarkers; C-Reactive Protein; Dyspnea; Emergency Service, Hospital; Female; Growth Differentiation Factor 15; Humans; Interleukin-8; Male; Oxygen; Predictive Value of Tests; Prognosis; Respiratory Rate; Risk Factors; Sex Factors; Sweden; Triage

Respiratory pathogens are frequently isolated from the airways of patients with chronic obstructive pulmonary disease (COPD) in the absence of an exacerbation. This bacterial "colonization" by potential pathogens is associated with host inflammatory and immune responses, which could increase respiratory symptoms.. To study whether bacterial colonization impacts daily respiratory symptoms in COPD.. In a longitudinal prospective observational study of COPD, patients recorded daily symptoms electronically on the Breathlessness, Cough, and Sputum Scale (BCSS). Sputum cultures and quantitative polymerase chain reaction (PCR) were performed every 2 weeks. The relationship of BCSS and bacterial colonization was analyzed with generalized linear mixed effects models, after controlling for exacerbations, weather conditions, lung function, and demographic variables.. A total of 41 patients recorded daily symptoms for 12,527 days. The average BCSS score was higher during the periods of colonization, determined by sputum culture with one or more of the following pathogens: nontypeable Haemophilus influenzae, Moraxella catarrhalis, Streptococcus pneumoniae, and Pseudomonas aeruginosa, compared to periods without colonization (5.28 vs. 4.46; P = 0.008) after controlling for confounding variables. The finding did not change when colonization was defined by quantitative PCR (average BCSS, 4.77 vs. 4.25; P = 0.006). Sputum IL-8 levels were elevated with bacterial colonization.. Even in the absence of clinical exacerbation, colonization by bacterial pathogens in COPD was associated with a clinically significant moderate increase in daily symptoms, likely mediated by increased airway inflammation. Novel therapies that decrease bacterial colonization in COPD could improve daily symptoms and quality of life.

Topics: Aged; Cough; Dyspnea; Female; Haemophilus influenzae; Humans; Interleukin-8; Longitudinal Studies; Male; Middle Aged; Moraxella catarrhalis; Prospective Studies; Pseudomonas aeruginosa; Pulmonary Disease, Chronic Obstructive; Sputum; Streptococcus pneumoniae

When exacerbation of chronic obstructive pulmonary disease (AECOPD) occurs frequently, patients have high levels of airway and systemic inflammation and a poor quality of life. This study compared the nature and course of systemic and airway inflammation during AECOPD between patients who experienced frequent exacerbations and those with non-frequent exacerbations.. Consecutive hospitalized patients with AECOPD were recruited and divided into 2 groups according to the frequency of AECOPD they had experienced in the previous year. Frequent exacerbators (defined as 2 or more AECOPD in the previous year) and non-frequent exacerbators (defined as zero or 1 AECOPD in the previous year). Inflammatory (interleukin 6, interleukin 8, myeloperoxidase, and C-reactive protein) and clinical (dyspnea, COPD assessment test (CAT), and peak expiratory flow) indices were assessed on the day of admission before starting therapy, day 7 of treatment, the day of planned discharge (day 10-14), and 8 weeks after discharge.. We analyzed data from 135 patients; 78 (57.8%) were non-frequent exacerbators and 57 (42.2%) were frequent exacerbators. In both groups, the inflammatory and clinical indices at day 7, the day of planned discharge (day 10-14), and 8 weeks were significantly improved compared to those at admission. Frequent exacerbators had a smaller reduction in their inflammatory indices and CAT scores between exacerbation onset and all the other time points compared with infrequent exacerbators.. Frequent exacerbators have a reduced response to treatment of AECOPD in terms of inflammatory indices and quality of life.

Topics: Aged; Bronchitis; C-Reactive Protein; China; Dyspnea; Female; Humans; Inflammation; Interleukin-6; Interleukin-8; Lung Diseases, Obstructive; Male; Middle Aged; Peak Expiratory Flow Rate; Peroxidase; Prospective Studies; Quality of Life; Recurrence; Statistics, Nonparametric; Time Factors

The BODE index, based on BMI, obstructive ventilatory impairment, dyspnoea scale and exercise capacity, has been used to evaluate the severity of patients with COPD. However, the correlations between serum biomarkers and the BODE index in patients with stable COPD are not widely studied. This study evaluated potential serum biomarkers for their ability to identify smokers with COPD and reflect disease severity.. A comparative study was conducted of 100 clinically stable COPD patients and 50 matched healthy smokers and the difference in levels of biomarkers between the COPD patients and healthy smokers was measured. Serum inflammatory mediators measured were growth-related oncogene-alpha (GRO-alpha), IL-8, tumour necrosis factor-alpha (TNF-alpha), matrix metalloproteinase-9 (MMP-9) and monocyte chemoattractant protein-1 (MCP-1). Variables included age, pack-years, current or ex-smoker status, inhaler or oral steroid use and BODE index components, including airflow obstruction, the distance walked in 6MWD, modified Medical Research Council (MMRC) dyspnoea scale and BMI. The association between serum biomarkers and the components of the BODE index was assessed in the COPD patients.. The level of serum MCP-1 was significantly different between the COPD group and the healthy smoker group (P = 0.003). Significant results in univariate and multivariate analysis of the association between biomarkers and BODE components were: serum MCP-1 correlated with FEV(1)% and 6MWD; serum IL-8 and GRO-alpha correlated with steroid use; serum TNF-alpha correlated with steroid use and FEV(1)%; and serum MMP-9 correlated with MMRC dyspnoea scale.. No single specific serum inflammatory mediator was completely correlated with BODE variable parameters in patients with stable COPD. Serum MCP-1 may be an important biomarker for identifying COPD subjects from healthy smokers and classifying COPD severity.

Topics: Aged; Aged, 80 and over; Biomarkers; Body Mass Index; Case-Control Studies; Chemokine CCL2; Chemokine CXCL1; Dyspnea; Exercise Tolerance; Forced Expiratory Volume; Humans; Interleukin-8; Lung; Matrix Metalloproteinase 9; Middle Aged; Pulmonary Disease, Chronic Obstructive; Severity of Illness Index; Smoking; Tumor Necrosis Factor-alpha

Sulfur mustard (SM) is a blistering chemical agent which has short and long term toxicity against many organs. The respiratory tract is one of the main targets, and is the most disabling long term complication of SM. Inflammatory mediators especially IL-8 and IL-6 play the primary role in the various chronic pulmonary diseases. Sardasht-Iran Cohort Study (SICS) was designed to evaluate immunological and molecular parameters in SM exposed people 20 years after exposure. In the present study, the association of the serum levels of IL-8, IL-6, C reactive protein (CRP) and rheumatoid factor (RF) with long term pulmonary involvement was evaluated. There were 348 exposed and 120 control participants. The clinical evaluations were done for all subjects and Spirometry was performed according to American Thoracic Society Criteria. Severity of pulmonary involvement was assessed by Global Initiative for chronic Obstructive Lung Disease (GOLD) classification. The serum levels of IL-8, IL-6 and RF were assessed by ELISA assay. CRP was assessed by photometric method. The serum levels of IL-8 and IL-6 significantly decreased in the SM exposed participants compared to the control group. There were no significant associations between the serum levels of IL-8 and pulmonary symptoms (chronic cough, sputum, hemoptysis, and dyspnea), pulmonary findings (crackles, rales, and wheezing) as well as spirometry parameters. IL-6 was associated with wheezing and CRP was associated with wheezing and rales in SM exposed group. We concluded the serum levels of these inflammatory mediators probably do not have any major role in pathogenesis and persistence of pulmonary complications and do not reflect the degree of severity of pulmonary involvement following SM exposure.

Topics: C-Reactive Protein; Chemical Warfare Agents; Cohort Studies; Cough; Dyspnea; Humans; Interleukin-6; Interleukin-8; Iran; Mustard Gas; Pulmonary Disease, Chronic Obstructive; Respiratory Function Tests; Respiratory Sounds; Rheumatoid Factor; Time Factors

Sarcoidosis (SAR) is a systemic granulomatous inflammatory disease characterized by recruitment and activation of peripheral blood mononuclear cells to the sites of disease. Neovascularisation is a principal vascular response in chronic inflammation and hypoxia. The aim of the study was to evaluate the effect of sera from sarcoidosis patients on angiogenic capability of different subsets of normal peripheral human mononuclear cells (MNC) in relation to IL-6 and IL-8 serum levels, to radiological stages of disease and to the presence of extrapulmonary changes. Serum samples obtained from 42 sarcoidosis patients were examined. There were 12 patients in stage I, 16 patients in stage II, and 14 in stage III. In order to quantify angiogenesis, a leukocyte-induced angiogenesis assay was performed by a method of Sidky and Auerbach. MNC were depleted in monocytes by glass adherence and phagocytosis of iron particles techniques. IL-6 and IL-8 in sera from sarcoidosis patients were evaluated by an ELISA-based assay. Sera from sarcoidosis patients enhanced angiogenic capability of normal MNC significantly stronger than sera from healthy donors (P<0.001). Angiogenic activity of sera in sarcoidosis depended on the stage of disease and appeared most pronounced in stage II (P<0.05). Sera from patients with extrapulmonary changes exerted stronger effect on angiogenesis than sera from patients with thoracic changes only (P<0.001). IL-6 and IL-8 serum level correlated with each other, but no correlation was found between IL-6 and IL-8 serum level and angiogenic activity of the examined sera. Removal of monocytes from MNC eliminated the effect of sera from sarcoidosis patients on angiogenesis compared with the effect of these sera on intact MNC (P<0.001). Sera from sarcoidosis patients and from healthy people constitute a source of mediators participating in angiogenesis. Sera from sarcoidosis patients prime monocytes for production of proangiogenic factors.

Topics: Adult; Aged; Animals; Cough; Dyspnea; Enzyme-Linked Immunosorbent Assay; Female; Humans; Interleukin-6; Interleukin-8; Lymphocyte Subsets; Male; Mice; Mice, Inbred BALB C; Middle Aged; Monocytes; Neovascularization, Pathologic; Radiography; Sarcoidosis; Smoking

Leukocytopenia can be caused by depressed production, increased peripheral destruction, or excessive peripheral pooling. Leukocyte margination is one of the mechanisms responsible for excessive peripheral pooling. A reversible leukocyte margination is caused by an increase in pro-inflammatory cytokines. However, there are limited data for this phenomenon in clinical conditions. We describe a case of unexpected transient leukocytopenia after exchanging an extracorporeal membrane oxygenation (ECMO) system used to treat severe cardiogenic pulmonary edema. To assess the cause of the leukocytopenia, the serum concentrations of pro-inflammatory cytokines and selectins were measured. The concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and IL-8 were markedly, but transiently, elevated in relation to the leukocytopenia. The transient leukocytopenia with pulmonary margination appeared to be caused by a steep surge of pro-inflammatory cytokines stimulated by hypoxia/reoxygenation during the exchange of the ECMO system. This case may suggest the mechanisms responsible for leukocytopenia in the clinical entity referred to as "systemic inflammatory response syndrome"

Topics: Chordae Tendineae; Cytokines; Dyspnea; Extracorporeal Membrane Oxygenation; Heart Valve Diseases; Humans; Hypoxia; Interleukin-6; Interleukin-8; Intra-Aortic Balloon Pumping; Leukopenia; Male; Middle Aged; Mitral Valve Insufficiency; Positive-Pressure Respiration; Pulmonary Edema; Rupture, Spontaneous; Systemic Inflammatory Response Syndrome; Tumor Necrosis Factor-alpha

Topics: Administration, Inhalation; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Dose-Response Relationship, Drug; Dyspnea; Humans; Interleukin-8; Neutrophil Activation; Pulmonary Disease, Chronic Obstructive; Receptors, Interleukin-8A; Respiratory Function Tests

We report a rare case of a cute lymphoblasticleukemia (ALL) who developed dyspnea, neurological disturbance with illusions, pancytopenia, phagocytosis and coagulation disturbances following bacterial tonsillitis. The values of soluble interleukin-2 receptor (sIL-2R), IL-6 and IL-8 were also elevated. Her clinicolaboratory findings were similar to hemophagocytic lymphohistiocytosis (HLH), which is a cytokine disease induced by activated T cells and macrophages. Atypical HLH following bacterial tonsillitis should be kept in mind in leukemia patients.

Topics: Antigens, CD; Antineoplastic Agents; Blood Coagulation; Child; Dyspnea; Female; Histiocytosis, Non-Langerhans-Cell; Humans; Interleukin-6; Interleukin-8; Pancytopenia; Phagocytosis; Precursor Cell Lymphoblastic Leukemia-Lymphoma; Pseudomonas aeruginosa; Pseudomonas Infections; Receptors, Interleukin-2; Streptococcal Infections; Tonsillitis

Topics: Dyspnea; Gene Expression; Granulocyte Colony-Stimulating Factor; HLA-B Antigens; HLA-B51 Antigen; HLA-B52 Antigen; Humans; Interleukin-8; Respiratory Distress Syndrome; Systemic Inflammatory Response Syndrome; Tumor Necrosis Factor-alpha