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

Inflammation of the central airways is a prominent feature in subjects with chronic bronchitis. The pathology of chronic bronchitis includes an inflammatory mononuclear cell infiltrate in the airway wall and a neutrophil influx into the airway lumen. The molecular events that produce the inflammation and its pathogenetic role in causing mucus hypersecretion are beginning to be elucidated. The inflammatory cell recruitment to the airways likely involves chemotactic agents derived not only from tissue fluid and invading microbes but also generated by the diseased bronchial epithelium. For example, bronchial epithelial cells synthesize interleukin (IL-8), a potent chemoattractant and activator of neutrophils and lymphocytes. Adhesion of infiltrating leukocytes to resident parenchymal cells in the bronchi and to extracellular matrix also is crucial for the development of airway inflammation. The resultant inflammation likely plays a direct role in the clinical features of the disorder. There is growing evidence incriminating neutrophil and lymphocytes constituents in the initiation and maintenance of cough and mucus expectoration that occurs in subjects with chronic bronchitis.
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PMID:Pathogenesis of chronic bronchitis. 797 68

CM101 is a bacterial polysaccharide that induces neovascular inflammation in malignant tumors. Fifteen patients with refractory malignancies received CM101 i.v. by a 15-min infusion every other day, three times in 1 week, at doses ranging from 1 unit (7.5 microgram)/kg to 5 units/kg. Serum was analyzed for anti-CM101 IgG and IgM weekly. Plasma levels of inflammatory cytokines, including tumor necrosis factor alpha, interleukin 8, interleukin 10, MIP-1alpha, and soluble E-selectin, were analyzed from -15 min to 12 h during each treatment. Dose-limiting toxicities, including grade IV dyspnea and arrhythmia, were encountered at the 5-unit/kg level. Toxicities occurred primarily within the first 12 h after therapy and included mild-to-moderate fever and chills, nausea, cough, headache, facial flushing, dyspnea, myalgias, and acute tumor-related pain. No patient developed detectable antibodies to CM101. All patients experienced marked time- and dose-dependent elevations in all cytokines studied. Three patients experienced tumor shrinkage. The results show that CM101 can be safely administered at doses that produce evidence for severe, and possibly tumor-specific, inflammation. Further study is necessary to better characterize the mechanism of action and determine the optimal dose and schedule of this new agent.
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PMID:Phase I study of the antineovascularization drug CM101. 981 93

Endotoxins, cell-wall fragments of gram-negative bacteria, are found in various work environments and first measurements have been made in general indoor environments. Endotoxins cause an inflammatory response of the respiratory tract. The response is mediated by the proinflammatory cytokines IL-1, IL-6, IL-8, and TNF-alpha and gives rise to general symptoms (fever, headache, malaise), respiratory symptoms (tightness of chest, dry cough), and lung function decrements. In the work environment endotoxins have been identified in all environments which produce similar symptoms. The qualitative results of experimental and epidemiological studies agree well. The related question whether endotoxins are the biologically active component of organic dust cannot yet be answered because of the gap between the concentration of lipopolysaccharides and of endotoxins necessary to induce the same quantitative effect. Different possible explanations are discussed. Endotoxins are also found in the general environment, especially indoors. Their health relevance needs to be assessed in more detail, especially in subjects with bronchial hyperreactivity.
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PMID:[Endotoxins in the workplace and in the environment]. 1023 2

Exposure to airborne endotoxin in infancy may protect against asthma by promoting enhanced T(H)1 response and tolerance to allergens. On the other hand, later in life, it adversely affects patients with asthma. Endotoxin binding to receptors on macrophages and other cells generates IL-12, which inhibits IgE responses. It also generates cytokines like IL-1, TNF-alpha, and IL-8, which cause inflammation. These signal transduction pathways resemble those leading to the generation of cytokines, such as IL-4, IL-13, and IL-5, which are responsible for the inflammation of IgE-mediated allergic disease. The main difference seems to be that endotoxin recruits neutrophils, but IgE recruits eosinophils, and the details of the tissue injury from these granulocytes differ. Sources of airborne endotoxin include many agricultural dusts, aerosols from contaminated water in many industrial plants, contaminated heating and air-conditioning systems, mist-generating humidifiers, and damp or water-damaged homes. Acute inhalation of high concentrations of endotoxin can cause fever, cough, and dyspnea. Chronic inhalation of lesser amounts causes chronic bronchitis and emphysema and is associated with airway hyperresponsiveness. Airborne endotoxin adversely affects patients with asthma in 3 ways: (1) by increasing the severity of the airway inflammation; (2) by increasing the susceptibility to rhinovirus-induced colds; and (3) by causing chronic bronchitis and emphysema with development of irreversible airway obstruction after chronic exposure of adults. The most effective management is mitigating exposure. The potential of drug treatments requires further clinical investigation.
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PMID:Endotoxin-stimulated innate immunity: A contributing factor for asthma. 1149 29

In childhood asthma, cough is a major symptom in some but not in others. There is only limited data on the frequency, severity and prevalence of cough in children with classical asthma. Studies have largely shown no relationship between cough frequency and cough receptor sensitivity with various asthma severity indices. However relating cough severity with asthma severity is limited by various methodological and sensitivity issues, and these are presented in this paper. Mild asthma exacerbations in a group of children with cough as a dominant symptom were characterised by an increase in cough severity (daytime cough scores) and eosinophilic inflammation but not neutrophilic inflammation. However neither cough receptor sensitivity or cough scores related to airway IL-8, eosinophil cationic protein, myeloperoxidase or serum eosinophil cationic protein, and, asthma scores consistently related to cough score only early in the asthma exacerbation phase.
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PMID:Relationship between cough, cough receptor sensitivity and asthma in children. 1209 81

Acute exacerbations (AE) represent one of the hallmarks of Chronic Obstructive Pulmonary Disease (COPD). They are characterised by increased from baseline dyspnoea, cough and sputum production and/or purulence, variably associated with fever and systemic symptoms. As in stable COPD, airway inflammation is an important part of the disease underlying the clinical manifestations. Studies on airway inflammation in AE by means of invasive methodologies (e.g. fiberoptic bronchoscopy with bronchial biopsy and/or bronchoalveolar lavage) are difficult due to clinical, practical and ethical issues. New and less- (sputum) or non-invasive methodologies (exhaled markers) are becoming increasingly applied also to the study of AE in COPD. The overall data on airway inflammation during AE seems to indicate an "acute on chronic" picture of inflammation, with increased proportions of inflammatory cells in tissue and lavage/sputum samples and with the change in the proportions of some of the cell types, such as a substantial increase in the numbers of eosinophils. Cytokines and inflammatory mediators involved in AE seem to be those related to PMN chemotaxis (IL-8 and LT) and those related to eosinophilic inflammation. A more precise categorisation of the event causing AE (e.g. viral vs. bacterial), and of the baseline patients' characteristics (e.g. severe vs. mild-moderate stage) associated with a wider application of well-standardised non-invasive methodologies could bring us in the future better clues on the pattern of airway inflammation during AE.
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PMID:Acute exacerbations of COPD: is inflammation central to prevention and treatment strategies? 1281 45

The aims of this study were (1) to correlate cough and body temperature (BT) with the severity of bronchopneumonia in pigs, (2) to determine whether these clinical signs can be used to early diagnose bronchopneumonia and (3) to assess the predictive values of cough and BT regarding lung lesions. Bronchopneumonia was induced by administering E. coli endotoxin (LPS) combined with Pasteurella multocida type A (PmA) in the trachea of 13 piglets. Saline-instilled negative controls (n = 8), PmA inoculated (n = 6) and LPS instilled (n = 5) groups were also constituted. Cough and BT were recorded daily while the bronchopneumonia severity was assessed using bronchoalveolar lavage fluid (BALF) cytology, cytokines and measurement of lung lesion volume. Changes in expiratory breathing pattern were also measured (Penh). The combination of LPS and PmA induced a subacute bronchopneumonia characterised by macrophage, neutrophil, and lymphocyte infiltration, changes in Penh and an increase in the mRNA level of IFN-gamma while IL8, IL-18 and TNF-alpha mRNA levels remained unchanged. The daily body weight gain of infected animals was significantly reduced. Cough and BT changes were proportional to the intensity of the lung inflammatory process, functional respiratory changes and to the extent of macroscopic lesions. When comparing the individual values of cough and BT to thresholds defined for both parameters, an early diagnosis of pneumonia was possible. Considering the pooled data of each group, it was possible to define thresholds allowing an early segregation between the groups of diseased and healthy piglets. The daily values of cough and BT were predictive for the volume of lung lesions recorded at the end of the trial. In conclusion, cough and BT appear as potential indicators for the intensity and the evolution of the respiratory disease. They also seem to be good predictors for the magnitude of lung lesions and weight gain recorded at the study endpoint.
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PMID:Pathophysiological changes occurring during Escherichia coli endotoxin and Pasteurella multocida challenge in piglets: relationship with cough and temperature and predicitive value for intensity of lesions. 1521 80

The postoperative period is associated with an increased production of cytokines, which augment pain sensitivity. We investigated the hypothesis that epidural clonidine premedication and postoperative patient-controlled epidural analgesia (PCEA) including clonidine would decrease the release of proinflammatory (interleukin (IL)-6, IL-1beta, IL-8, and tumor necrosis factor (TNF)-alpha) and antiinflammatory (IL-1 receptor antagonist (RA)) cytokines in patients who underwent elective colorectal surgery and that they would provide better postoperative analgesia. Forty patients were randomly assigned to 1 of 2 groups of 20 each: the control group received normal saline 10 mL, whereas the clonidine group received epidural clonidine 150 microg diluted with 9 mL of normal saline 30 min before surgery. Venous blood samples for cytokine levels were obtained before induction, at the end of surgery, and after surgery at 12 and 24 h. After surgery, the clonidine group patients received PCEA with morphine (0.1 mg/mL) and clonidine (1.5 microg/mL) in 0.2% ropivacaine 100 mL, whereas control group patients received only PCEA morphine and ropivacaine. Patients in the clonidine group exhibited longer PCEA trigger times, lower pain scores at rest and while coughing, less morphine consumption, and a faster return of bowel function throughout the 72-h postoperative observation period, compared with patients in the control group. For patients in the clonidine group, production of IL-1RA, IL-6, and IL-8 was significantly less increased at the end of the surgical procedure and at 12 and 24 h after surgery. However, the concentrations of IL-1beta and TNF-alpha were not significantly increased.
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PMID:The effect of epidural clonidine on perioperative cytokine response, postoperative pain, and bowel function in patients undergoing colorectal surgery. 1527 31

Fumonisin B(1) (FB(1)) is a mycotoxin produced by Fusarium verticillioides and F. proliferatum that commonly occurs in maize. In swine, consumption of contaminated feed induces liver damage and pulmonary edema. Pasteurella multocida is a secondary pathogen, which can generate a respiratory disorder in predisposed pigs. In this study, we examined the effect of oral exposure to fumonisin-containing culture material on lung inflammation caused by P. multocida. Piglets received by gavage a crude extract of fumonisin, 0.5mg FB(1)/kg body weight/day, for 7 days. One day later, the animals were instilled intratracheally with a non toxin producing type A strain of P. multocida and followed up for 13 additional days. Pig weight and cough frequency were measured throughout the experiment. Lung lesions, bronchoalveolar lavage fluid (BALF) cell composition and the expression of inflammatory cytokines were evaluated at the autopsy. Ingestion of fumonisin culture material or infection with P. multocida did not affect weight gain, induced no clinical sign or lung lesion, and only had minimal effect on BALF cell composition. Ingestion of mycotoxin extract increased the expression of IL-8, IL-18 and IFN-gamma mRNA compared with P. multocida infection that increased the expression of TNF-alpha. The combined treatment with fumonisin culture material and P. multocida delayed growth, induced cough, and increased BALF total cells, macrophages and lymphocytes. Lung lesions were significantly enhanced in these animals and consisted of subacute interstitial pneumonia. TNF-alpha, IFN-gamma and IL-18 mRNA expression was also increased. Taken together, our data showed that fumonisin culture material is a predisposing factor to lung inflammation. These results may have implications for humans and animals consuming FB(1) contaminated food or feed.
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PMID:Oral exposure to culture material extract containing fumonisins predisposes swine to the development of pneumonitis caused by Pasteurellamultocida. 1597 25

Swine influenza viruses are an important pathogen in pig industry. In this study, we wanted to know whether swine H1N2 influenza viruses circulating in Korean pigs would cause clinical signs in pigs when experimentally infected. When pigs were infected with swine H1N2 viruses isolated from Korean pigs, pigs suffered from severe clinical signs of coughing, nasal discharge, labored breathing, facial edema, anorexia, and diarrhea. When the level of cytokine induction was measured using lung tissues, pro-inflammatory cytokines such as TNF-alpha, IL-1, and IL-8 were induced higher in lungs of infected pigs than in lungs of uninfected pigs. However, no increased induction of the anti-inflammatory cytokines such as IL-4 and IL-10 was observed in lungs of infected pigs. These results suggest that the pathogenesis induced in pigs by H1N2 influenza viruses may be induced by pro-inflammatory cytokines instead of anti-inflammatory cytokines.
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PMID:Pathogenesis and inflammatory responses of swine H1N2 influenza viruses in pigs. 1757 May 53


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