interleukin-8 and Dilatation--Pathologic

In-hospital outcomes are generally acceptable in patients with type B dissection; however, some patients present with undesirable complications, such as aortic expansion and rupture. Excessive inflammation is an independent predictor of adverse clinical outcomes.. We have investigated the underlying mechanisms of catastrophic complications after acute aortic dissection (AAD) in mice.. When angiotensin II was administered in lysyl oxidase inhibitor-preconditioned mice, AAD emerged within 24 hours. The dissection was initiated at the proximal site of the descending thoracic aorta and propagated distally into an abdominal site. Dissection of the aorta caused dilatation, and ≈70% of the mice died of aortic rupture. AAD triggered CXCL1 and granulocyte-colony stimulating factor expression in the tunica adventitia of the dissected aorta, leading to elevation of circulating CXCL1/granulocyte-colony stimulating factor levels. Bone marrow CXCL12 was reduced. These chemokine changes facilitated neutrophil egress from bone marrow and infiltration into the aortic adventitia. Interference of CXCL1 function using an anti-CXCR2 antibody reduced neutrophil accumulation and limited aortic rupture post AAD. The tunica adventitia of the expanded dissected aorta demonstrated high levels of interleukin-6 (IL-6) expression. Neutrophils were the major sources of IL-6, and CXCR2 neutralization significantly reduced local and systemic levels of IL-6. Furthermore, disruption of IL-6 effectively suppressed dilatation and rupture of the dissected aorta without any influence on the incidence of AAD and neutrophil mobilization.. Adventitial CXCL1/granulocyte-colony stimulating factor expression in response to AAD triggers local neutrophil recruitment and activation. This leads to adventitial inflammation via IL-6 and results in aortic expansion and rupture.

Topics: Acute Disease; Adventitia; Aged; Aminopropionitrile; Angiotensin II; Animals; Antibodies, Monoclonal; Aorta, Thoracic; Aortic Aneurysm, Thoracic; Aortic Dissection; Aortic Rupture; Aortography; Chemokine CXCL1; Chemokine CXCL12; Chemotaxis, Leukocyte; Dilatation, Pathologic; Disease Models, Animal; Female; Granulocyte Colony-Stimulating Factor; Humans; Inflammation Mediators; Interleukin-6; Interleukin-8; Male; Mice, Inbred C57BL; Mice, Knockout; Middle Aged; Neutrophil Activation; Neutrophil Infiltration; Neutrophils; Receptors, Interleukin-8B; Signal Transduction; Time Factors

Our aim was to evaluate the effect of a gingival gel containing chlorhexidine and Rheum Palmatum extract on gingival fragments stimulated by SP (substance P) and lipopolysaccharides (LPS).. Gingival fragments were maintained in survival for 3 days at 37 degrees C. To induce inflammation, SP and LPS were applied to the culture medium in contact with the corium. The gingival gel was applied on epithelium. Histological analysis was then performed on hematoxylin and eosin stained slides. Edema was evaluated with semi-quantitative scores. Vasodilation was studied by counting the percent of dilated vessels according to scores and the surface of these dilated vessels by morphometrical image analysis. An inflammatory cytokine, IL8, was measured in culture supernatants. Immunohistochemical expression of metalloproteinase type 9 (MMP9) implicated in inflammatory processes, was also studied (% of positive cells).. Edema, vasodilation and IL8 were significantly increased after application of SP and LPS. Application of gingival gel showed a significant decrease of these parameters. A significant decrease of MMP9 on fibroblasts and mononuclear cells was observed after use of gingival gel.

Topics: Anti-Infective Agents, Local; Capillaries; Cells, Cultured; Chlorhexidine; Coloring Agents; Dilatation, Pathologic; Gels; Gingiva; Gingivitis; Humans; Image Processing, Computer-Assisted; Interleukin-8; Lipopolysaccharides; Matrix Metalloproteinase 9; Phytotherapy; Plant Extracts; Rheum; Substance P

Posthaemorrhagic ventricular dilatation (PHVD) is closely associated with white matter damage and neurological disability in the preterm infant. Proinflammatory cytokines have been implicated in the pathogenesis of white matter injury and subsequent cerebral palsy. The aim of this study was to determine the levels of proinflammatory cytokines in cerebrospinal fluid (CSF) from preterm infants with PHVD and to correlate the levels to white matter damage and neurodevelopmental outcome.. CSF samples were obtained from 24 preterm infants with expanding PHVD and 19 preterm infants with normal ultrasound. Tumour necrosis factor-alphaa (TNF-alpha ), interleukin-1beta (IL-1beta), interleukin-8 (IL-8) and interferon-gamma (IFN-gamma) in CSF were measured by enzyme-linked immunosorbent assay, and IL-6 was measured by bioassay.. The concentrations of TNF-alpha, IL-1beta, IL-6 and IL-8 were significantly elevated in CSF from infants with PHVD. TNF-alpha was detected in 43% of PHVD infants and 11% of controls (p = 0.04). IL-1beta was detected in 67% of PHVD infants and 0% of controls (p < 0.0001). The concentrations of IL-6 were 368 (145-460) pg ml(-1) in the PHVD group and 30 (25-41) pg ml(-1) in the control group (p < 0.0001), and those of IL-8 were 3000 (1620-3400) pg ml(-1) in the PHVD group and 35 (0-230) pg ml(-1) in the control group (p < 0.0001). Cytokine concentrations did not correlate with white matter lesions on ultrasound, shunt dependence or neurological outcome within the PHVD group.. There was an intense and prolonged inflammatory reaction in CSF from preterm infants with PHVD and a high risk for subsequent white matter injury and permanent neurological impairment.

Topics: Cerebral Hemorrhage; Cerebral Ventricles; Cytokines; Dilatation, Pathologic; Humans; Infant, Newborn; Infant, Premature; Interferon-gamma; Interleukin-1; Interleukin-6; Interleukin-8; Tumor Necrosis Factor-alpha; Ultrasonography