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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Several epidemiological studies have described an association between adverse health effects and exposure to mould and microbes present in the indoor air of moisture-damaged buildings. However, the biochemical linkage between microbial exposure and the large variety of reported respiratory symptoms is poorly understood. In the present study, the authors compared the respiratory symptoms, the production of inflammatory mediators interleukin (IL)-1, IL-4, IL-6, tumour necrosis factor-alpha (TNF-alpha) and cell count in nasal lavage fluid and induced sputum samples of subjects working in moisture-damaged and control school buildings. The sampling was performed and the questionnaires were completed at the end of the spring term, at the end of the summer vacation (2.5 months), during the winter term and after a 1-week winter holiday. The authors found a significant elevation of IL-1, TNF-alpha and IL-6 in nasal lavage fluid and IL-6 in induced sputum during the spring term in the subjects from the moisture-damaged school building compared to the subjects from the control building. The exposed workers reported sore throat, phlegm, eye irritation, rhinitis, nasal obstruction and cough in parallel with these findings. The present data suggests an association between microbial exposure, and symptoms as well as changes in pro-inflammatory mediators detected from both the upper and lower airways.
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PMID:Changes in pro-inflammatory cytokines in association with exposure to moisture-damaged building microbes. 1182 1

The herb, Chrysanthemum zawadskii var, latilobum commomly known as Gu-Jul-Cho in Korea, used in traditional medicine to treat pneumonia, bronchitis, cough, common cold, pharyngitis, bladder-related disorders, gastroenteric disorders, and hypertension. Linarin is the main active compound and the biological mechanisms of its activity are unclear. It is believed that effects of this herb may be exerted through the pluripotent effectors of linarin due to its ability to treat a variety of afflictions. In this study, the effects of linarin on the mouse macrophages cell line, RAW 264.7, were investigated. It was found that linarin could activate macrophages by producing cytokines. Monocytes and tissue macrophages produce at least two groups of protein mediators of inflammation, interleukin 1 (IL-1) and the tumor necrosis factor (TNF). Recent studies have shown that TNF and IL-1 modulate the inflammatory function of endothelial cells, leukocytes, and fibroblasts. TNF-alpha production by macrophages treated with linarin occured in a dose dependent manner. However, IL-1 production was largely unaffected by this natural product. This study demonstrated the ability of linarin to activate macrophages both directly and indirectly. Linarin also affect both cytokine production and nitric oxide inhibition, in addition to the expression of some surface molecules. Nitric oxide (NO), derived from L-argin-ine, is produced by two forms(constitutive and inducible) of nitric oxide synthase (NOS). The NO produced in large amounts by inducible NOS is known to be responsible for the vasodilation and hypotension observed in septic shock. Linarin was found to inhibit NO production in the LPS-activated RAW 264.7 cells. Linarin may be a useful candidate as a new drug for treating endotoxemia and the inflammation accompanied by NO overproduction. The linarin-treated total lymphocytes exhibited cytotoxicity in a dose dependent manner between 20 microg/ml and 40 microg/ml. These results suggest that linarin may function through macrophage activation.
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PMID:The effect of linarin on LPS-induced cytokine production and nitric oxide inhibition in murine macrophages cell line RAW264.7. 1200 31

A decline in T-cell-mediated immunity and transient state of immunosuppression after immunization has been reported in dogs. Nevertheless, dogs are still routinely vaccinated with polyvalent live vaccines and severe disease does not generally occur. In order to investigate these effects on the canine immune system and to elucidate possible mechanisms we determined the following immune parameters in the blood of 33 clinically sound German shepherd dogs before and after standard vaccination with a polyvalent vaccine against distemper, parvovirus, viral hepatitis, leptospirosis, kennel cough and rabies: white and differential blood cell count, the serum concentrations and/or activities of IL-1, IL-2, IFN-gamma, TNF-alpha, neopterin and IgG, natural killer (NK) cell activity, bactericidal activity and complement hemolytic activity, lymphocyte proliferation test (LPT) and nitroblue tetrazolium test (NBT). Our major findings were that significant postvaccinal decreases in T-cell mitogenic response to PHA and in neutrophil function and neopterin serum concentration were accompanied by simultaneous increase in plasma IgG and hemolytic complement activity. This suggests a transient shift in the balance between cell-mediated and humoral (T(H)1/T(H)2) immunity rather than immunosuppression. These results do not imply that dogs should not receive live vaccines, as the response to vaccines just seems to create a state of altered homeostasis when immunization elicits protection by humoral and cell-mediated immunity. However, these recognized compromises of immune function should be considered and vaccines still be applied only in healthy animals and strictly according to the rules and regulations given by the manufacturer.
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PMID:Immune modulation following immunization with polyvalent vaccines in dogs. 1290 8

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

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

Schistosoma mansoni infection may occur either as an acute infection in individuals who have recently visited an endemic area, with no previous contact with the parasite, or as a lasting chronic disease, if not interrupted by specific chemotherapy. The acute phase is characterized by symptoms such as fever, cough, diarrhea, anorexia, and arthralgias in combination with leukocytosis and eosinophilia, and a high cellular immune response to schistosome antigens especially those from the parasite's eggs. In the chronic phase, most patients living in endemic areas are asymptomatic, and their immune responses to egg antigens are modulated. A few develop periportal fibrosis of the liver, which may result in the hepatosplenic form of the disease. The humoral response (IgG, IgM and IgE) in acute patients to egg and worm antigens does not differ from the chronic phase. However, a high level of IgG and IgM antibodies to KLH were detected in acute patients. Acute patients express a considerably higher in vitro cellular responsiveness than do chronic patients, especially to egg antigens. They present a mixed profile of Th1 and Th2 cytokines. Ultrasound examinations of endemic population reveal a high heterogeneity between the patients as regards the presence and intensity of periportal fibrosis. Most patients are asymptomatic and their immune responses to schistosoma egg antigens (SEA) are modulated. In contrast, a high percentage of patients with incipient fibrosis (early stage of hepatosplenic) responded strongly to SEA. Patients with advanced hepatosplenic disease were likely to be non-responders to SEA. Most of the chronic patients presented a Th2 profile with low production of interferon-gamma (IFN-gamma). The intensity of infection favors the production of interleukin (IL)-10. After adjusting for age, sex, and intensity of infection, a strong correlation was observed between the production of IL-13 and the degree of fibrosis. Chronic asymptomatic patients and those with incipient fibrosis expressed very high levels of heterogeneity of their antibody responses. IgG response to soluble worm antigen preparation (SWAP) was distinct and significantly higher in hepatosplenic patients than in those asymptomatic or with incipient fibrosis. Levels of IgG4 to SEA were significantly higher in sera from patients with incipient fibrosis as compared to uninfected and hepatosplenic groups. Polyclonal idiotypic antibodies and their fragments F(ab')2, directly stimulate in culture T cells of schistosomiasis patients in presence of IL-1. Polyclonal idiotypic antibodies are able to modulate in vitro granuloma formation around SEA-polyacrylamide. The importance of idiotypes for protection or pathology in schistosomiasis is still not clear.
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PMID:Human schistosomiasis mansoni: immune responses during acute and chronic phases of the infection. 1857 64

Airborne organic dusts in swine confinement facilities have detrimental effects on workers health. Bacterial endotoxins (i.e., lipopolysaccharides [LPS]) that contaminate these dusts have been implicated in their pro-inflammatory effects in the airways. Exposure to such dusts induces expression of ELR-CXC chemokines (e.g., interleukin [IL]-8), prototypical neutrophil chemoattractants and activators, and neutrophilic pathology. To confirm the roles of the ELR-CXC chemokines in LPS-driven airway pathology, the authors exposed swine to bacterial LPS and tested whether blocking ELR-CXC chemokines would have beneficial effects. Delivery of the ELR-CXC chemokine antagonist CXCL8(3-74)K11R/G31P (G31P) blocked reactive oxygen intermediate production and chemotactic responses by IL-8-challenged neutrophils in vitro. In vivo, one treatment with G31P (100 microg/kg) blocked neutrophil inflammatory responses to intradermal LPS challenge for > or =2 days. It also ameliorated pathology in piglets challenged via the airway with 1 mg of Eschericia coli LPS. On physical examination the saline-treated endotoxemic animals were depressed, pyrexic, and displayed labored breathing, whereas the G31P-treated animals were bright, active, and alert and had a low-grade fever and occasional cough. The lungs of the saline-treated animals displayed evidence of pleural surface hemorrhagic consolidation, and their airways contained large numbers of neutrophils (>80%) as well as substantial amounts of tumor necrosis factor (TNF) and IL-1. The G31P treatments of the LPS-challenged piglets reduced their airway neutrophilic inflammatory responses by approximately 86% and reduced the airway TNF (approximately 70%) and IL-1 (approximately 83%) levels. These data implicates the ELR-CXC chemokines in the neutrophilic inflammation observed after airways exposure to bacterial LPS.
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PMID:Amelioration of pathology by ELR-CXC chemokine antagonism in a swine model of airway endotoxin exposure. 1943 83

A 24-year-old man presented with cough, sore throat, fever, maculopapulous exanthema, pericardial and pleural effusion. Despite extensive evaluation neither infectious, autoimmune, hematological nor oncological disorders were revealed. Broad spectrum antibiotic and subsequently corticosteroid treatment failed to resolve the symptoms. Multiorgan failure with rapid progress of acute respiratory distress syndrome and circulatory failure developed and patient died. Adult onset Still's disease (AOSD), a diagnosis considered in this patient, is a rare disease with unknown prevalence, pathogenesis and etiology. Clinically it is characterized by spiking fever, arthritis, rash, and impairment of multiple organs. There is no single diagnostic test for AOSD. Rather, the diagnosis is based on the clinical criteria and requires the exclusion of infectious, neoplastic, and other autoimmune diseases. Rarely the course of the disease can be rapidly progressive to death. Treatment includes the use of non-steroid antirheumatic drugs and corticosteroids. Limited data suggest that biological agents (e.g. anti-TNF-alpha, anti-IL-1), rituximab or intravenous immunoglobulins might be promising for the treatment of severe cases.
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PMID:[24-year old male with fever, multi-organ dysfunction and fast progressing ARDS]. 1994 45


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