interleukin-8 and Rupture--Spontaneous

Platelets foster an inflammatory environment that influences atherosclerotic lesion progression and facilitates plaque rupture, in addition to their role in acute thrombus formation. The route of entry of platelets into the atherosclerotic plaque and their exact location inside the plaque are however not completely understood.. 188 carotid plaques were examined for the presence of platelets using immunohistochemistry (CD42b), and 76/188 (40.4%) were platelet positive. Platelets were observed in intraplaque hemorrhages, around plaque microvessels, mostly without leakage of erythrocytes; and in mural thrombi. Platelet positive staining was associated with a higher plaque microvessel density, and elevated plaque-levels of interleukin-8.. Due to their short life span, platelets reflect recent bleeding. It can be hypothesized that platelets might serve as a marker for leaky microvessels inside atherosclerotic plaques that are at risk for development, or progression of plaque hemorrhage.

Topics: Aged; Biomarkers; Blood Platelets; Capillary Permeability; Carotid Arteries; Carotid Artery Diseases; Disease Progression; Female; Hemorrhage; Humans; Immunohistochemistry; Interleukin-8; Male; Microvessels; Middle Aged; Plaque, Atherosclerotic; Platelet Glycoprotein GPIb-IX Complex; Rupture, Spontaneous

Spontaneous intracerebral hemorrhage (ICH) represents about 15% of all strokes and is associated with high mortality rates. Our aim was to identify the gene expression changes and biological pathways altered in the brain following ICH.. Twelve brain samples were obtained from four deceased patients who suffered an ICH including perihematomal tissue (PH) and the corresponding contralateral white (CW) and grey (CG) matter. Affymetrix GeneChip platform for analysis of over 47,000 transcripts was conducted. Microarray Analysis Suite 5.0 was used to process array images and the Ingenuity Pathway Analysis System was used to analyze biological mechanisms and functions of the genes. We identified 468 genes in the PH areas displaying a different expression pattern with a fold change between -3.74 and +5.16 when compared to the contralateral areas (291 overexpressed and 177 underexpressed). The top genes which appeared most significantly overexpressed in the PH areas codify for cytokines, chemokines, coagulation factors, cell growth and proliferation factors while the underexpressed codify for proteins involved in cell cycle or neurotrophins. Validation and replication studies at gene and protein level in brain samples confirmed microarray results.. The genomic responses identified in this study provide valuable information about potential biomarkers and target molecules altered in the perihematomal regions.

Topics: Aged; Aged, 80 and over; Brain Diseases; Cerebral Hemorrhage; Female; Gene Expression Profiling; Genome, Human; Hematoma; Humans; Interleukin-8; Male; Oligonucleotide Array Sequence Analysis; Rupture, Spontaneous; Validation Studies as Topic

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

Appendicitis is a common surgical problem that is associated with a systemic inflammatory response. Previous studies have shown that cytokines are activated early in acute inflammation and sepsis and may serve as indicators of clinical severity. In this study we examined the role of cytokines as serum markers to distinguish nonperforated versus perforated appendicitis. Patients with the presumptive diagnosis of appendicitis had serum drawn preoperatively. Only patients (n = 59) with an intraoperative diagnosis of nonperforated (n = 34) and perforated (n = 25) appendicitis had serum drawn 12 hours postoperatively. Diagnosis was later confirmed by pathologic examination. The serum specimens were batch analyzed using enzyme-linked immunosorbent assays specific for interleukin (IL)-1beta, IL-2, IL-6, IL-8, and IL-10. Serum from normal healthy subjects served as control specimens (n = 9). Patients in the nonperforated and perforated groups were similar with regard to age, gender, race, white blood cell count, and fever. All cytokine levels including preoperative, postoperative, nonperforated, and perforated were higher in patients with appendicitis as compared with controls. IL-1beta, IL-2, and IL-10 levels were not different between groups with appendicitis. Preoperative serum levels of IL-6 (P = 0.036) and IL-8 (P = 0.047) were higher in patients with perforated versus nonperforated appendicitis. In addition postoperative serum levels of IL-6 (P = 0.0001) remained higher in the perforated group versus the nonperforated group. Serum levels of IL-6 and IL-8 may have a role in discerning the extent of disease in this condition. This initial step in systemically studying the role of cytokines in this disease may ultimately lead to the development of molecular indicators to aid in diagnosis and differentiate appendicitis from other conditions.

Topics: Adult; Aged; Appendicitis; Biomarkers; Enzyme-Linked Immunosorbent Assay; Female; Humans; Interleukin-1; Interleukin-10; Interleukin-2; Interleukin-6; Interleukin-8; Interleukins; Intestinal Perforation; Male; Middle Aged; Postoperative Period; Predictive Value of Tests; Preoperative Care; Rupture, Spontaneous