interleukin-8 and Nervous-System-Diseases

Autoimmune diseases afflict more than 3% of the U.S. population. Current therapy for mild to moderate cases is symptomatic, however advanced cases suffer high morbidity and mortality. Advanced patients have benefited from stem cell therapy in the form of bone marrow transplantation in conjunction with high-dose cytotoxic therapy. Broader application of stem cell therapy requires better understanding of how adult stem cells affect development and foster treatment of autoimmune pathologies, and of better ways to manipulate the host immune responses. While extensive research documents the role of hematopoietic stem cells (HSCs) in autoimmune disease, few studies have addressed if and how mesenchymal stem cells (MSCs) contribute to their etiopathology. Recent characterization of MSCs and their role in hematopoiesis and immune modulation suggest that their potential for cell therapy extends beyond their traditional accessory function in HSC engraftment. MSCs contribute significantly to tissue restructuring and immune functioning, in addition to facilitating durable, long-lasting stem cell engraftment. MSCs are relatively easy to obtain and expand in in vitro cultures, rendering them a prime candidate for genetic manipulations for stem cell therapy. They have the potential to differentiate into multiple lineages such as osteoblasts, adipose tissue, cartilage, tendon, and stromal cells. The role of MSCs for autoimmune disease therapy could thus be based both on immune function modulation and contribution to hematopoiesis. In this review, we examine the biology of MSCs, and their potential for cell therapy of autoimmune disease.

Topics: Adipose Tissue; Animals; Autoimmune Diseases; Cartilage; Cell Lineage; Chemokines, CXC; Hematopoietic Stem Cell Transplantation; Hematopoietic Stem Cells; Humans; Interleukin-8; Lupus Vulgaris; Mesenchymal Stem Cells; Models, Biological; Nervous System Diseases; Stem Cell Transplantation; Stem Cells; Stromal Cells

Several recent findings indicate that various interactions between nervous and immune system are important in the pathophysiology of alexithymia. These findings show that a significant role in developing alexithymia may play proinflammatory cytokines. Recent data also indicate that negative emotions related to depressive symptoms and anxiety are related to disturbed levels of interleukin-8 (IL-8). These findings suggest that IL-8 could present also useful immunological marker related to emotional dysregulation in alexithymia. In the present study we have performed psychometric measurement of alexithymia (TAS-20), depression (BDI-II) and anxiety (SAS), and immunochemical measure of cerebrospinal fluid (CSF) and serum levels of IL-8 in 33 inpatients with non-inflammatory neurological disorders (NIND) (mean age 38.8±12.5). The results show that IL-8 in CSF is significantly correlated with TAS-20 (Spearman R=0.46, p=0.007) and SAS (Spearman R=0.44, p=0.009) but not to BDI-II. The findings of the present study indicate that increased level of IL-8 (in CSF) may be related to symptoms of alexithymia and anxiety in patients with NIND.

Topics: Adult; Affective Symptoms; Anxiety; C-Reactive Protein; Encephalitis; Female; Humans; Interleukin-8; Male; Middle Aged; Nervous System Diseases; Personality Inventory; Psychiatric Status Rating Scales; Severity of Illness Index; Young Adult

Bacterial meningitis is a life-threatening disease with high mortality and common long-term sequelae. The inflammatory response in the subarachnoid space, modulated by different cytokines, plays a major role in the pathogenesis of acute central nervous system infections. We aimed to examine correlations of interleukin (IL)-6, IL-8, IL-10, IL-12(p40), and tumor necrosis factor (TNF)-α levels with disease severity, complications, and outcome in patients with acute bacterial meningitis.. The study involved 30 patients with bacterial meningitis/meningoencephalitis admitted to the University Hospital St. George, Plovdiv over a period of 4 years. Patients were selected based on clinical presentation and laboratory abnormalities, consistent with a neuroinfection. Enzyme-linked immunosorbent assay was used to measure the studied cytokines in both cerebrospinal fluid (CSF) and serum in parallel. For microbiological diagnosis multiplex, polymerase chain reaction, and CSF culture were used.. In patients with acute bacterial meningitis CSF levels of IL-6, IL-8, IL-10, and TNF-α are significantly increased than in serum. CSF TNF-α, CSF IL-8, and CSF IL-10 had a moderate negative correlation to CSF glucose. It was found that serum IL-8 is significantly elevated in patients who experienced neurological complications, have severe clinical course, and in deceased patients. CSF IL-10 is increased only in patients with severe acute bacterial meningitis.. Among patients with acute bacterial meningitis serum IL-8 could delineate these with increased risk of neurological complications, severe clinical course, and fatal outcome. Serum IL-8 and CSF IL-10 could be used as indicators of disease severity.

Topics: Cytokines; Disease Progression; Humans; Interleukin-10; Interleukin-6; Interleukin-8; Meningitis, Bacterial; Nervous System Diseases; Tumor Necrosis Factor-alpha

Topics: Aged; APACHE; Cardiovascular Diseases; Cohort Studies; Critical Illness; Disseminated Intravascular Coagulation; Extracellular Traps; Female; Gastrointestinal Diseases; Humans; Intensive Care Units; Interleukin-8; Kidney Diseases; Male; Middle Aged; Mitogen-Activated Protein Kinases; Mortality; Multivariate Analysis; Nervous System Diseases; Neutrophils; Organ Dysfunction Scores; Prospective Studies; Reproducibility of Results; Respiratory Tract Diseases; Risk Assessment; Sepsis; Wounds and Injuries

The maternal-fetal inflammatory response contributes to both preterm premature rupture of membranes (PPROM) and adverse neurological outcomes. Additionally, cytokines associated with fetal placental inflammation can be detrimental to brain development regardless of inciting infection. We investigated whether differential patterns of cytokine markers in maternal and fetal plasma samples reflect subtypes of placental inflammation and neurological outcomes at 6 months in infants born to mothers with PPROM.. Within a prospective cohort study of 25 women with PPROM, plasma cytokines (interleukin [IL]-1β, IL-6, IL-8, and tumor necrosis factor-α) were measured by enzyme-linked immunosorbent assay from maternal blood samples at rupture and delivery, and from fetal umbilical cord blood samples. Patterns of cytokine expression were correlated with specific placenta pathologies. Infants underwent cranial ultrasound after birth and standardized neurological examinations at 6 months' corrected gestational age. Predictors of inflammation and adverse neurological outcome were assessed by logistic regression, adjusting for gestational age at birth.. Inflammation of the fetal side of the placenta was associated with elevated maternal IL-6 and IL-8 at delivery and fetal IL-1β, IL-6, IL-8, and tumor necrosis factor-α. Worse neurological outcome at 6 months was associated with inflammation of the fetal side of the placenta and shorter duration from rupture of membrane to delivery, independent of gestational age at birth or cranial ultrasound results.. Our findings support the connection between fetal inflammation with adverse neurological outcome with PPROM, regardless of cranial ultrasound results. Further longitudinal studies are needed to adequately examine these patterns, and will aid in risk assessment and intervention strategies.

Topics: Adult; Chorioamnionitis; Cohort Studies; Cytokines; Enzyme-Linked Immunosorbent Assay; Female; Fetal Blood; Fetal Membranes, Premature Rupture; Gestational Age; Humans; Infant, Newborn; Inflammation; Interleukin-1beta; Interleukin-6; Interleukin-8; Male; Nervous System Diseases; Placenta; Pregnancy; Prospective Studies; Tumor Necrosis Factor-alpha; Young Adult

The management of complex patients with neuroimmunological diseases is hindered by an inability to reliably measure intrathecal inflammation. Currently implemented laboratory tests developed >40 years ago either are not dynamic or fail to capture low levels of central nervous system (CNS) inflammation. Therefore, we aimed to identify and validate biomarkers of CNS inflammation in 2 blinded, prospectively acquired cohorts of untreated patients with neuroimmunological diseases and embedded controls, with the ultimate goal of developing clinically useful tools.. Because biomarkers with maximum utility reflect immune phenotypes, we included an assessment of cell specificity in purified primary immune cells. Biomarkers were quantified by optimized electrochemiluminescent immunoassays.. Among markers with cell-specific secretion, soluble CD27 is a validated biomarker of intrathecal T-cell activation, with an area under the receiver operating characteristic curve of 0.97. Comparing the quantities of cerebrospinal fluid (CSF) immune cells and their respective cell-specific soluble biomarkers (released by CSF cells as well as their counterparts in CNS tissue) provided invaluable information about stationary CNS immune responses, previously attainable via brain biopsy only. Unexpectedly, progressive and relapsing-remitting multiple sclerosis (MS) patients have comparable numbers of activated intrathecal T and B cells, which are preferentially embedded in CNS tissue in the former group.. The cell-specific biomarkers of intrathecal inflammation may improve diagnosis and management of neuroimmunological diseases and provide pharmacodynamic markers for future therapeutic developments in patients with intrathecal inflammation that is not captured by imaging, such as in progressive MS.

Topics: Adult; Aged; B-Lymphocytes; Biomarkers; Case-Control Studies; Cerebrospinal Fluid; Cohort Studies; Female; Humans; Inflammation; Interleukin-12 Subunit p40; Interleukin-8; Lipopolysaccharide Receptors; Lymphocyte Count; Male; Middle Aged; Multiple Sclerosis, Chronic Progressive; Multiple Sclerosis, Relapsing-Remitting; Nervous System Diseases; Prospective Studies; Receptors, Complement 3d; T-Lymphocytes; Tumor Necrosis Factor Receptor Superfamily, Member 7; Young Adult

Topics: Biomarkers; Cardiopulmonary Resuscitation; Critical Care; Female; Heart Arrest; Humans; Intensive Care Units; Interleukin-8; Male; Monitoring, Physiologic; Nervous System Diseases; Predictive Value of Tests; Prognosis; Sensitivity and Specificity

Some mediators of inflammation are associated with sepsis, involving nervous system. Proinflammatory cytokines, TNF-alpha, IL-6, and IL-8, and procalcitonin (PCT), proinflammatory protein, were investigated in patients with neurologic complications in sepsis. TNF-alpha, IL-6, IL-8, and PCT were prospectively investigated in 62 patients with neurologic complications in sepsis. TNF-alpha and IL-6 were studied both in serum as in the CSF, IL-8 and PCT were studied only in serum. TNF-alpha, IL-6, and IL-8 were studied by ELISA (R & D Systems), and the PCT by immunoluminometric assay (BRAHMS). Mean value of TNF-alpha in serum was 578+/-214 pg/ml, and in CSF was 458+/-167 pg/ml (p<0.01). Mean value of IL-6 in serum was 749+/-213 pg/ml, and in CSF was 617.5+/-182 pg/ml (p<0.01). Mean value of IL-8 in serum was 332+/-196 pg/ml (p<0.01). Mean value of PCT in serum was 80+/-16 ng/ml (p<0.01). The investigated parameters do not permit the identifying of cases with neurologic complications. The increased correlation coefficient between cytokines in serum and in CSF suggests the damage of the blood-brain barrier. The raise of PCT in serum, induced by TNF-alpha and IL-6, is an argument of the severity of sepsis.

Topics: Aged; Calcitonin; Calcitonin Gene-Related Peptide; Female; Humans; Interleukin-6; Interleukin-8; Male; Nervous System Diseases; Protein Precursors; Sepsis; Tumor Necrosis Factor-alpha