Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P10145 (IL-8)
 23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bluetongue is an insect-transmitted disease of sheep and wild ruminants that is caused by bluetongue virus (BTV). Cattle are asymptomatic reservoir hosts of BTV. Infection of lung microvascular endothelial cells (ECs) is central to the pathogenesis of BTV infection of both sheep and cattle, but it is uncertain as to why sheep are highly susceptible to BTV-induced microvascular injury, whereas cattle are not. Thus, to better characterize the pathogenesis of bluetongue, the transcription of genes encoding a variety of vasoactive and inflammatory mediators was quantitated in primary ovine lung microvascular ECs (OLmVECs) exposed to BTV and/or inflammatory mediators. BTV infection of OLmVECs increased the transcription of genes encoding interleukin- (IL) 1 and IL-8, but less so IL-6, cyclooxygenase-2, and inducible nitric oxide synthase. In contrast, we previously have shown that transcription of genes encoding all of these same mediators is markedly increased in BTV-infected bovine lung microvascular ECs and that BTV-infected bovine ECs produce substantially greater quantities of prostacyclin than do sheep ECs. Thus, sheep and cattle were experimentally infected with BTV to further investigate the role of EC-derived vasoactive mediators in the pathogenesis of bluetongue. The ratio of thromboxane to prostacyclin increased during BTV infection of both sheep and cattle, but was significantly greater in sheep (P = 0.001). Increases in the ratio of thromboxane to prostacyclin, indicative of enhanced coagulation, coincided with the occurrence of clinical manifestations of bluetongue in BTV-infected sheep. The data suggest that inherent species-specific differences in the production and activities of EC-derived mediators contribute to the sensitivity of sheep to BTV-induced microvascular injury.
 ...
PMID:The role of endothelial cell-derived inflammatory and vasoactive mediators in the pathogenesis of bluetongue. 1206 31

The responses of five lactating ewes to experimental mammary infection with Staphylococcus epidermidis were examined. Infection caused an intense but transient influx of neutrophils into milk, which peaked at 8 h and was accompanied by mild fever and mild leukopaenia in blood. No other signs of systemic infection were observed. Number of staphylococci in milk decreased logarithmically until 24 h, were absent from three ewes at 48 h and then increased in number or re-emerged in four of the five ewes at 72 or 144 h. At all times milk appeared grossly normal. Expression of the adhesion molecules CD11b and CD18 increased on neutrophils in milk at 24 h then tended to decline over subsequent days. The proportion of lymphocytes positive for CD4, CD8, WC1 and MHCII tended to decrease from 24 to 72 h then increased at 144 h. Cytokines in milk were measured by ELISA. IL-8 was elevated in infected glands at 2 h, peaked at 24 h and remained elevated until the final sampling at 144 h. IL-6 was transiently elevated at 4 and 8 h while IL-1beta remained elevated from 8 until 144 h. The results suggest that the intense early neutrophil infiltrate eliminated most but not all bacteria and a state of subclinical infection ensued. After 24 h , leukocyte numbers in milk declined while cytokines, especially IL-8 remained elevated, suggesting that sensitivity or responsiveness of gland to inflammatory signals decreased as infection progressed. This attenuation of the host defence response may have contributed to the failure of the gland to eliminate bacteria and may be an important feature of the development of chronic and subclinical mastitis.
 ...
PMID:Immunological responses of the lactating ovine udder following experimental challenge with Staphylococcus epidermidis. 1220 51

Alveolar macrophages are likely the first cell type to encounter Mycobacterium tuberculosis in a pulmonary infection, resulting in the production of chemokines. In order to evaluate this response, alveolar macrophages harvested from nonvaccinated and Mycobacterium bovis BCG-vaccinated guinea pigs were infected in vitro with live M. tuberculosis H37Ra or H37Rv (multiplicity of infection, 1:1) or cultured with lipopolysaccharide (10 micro g/ml) for 3, 12, and 24 h. Interleukin-8 (IL-8) and monocyte chemoattractant protein 1 (MCP-1) mRNA expression was determined by real-time PCR. Culture supernatants were assayed for guinea pig IL-8 protein by using a human IL-8 enzyme-linked immunosorbent assay kit. Alveolar macrophages harvested from BCG-vaccinated guinea pigs produced significantly more mRNA and protein for IL-8 than alveolar macrophages harvested from nonvaccinated guinea pigs at 12 and 24 h poststimulation or postinfection. Infection with attenuated M. tuberculosis (H37Ra) stimulated alveolar macrophages isolated from BCG-vaccinated guinea pigs to produce significantly more IL-8 mRNA than did alveolar macrophages infected with a virulent strain (H37Rv) at 12 and 24 h postinfection. Significant MCP-1 mRNA production was also detected in stimulated or infected alveolar macrophages; however, prior vaccination did not significantly affect levels of MCP-1 mRNA. Alveolar macrophages isolated from BCG-vaccinated guinea pigs produced significantly more IL-8 mRNA and protein when stimulated for 24 h with heat-killed H37Ra, heat-killed H37Rv, and H37Rv cell wall, but not mannose-capped lipoarabinomannan (ManLAM), than did cells stimulated with media alone. These observations indicate that prior vaccination may alter very early events in the M. tuberculosis-infected lung.
 ...
PMID:Mycobacterium bovis BCG vaccination augments interleukin-8 mRNA expression and protein production in guinea pig alveolar macrophages infected with Mycobacterium tuberculosis. 1222 72

The aim of this study was to investigate the effects of stent carbon coating on inflammatory response. The authors serially measured plasma concentrations of C-reactive protein (CRP), fibrinogen, and several cytokines (tumor necrosis factor, interleukin [IL]-1-beta, IL-6, and IL-8) in patients with single-vessel coronary stenosis who underwent primary stent implantation. None of the subjects had inflammatory or infectious disease at the time of the procedure. Forty-six patients (38 males; mean age 55 +/-9 years) were studied. Blood samples were collected before and at 2, 4, 6, 24, and 48 hours after stent implantation. Patients were randomly assigned 1 of 2 different stent types, an uncoated MAC (AMG Raesfeld-Erle, Germany) (UC-MAC) or a carbon-coated MAC (CC-MAC) stent. Implantations were performed without predilatation, and stents were deployed at a maximum pressure of 6 atmospheres for 90 seconds. Of the 46 patients, 14 had stable, 27 had unstable, and 5 had atypical angina. According to ACC/AHA classification, 35 lesions (76.1%) were type A, 10 (21.7%) were type B, and 1 (2.2%) was type C. Single stenosis of 28 left anterior descending, 12 circumflex, and 6 right coronary arteries were treated. Serum IL-6 increased in both the UC-MAC and CC-MAC groups, with concentrations significantly elevated above baseline at 6 hours, and then decreasing after 24 hours (baseline, 6-hour, and 24-hour values = 3.1 +/-2.3, 5.7 +/-3.8, and 6.3 +/-4.6 pg/mL, respectively, in UC-MAC; 3.7 +/-2.6, 6.2 +/-6.0, and 4.6 +/-3.7 pg/mL, respectively, in CC-MAC [p=0.002]). Plasma fibrinogen, CRP, and leukocyte concentrations also increased in both groups over the 24 hours (p < 0.05). The elevations of IL-6, CRP, and fibrinogen were similar in the 2 groups. The percent increases in IL-6, fibrinogen, and CRP were not associated with stent length, size, or clinical presentation (all p > 0.05). The results showed that stent implantation increases plasma IL-6, fibrinogen, and CRP concentrations, but carbon coating of the stent does not seem to affect this inflammatory response.
 ...
PMID:Carbon coating of stents has no effect on inflammatory response to primary stent deployment. 1236 64

Enterohaemorrhagic Escherichia coli O157:H7 (EHEC) is a gastrointestinal pathogen that is generally non-invasive for intestinal epithelial cells, yet causes acute intestinal inflammation, diarrhoea, haemorrhagic colitis and haemolytic uraemic syndrome. To study signal transduction pathways activated in human intestinal epithelial cells by EHEC, we took advantage of EHEC O157:H7 and isogenic mutants deficient in the major EHEC virulence factors, intimin (eae-) and Shiga toxin (stx-). Infection with wild-type EHEC activated p38 and ERK MAP kinases and the nuclear translocation of the transcription factor NF-kappaB. Downstream, this was accompanied by increased expression of mRNA and protein for the neutrophil chemoattractant IL-8. Isogenic eae- and stx- mutants also activated p38 and ERK MAP kinases, and NF-kappaB and stimulated increases in IL-8 protein secretion similar to those of wild-type EHEC. Further, inhibition of either p38, ERK or NF-kappaB activation abrogated the IL-8 response induced by wild-type EHEC and the mutants. Epithelial cell MAP kinase and NF-kappaB pathways leading to IL-8 secretion were also activated by isolated EHEC H7 flagellin, which was active when added to either the apical or basolateral surface of polarized human intestinal epithelial cells. We conclude that EHEC interacting with intestinal epithelial cells activates intracellular signalling pathways and an epithelial cell proinflammatory response independent of either Shiga toxin or intimin, two of the major known virulence factors of EHEC. The activation of proinflammatory signals in human colon epithelial cells in response to this non-invasive pathogen appears to depend to a significant extent on H7 flagellin.
 ...
PMID:Role of EHEC O157:H7 virulence factors in the activation of intestinal epithelial cell NF-kappaB and MAP kinase pathways and the upregulated expression of interleukin 8. 1236 1

Immune responses and illness severity during viral upper respiratory infections may be influenced by the local elaboration of cytokines. Cytokine gene polymorphisms moderate immune responses and severity of illness in various inflammatory and infectious diseases. We performed cytokine genotyping on 29 adults experimentally inoculated with respiratory syncytial virus (RSV) to determine whether specific cytokine gene polymorphisms are associated with immune responses or illness severity. DNA was extracted from leukocytes and assayed for TNF-alpha, IFN-gamma, IL-6, IL-10 and TGF-beta1 genotypes using polymerase chain reaction-sequence-specific primer technology. Outcomes consisted of baseline and convalescent RSV-specific serum IgG and nasal IgA titers, nasal secretion weights, nasal, throat and general symptom scores, and nasal cytokine protein levels. IFN-gamma genotype was directly related with the frequency of subjects having at least a four-fold increase in RSV-specific serum IgG and TNF-alpha genotype was inversely associated with the frequency of subjects having at least a twofold increase in RSV-specific nasal IgA. Additionally, IL-6 genotype was predictive of certain measures of illness expression, while IFN-gamma genotype predicted IL-1 protein levels, and TNF-alpha genotype predicted IL-6 and IL-8 protein levels in nasal lavage fluids. There were no associations between IL-10 or TGF-beta1 and any of the outcome parameters. These results suggest that certain cytokine gene polymorphisms moderate immune responses and illness severity in adults experimentally exposed to RSV.
 ...
PMID:Cytokine gene polymorphisms moderate responses to respiratory syncytial virus in adults. 1250 18

The NF-kappaB family of transcription factors forms one of the first lines of defense against infectious disease by inducing the expression of genes involved in inflammatory and immune responses. In this study, we analyzed the impact of Shiga toxin-producing Escherichia coli (STEC) on the NF-kappaB DNA-binding activity in HeLa cells. After a period of weak initial activation, DNA binding of NF-kappaB was actively suppressed by viable, E. coli secreted protein B (EspB)-secreting STEC. Sustained NF-kappaB activity was observed either using an isogenic mutant lacking EspB or after gentamicin-based killing of STEC after allowing bacterial attachment. These observations indicate that the ability of STEC to cause NF-kappaB activation is suppressed by a translocated bacterial effector protein, which is either EspB itself or requires EspB for delivery into the host cell. We found that STEC, enterohemorrhagic E. coli, and enteropathogenic E. coli all interfere with NF-kappaB activation initiated by TNF-alpha, indicating that suppression of signal-induced NF-kappaB activity is a property common to several attaching and effacing bacteria. As a consequence of NF-kappaB suppression, wild-type STEC induces significantly lower mRNA levels of IL-8, IL-6, and IL-1alpha upon prolonged infection periods compared with bacteria lacking EspB. For IL-8 and IL-6, the suppressive effect was also reflected at the level of cytokine secretion. Suppression of both basal and signal-induced NF-kappaB DNA binding by attaching and effacing-inducing bacteria appears to be an active strategy to counteract host defense responses, thus favoring intestinal colonization by these pathogens.
 ...
PMID:Suppression of NF-kappa B activation and proinflammatory cytokine expression by Shiga toxin-producing Escherichia coli. 1257 78

Foals are uniquely susceptible to a wide variety of opportunistic infections normally associated with immunodeficiencies. Little is understood about the immune system of foals during the neonatal period. An apparent age-related susceptibility predisposes neonatal foals to infectious diseases and hinders therapeutic and preventative interventions for these diseases. Cytokine expression is correlated with the type of immune response as well as the severity of a disease. In this study, we measured foal peripheral blood mononuclear cell (PBMC)-specific mRNA cytokine expression from 72 foals from three different farms during the first 4 weeks of life. Interleukin-1alpha (IL-1alpha), IL-1beta, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12p35, IL-12p40, interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), and transforming growth factor-beta1 (TGF-beta1) were cloned and transcribed in vitro to generate antisense probes for ribonuclease protection assays. Using linear mixed-effect models, we determined that IFN-gamma, TGF-beta1, and IL-1alpha increased significantly (P<0.05) with age.
 ...
PMID:Temporal changes in cytokine expression of foals during the first month of life. 1262 65

The responses of five lactating East Friesian milk ewes to experimental mammary infection with Staphylococcus epidermidis and of five control ewes were examined over a period of 10 weeks. Infection caused an influx of neutrophils into milk, the numbers of which started to rise 4 h post infection and peaked 24 h after infection. The initial response was accompanied by mild fever and mild leucopaenia in blood (8 h after infection). No other signs of systemic infection were observed. Milk appeared normal at all times, although the milk yield of infected ewes tended to decline. Staphylococci were absent in milk from four ewes at 2 d and at 3 d after infection, but re-emerged intermittently in four of five ewes at subsequent samplings. Cytokines in milk were measured by ELISA. IL-8 was elevated in infected glands at 2 h and peaked at 8 h. In the four ewes intermittently shedding bacteria, IL-8 remained elevated until the final sampling at 10 weeks. IL-1beta was transiently elevated at 1 d and 2 d and showed a pronounced peak in one sheep. Milk samples from this ewe were bacteriologically negative, somatic cell count (SCC) was within the normal range and the concentrations of IL-1beta, as well as IL-8, were similiar to the control group (n=5) from 1 week after infection until the final sampling. Histological examination revealed leucocytic infiltrates in the four glands remaining infected at the end of the experiment, and a high level of CD5+ lymphocytes in three ewes. The results suggest that the relationship between the initial neutrophil influx and the proinflammatory cytokines may be responsible for determining the course of infection. Subclinical mastitis due to coagulase-negative staphylococci leads to minor changes in milk yield and milk constituents.
 ...
PMID:Dynamics of experimentally induced Staphylococcus epidermidis mastitis in East Friesian milk ewes. 1280 Aug 69

Numerous studies indicate that enteroviruses, such as the Coxsackievirus (CV) group, are linked to autoimmune diseases. Virus tropism and tissue access are modulated by vascular endothelial cells (ECs), mainly at the level of the microvasculature. Data on the permissiveness of ECs to CV are, however, scanty and derived from studies on large vessel ECs. To examine the susceptibility of microvascular ECs to infection of group B CV (CVB), human dermal microvascular ECs (HMEC-1) were infected with three CVB strains, and the immunological phenotype of the infected cells was analyzed. All CVB persistently infected the EC cultures without producing overt cytopathic effects. Infected ECs retained endothelial characteristics. Release of infectious particles in cell supernatants persisted for up to 3 mo of culture. Infection up-regulated expression of the adhesion molecules ICAM-1 and VCAM-1, with the highest values detected during the first 30 days of infection (p < 0.05 vs uninfected HMEC-1). CVB infection increased production of the proinflammatory cytokines, IL-6, IL-8, and TNF-alpha, which may account for the enhanced expression of adhesion molecules. Parallel infection of macrovascular HUVEC had less evident effects on induction of ICAM-1 and did not significantly increase expression of VCAM-1. Moreover, mononuclear cell adhesion to CVB-infected HMEC-1 monolayers was increased, compared with uninfected monolayers. These results provide evidence that small vessel ECs can harbor a persistent viral infection, resulting in quantitative modification of adhesion molecule expression, which may contribute to the selective recruitment of subsets of leukocytes during inflammatory immune responses. Furthermore, our data confirm that the behavior against a viral challenge of ECs in large vessels and microvessels may differ.
 ...
PMID:Persistent infection of human microvascular endothelial cells by coxsackie B viruses induces increased expression of adhesion molecules. 1281 28


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>