Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of recombinant interleukin (IL)-10 and the role of endogenous IL-10 were determined in C57B1/6 mice with pneumonia induced by intranasal inoculation with 10(6) cfu of Streptococcus pneumoniae. Pneumonia induced sustained expression of IL-10 mRNA and protein in lungs, but IL-10 remained undetectable in plasma. Intranasal inoculation of S. pneumoniae in combination with IL-10 (1500 U/mouse) resulted in decreased lung concentrations of tumor necrosis factor-alpha (TNF) and interferon (IFN)-gamma, increased bacterial counts in lungs and blood, and early lethality. Conversely, pretreatment (-2 h) of mice with an anti-IL-10 monoclonal antibody (2 mg/mouse) was associated with increased lung levels of TNF and IFN-gamma, reduced bacterial counts in lungs and plasma 40 h after the inoculation, and prolonged survival. These results indicate that during pneumococcal pneumonia, IL-10 attenuates the proinflammatory cytokine response within the lungs, hampers effective clearance of the infection, and shortens survival.
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PMID:Interleukin-10 impairs host defense in murine pneumococcal pneumonia. 889

A veal calf with chronic pneumonia was characterized by reduced weight gain, feed intake and increased feed/gain ratio. Concentrations of hemoglobin, packed cell volume, red blood cell number and blood plasma levels of iron, albumin, urea, glucose, insulin, insulin-like growth factor-I and triiodothyronine were decreased, while plasma levels of total protein, immunoglobulin G and nonesterified fatty acids were increased. White blood cell number, blood plasma concentrations of triglycerides, growth hormone, cortisol and tumor necrosis factor-alpha were not changed. Hematological, metabolic and endocrine changes were interpreted as expressions of reduced energy and protein intake and of nutrient partitioning which contributed to reduced growth performance.
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PMID:Endocrine, metabolic and hematological changes associated with reduced growth performance during chronic pneumonia in calves: a case study. 892 69

The present study was aimed at elucidating the role of inflammatory cells in the pathogenesis of cryptogenic organizing pneumonia, and the mode of action of erythromycin in inhibiting the progression of the disease. Bronchoalveolar lavage fluid was obtained from 16 patients with cryptogenic organizing pneumonia and 4 control subjects. Neutrophil chemotactic activity was determined in relation to the concentration of two cytokines, interleukin-8 and tumor necrosis factor-alpha. Eight patients with cryptogenic organizing pneumonia, 4 with bronchoalveolar lavage fluid neutrophilia and 4 without, received low dose oral erythromycin daily (600 mg) for 2 to 3 months. Bronchoalveolar lavage fluid was obtained before and after treatment. In the bronchoalveolar lavage fluid of cryptogenic organizing pneumonia patients with bronchoalveolar lavage fluid neutrophilia, the levels of neutrophil chemotactic activity, interleukin-8, and tumor necrosis factor-alpha were significantly increased compared with levels measured in control subjects and in cryptogenic organizing pneumonia patients without bronchoalveolar lavage fluid neutrophilia. The level of interleukin-8 correlated with the percent of neutrophils and neutrophil chemotactic activity of bronchoalveolar lavage fluid, while the level of tumor necrosis factor-alpha did not. Furthermore, the levels of interleukin-8 and neutrophil chemotactic activity in the bronchoalveolar lavage fluid of cryptogenic organizing pneumonia patients with bronchoalveolar lavage fluid neutrophilia were significantly decreased following treatment with erythromycin. In contrast, the level of tumor necrosis factor-alpha was not affected by treatment with erythromycin. It is possible that cryptogenic organizing pneumonia is caused by neutrophil-mediated inflammation, and that the favorable clinical effect of erythromycin is due to inhibition of neutrophil accumulation in the peripheral airways through a biological activity other than bacteriostasis, e.g., local suppression of interleukin-8 production.
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PMID:Neutrophil chemotactic activity in cryptogenic organizing pneumonia and the response to erythromycin. 894 40

Streptococcus pneumoniae is the most frequent cause of community-acquired pneumonia. We sought to determine the role of tumor necrosis factor-alpha (TNF) in the pathogenesis of pneumococcal pneumonia. Induction of pneumonia in C57B1/6 mice by intranasal inoculation with 10(6) colony-forming units (cfu) S. pneumoniae resulted in a sustained increase in TNF activity in lung homogenates reaching a plateau between 12 and 72 h (72 h: 185.49 +/- 54.41 ng/g), while plasma TNF activity remained low or undetectable. Treatment with a neutralizing anti-TNF monoclonal antibody 2 h before inoculation strongly reduced lung TNF activity, but only modestly diminished lung interleukin (IL)-1beta levels, and did not significantly influence lung IL-6, IL-10, and interferon-gamma concentrations. Anti-TNF-treated mice had fourfold more S. pneumoniae cfu isolated from lungs than control mice 40 h after inoculation (p < 0.05), although lung myeloperoxidase activities were similar in both treatment groups. Anti-TNF-treated mice died significantly earlier from pneumococcal pneumonia than control mice (p < 0.05). Endogenously produced TNF is important for host defense during pneumococcal pneumonia.
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PMID:Passive immunization against tumor necrosis factor-alpha impairs host defense during pneumococcal pneumonia in mice. 903 1

Alveolar macrophages (AM), which represent the major resident population of immunocompetent cells in the lower respiratory tract, have been implicated in the pathogenesis of acute lung injury in view of their exceptional capacity to release a large array of inflammatory mediators. The ex vivo analysis of these cells, accessible to bronchoalveolar lavage (BAL) is hampered by the fact that, under conditions of respiratory failure, the AM pool is heavily expanded by polymorphonuclear neutrophils (PMN), which necessitates separation of these cell populations. In the present study, we describe a flow cytometric approach to sort human AM obtained from BAL samples of both healthy volunteers (n = 10) and patients with severe pneumonia demanding mechanical ventilation (n = 10), using forward scatter and high autofluorescence characteristics to discriminate AM from PMN and lymphocytes. This technique yielded highly purified AM populations (>95%) as evidenced by morphological analysis, cytochemistry, and CD71 and CD14 expression of the sorted cells. The flow sorting process, per se, did not induce the expression of the acute-phase cytokine tumor necrosis factor-alpha (TNF-alpha) in control AM as determined by reverse transcriptase-polymerase chain reaction. Unstimulated and lipopolysaccharide-induced TNF-alpha protein secretion were comparable in sorted and unsorted AM as demonstrated by enzyme-linked immunosorbent assay. We suggest flow sorting of viable human AM as an efficient and nonperturbing separation technique to yield highly purified cell populations especially from PMN-rich BAL fluids of critically ill patients.
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PMID:Separation of human alveolar macrophages by flow cytometry. 912 15

Induction of pneumonia in C57Bl/6 mice by intranasal inoculation with 10(6) cfu of Streptococcus pneumoniae resulted in sustained expression of interleukin (IL)-6 mRNA in lungs and increases in lung and plasma IL-6 concentrations. In IL-6-deficient (IL-6-/-) mice, pneumonia was associated with higher lung levels of the proinflammatory cytokines tumor necrosis factor-alpha, IL-1beta, and interferon-gamma and of the antiinflammatory cytokine IL-10 than in wild type (IL-6+/+) mice (all P < .05). Also, the plasma concentrations of soluble tumor necrosis factor receptors were higher in IL-6-/- mice (P < .05), while the acute-phase protein response was strongly attenuated (P < .01). Lungs harvested from IL-6-/- mice 40 h after inoculation contained more S. pneumoniae colonies (P < .05). IL-6-/- mice died significantly earlier from pneumococcal pneumonia than did IL-6+/+ mice (P < .05). During pneumococcal pneumonia, IL-6 down-regulates the activation of the cytokine network in the lung and contributes to host defense.
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PMID:Interleukin-6 gene-deficient mice show impaired defense against pneumococcal pneumonia. 923 10

To determine the role of endogenous tumor necrosis factor (TNF) alpha on neutrophil influx into the lungs in acute Pseudomonas aeruginosa pneumonia, we evaluated TNF alpha activity, inflammatory cell response and neutrophil chemotactic activity in the bronchoalveolar lavage fluids (BALFs) of P. aeruginosa-infected mice. In the case of fatal pneumonia, the TNF alpha activity in the BALFs appeared within 3 hr, peaked at 6-12 hr and attenuated within 24 hr after intratracheal challenging, while no TNF alpha activity was detected in the plasma. The elevation of TNF alpha activity in the BALFs was closely associated with neutrophil accumulation. Mirroring the TNF alpha activity response and the influx of neutrophils into the murine airway, the number of neutrophils in the BALFs increased within 3 hr, peaked at 6-12 hr and remained elevated up to 24 hr after challenging. Neutralization of the TNF alpha activity in the BALFs with anti-murine TNF antiserum decreased the level of neutrophil migration by BALF 45.0-49.7% at 6 hr and 49.3-54.2% at 12 hr, while the neutralizing antiserum had no effect on the level of neutrophil migration by BALFs at 3 and 24 hr. Furthermore, the intravenous administration of anti-murine TNF antiserum 2 hr before challenging significantly inhibited neutrophil migration into the lungs of mice with sublethal pneumonia (P < 0.05; compared with mice receiving pre-immune serum). These data suggest that intra-alveolar TNF alpha plays an important role in causing lung neutrophil accumulation at the mid-phase of murine P. aeruginosa pneumonia.
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PMID:Endogenous tumor necrosis factor (TNF) alpha mediates neutrophil accumulation at the mid-phase of a murine model of Pseudomonas aeruginosa pneumonia. 931 Sep 39

Inflammatory cell recruitment contributes to respiratory impairment during Pneumocystis carinii pneumonia. We evaluated expression of intercellular adhesion molecule-1 (ICAM-1), a key participant in leukocyte accumulation, in rats with P. carinii pneumonia. Immunostaining for ICAM-1 was most marked on bronchiolar epithelium but was also evident on type II pneumocytes, endothelium, and macrophages. Lung from normal and dexamethasone-treated uninfected animals exhibited markedly less ICAM-1. We hypothesized that P. carinii promoted ICAM-1 expression in epithelium through tumor necrosis factor-alpha (TNF-alpha) release from macrophages or that P. carinii directly stimulated ICAM-1 expression. Alveolar macrophages were incubated with P. carinii, and the medium was added to A549 epithelial cells. Treatment of macrophages with P. carinii enhanced A549 ICAM-1, which was inhibited with antibody to TNF-alpha. To determine whether P. carinii alone also stimulated ICAM-1, A549 cells were cultured with P. carinii, also augmenting ICAM-1. Of note, A549 ICAM-1 expression from P. carinii alone was less than with P. carinii-exposed macrophages. Thus ICAM-1 is enhanced in lung epithelium during P. carinii infection, in part, through TNF-alpha-mediated mechanisms.
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PMID:Pneumocystis carinii induces ICAM-1 expression in lung epithelial cells through a TNF-alpha-mediated mechanism. 943 63

Biologically active interferon-alpha, tumor necrosis factor-alpha (TNF-alpha), and interleukin-1 (IL-1) were detected in bronchoalveolar lavage (BAL) fluids of 3-week-old cesarian-derived colostrum-deprived pigs inoculated with H1N1 influenza virus. Cytokine titers and lung virus titers were significantly higher 18-24 h after inoculation than at 48-72 h after inoculation in all 4 litters of pigs examined. All three cytokines were positively correlated with a 3- to 4-fold increase in BAL cell numbers (P < .036) and with a drastic neutrophil infiltration (24%-77% of BAL cells vs. 0-1.5% in controls) (P < .001). In addition, cytokine production coincided with the onset of general and respiratory symptoms of influenza and with the development of a necrotizing bronchopneumonia. This study is the first demonstration of TNF-alpha and IL-1 in BAL fluids of a natural influenza virus host. It documents that pigs may be a highly valuable experimental model in human influenza virus pneumonia.
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PMID:Bronchoalveolar interferon-alpha, tumor necrosis factor-alpha, interleukin-1, and inflammation during acute influenza in pigs: a possible model for humans? 953 86

Oral administration of the bacterial extract OM-85 BV has been shown to prime alveolar macrophages (AM) in such a way that they secrete significantly more nitric oxide, tumor necrosis factor-alpha and interleukin-1beta upon in vitro stimulation with lipopolysaccharide (LPS). As increased cytokine secretion by AM may account for the therapeutic effect of OM-85 BV in respiratory tract infections, we studied the effect of orally administered OM-85 BV on the outcome of Klebsiella pneumoniae-induced pneumonia. Mice received a daily oral dose of OM-85 BV (350 mg/kg body weight) for 5 days and were intratracheally infected with 333, 1000 or 3333 CFU K. pneumoniae on day 8. It was shown that OM-85 BV pretreatment of mice has no effect on bacterial clearance, neutrophil recruitment and survival in this acute respiratory tract infection. Also, OM-85 BV treatment had no protective effect in a recurrent infection with K. pneumoniae. It is concluded that AM activation by oral treatment with OM-85 BV is not sufficient to play a protective role in respiratory tract infection with K. pneumoniae.
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PMID:In vivo study on the immunomodulating effects of OM-85 BV on survival, inflammatory cell recruitment and bacterial clearance in Klebsiella pneumonia. 963 54


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