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 relationship of the production of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha) and interleukin-2 (IL-2) to the pattern and etiology was studied in patients with pulmonary tuberculosis (n = 74) and nontuberculous lung diseases (n = 28). There was an inverse correlation between the production of the proinflammatory cytokines IL-1 beta and TNF-alpha and the main T-cellular immunity IL-2. An exacerbation of a tuberculous process is accompanied by an increase in IL-1 beta and TNF-alpha productions and by a decrease in inducted IL-2 synthesis. With favourable changes, there was, on the contrary, a reduction in the levels of IL-1 beta and TNF-alpha and a rise in IL-2. There were differences in the rate of cytokine synthesis in pulmonary tuberculosis, lung cancer, and pneumonia. Patients with cancer are most typified by the spontaneous mononuclear production of serum TNF-alpha and by the low level of IL-2 when PGA is stimulated. On the contrary, the least TNF-alpha synthesis and pronounced IL-2 production in pneumonia. A combination of the high production of PPD-induced IL-1 beta and PGA-stimulated IL-2 is more specific to patients with infiltrative pulmonary tuberculosis.
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PMID:[Production of cytokines in different forms of pulmonary tuberculosis]. 969 96

The serum concentrations of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and interferon-gamma (IFN-gamma) were measured by enzyme immunoassays in 44 patients with Chlamydia (n = 13) or Mycoplasma (n = 14) pneumonia or influenza A infection (n = 17) and in 20 control subjects. The levels of IFN-gamma were raised in 29/44 patients. The concentrations of IL-6 were raised in 32/44 patients. Raised levels of TNF-alpha were seen in 26/44 but there was no significant difference between the levels of the different groups of patients. All three cytokines indicated clinical recovery when acute and convalescent samples from 10 patients with Chlamydia pneumonia were analyzed. IFN-gamma, IL6 and TNF-alpha are present in the circulation in the majority of patients with Chlamydia and Mycoplasma pneumonia and in influenza A infection. We suggest that repeated measurement of cytokines, such as IL-6, IFN-gamma and TNF-alpha, may be useful in the management of lower respiratory tract infections but further studies are needed to define the value of cytokine measurements in acute pneumonia.
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PMID:Cytokine responses in patients with pneumonia caused by Chlamydia or Mycoplasma. 973 Jul 97

The sequential pathogenesis of pulmonary aspergillosis was studied and the role of inflammatory cytokines in host response to Aspergillus fumigatus was characterized in immunocompetent and immunosuppressed mice. Two distinct phases were observed in immunocompetent mice: First, an intense clearance of A. fumigatus occurred, possibly through alveolar macrophages and recruited neutrophils (PMNL), accompanied by rapid release of tumor necrosis factor-alpha, interleukin (IL)-6, and IL-1beta, and second, cellular and fungal debris were cleaned by recruited monocytes, cytokine production rapidly decreased, and pneumonia self-healed. In contrast, cortisone-treated animals had, first, an altered clearance of conidia and delayed cytokine production and inflammatory cell recruitment; second, an invasive process in lungs, recruitment of PMNL, and release of IL-6 and IL-1beta; and third, widespread tissue necrosis, sustained release of IL-6 and IL-1beta, further increases in PMNL trafficking but no monocyte recruitment, respiratory failure, and 100% mortality within 5 days. These insights may be useful in the development of new treatment strategies for pulmonary aspergillosis.
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PMID:Kinetic study of host defense and inflammatory response to Aspergillus fumigatus in steroid-induced immunosuppressed mice. 978 Feb 70

The obligate intracellular pathogen Chlamydia pneumoniae is associated with chronic respiratory, atherosclerotic, and rheumatic disease. The alveolar macrophage (AM) is a potential target cell for the pathogen and may contribute to respiratory immunopathology. We therefore investigated in vitro the interaction between chlamydiae and macrophages with cocultures of C. pneumoniae and AM from 12 healthy volunteers. Inflammatory responses were evaluated through lucigenin-amplified chemiluminescence; secretion of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and interleukin 8 (IL-8); and expression of intercellular adhesion molecule-1 (ICAM-1) and human leukocyte antigen-DR (HLA-DR). C. pneumoniae readily induced productive infection in the AM. Inclusions containing replicating pathogens could be maintained for up to 120 h. Morphologically similar infection patterns were seen ex vivo in AM collected from six patients with known C. pneumoniae pneumonia. AM responded to the infection with a marked, dose-dependent release of reactive oxygen species, TNF-alpha, IL-1beta, and IL-8. ICAM-1 expression remained unchanged, but HLA-DR was significantly upregulated. Our data indicate that the release of antimicrobial mediators cannot prevent chlamydial infection and replication in AM, but may be involved in amplification of the local inflammatory response in C. pneumoniae pneumonia.
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PMID:Interaction of Chlamydia pneumoniae and human alveolar macrophages: infection and inflammatory response. 980 36

Sepsis and pneumonia are major causes of morbidity and mortality in the neonatal period. The symptoms are variable and unspecific. So far, no reliable diagnostic test for neonatal infection has been found. In this study we measured serum levels of soluble tumor necrosis factor receptors (sTNFR) p55 and p75 in non-infected and infected neonates, and evaluated the diagnostic value of these mediators as tests for early detection of neonates with sepsis or pneumonia. Blood was collected on admission and after 3-4 days from 161 neonates consecutively admitted to the Neonatal Intensive Care Unit (NICU) during the first week of life. Twenty two neonates suffered from infection and 127 were classified as non-infected (controls). Samples were analyzed for p55 and p75, C-reactive protein (CRP) and white blood cell count with differential. Both preterm and term infected neonates had initially higher concentrations of p55 (both p <0.01) and p75 (p = 0.01 and p = 0.05, respectively) than controls. In non-infected neonates p55 levels decreased in the perinatal period, whereas p75 levels remained stable. Levels of both p55 and p75 decreased in neonates with infection during the perinatal period. CRP was a more specific parameter than p55 and p75 (CRP: 97%, p55: 65% and p75: 75%) whereas the sensitivity of all three parameters was at similar levels (CRP: 59%, p55: 70% and p75: 67%). We conclude that assessment of sTNFR may not improve accuracy in the diagnosis of early onset neonatal sepsis compared to the use of CRP.
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PMID:Increased serum concentrations of soluble tumor necrosis factor receptors p55 and p75 in early onset neonatal sepsis. 980 75

We investigated the contribution of eicosanoids, platelet-activating factor, tumor necrosis factor and nitric oxide to the neutrophil influx and development of pulmonary haemorrhagic lesions following immune-complex-induced pneumonitis in rats and possible interactions between these mediators. Increased levels of leukotriene B4 and tumor necrosis factor, measured by enzyme immunoassay and L-929 cytotoxicity assay, were found in the bronchoalveolar lavage 1 and 4 h after induction of the reaction, respectively, and their release was dependent on the previous generation of platelet activating factor. Antagonism of leukotriene B4 receptors by RO-0254094 (2-[(5-carboxypentyl])oxy]-6-[6-[3,4-dihydro-4-oxo-8-propyl-2H-1-benzopy ran-7-yl)oxy]hexyl] benzenepropanoic acid), inhibition of nitric oxide synthesis by L-NAME (Nw-nitro-L-arginine methyl ester) and antagonism of PAF-receptors by WEB-2170 (5-(2-chlorphenyl)-3-4-dihydro-10-methyl-3-((4-morpholinyl)carbony l)-2 H,7H-cyclopenta (4,5)thieno(3,2-f)(1,2,4)-triazolo-4,3,a)91,4)diazepine), significantly inhibited the intensity of haemorrhage, evaluated by the increased levels of extravascular hemoglobin in homogenates of lung tissues. Little evidence support the role of tumor necrosis factor in these lesions. The infiltration of neutrophils, evaluated by measuring myeloperoxidase in homogenates of lungs, was reduced by compounds L-663,536 (3-[1-(4 chlorobenzyl)-3-t-butyl thio-5-isopropylindol-2-yl]-2-2-dimethylpropanoic acid), WEB-2170 and L-NAME. These results indicate that neutrophil infiltration and haemorrhagic lesions in immune-complex-induced lung inflammation are mediated by platelet activating factor, leukotriene B4 and nitric oxide and point out to interesting interactions between these mediators.
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PMID:Lipid mediators, tumor necrosis factor and nitric oxide and their interactions in immune-complex-induced lung injury. 980 71

Small bowel allograft rejection in large animals has yet to be well defined. There are no specific early signs of graft rejection. The present experiments were undertaken to compare acute small bowel allograft rejection in pigs with and without FK506 and also to examine the usefulness of mucosal biopsies. Thirty-six outbred Large-White pigs were divided into (1) group 1 (n = 9): nonimmunosuppressed recipients; (2) group 2 (n = 8): FK506-immunosuppressed recipients; (3) group 3 (n = 2): autotransplant controls; and (4) donors (n = 17). Orthotopic small bowel transplantations were performed with Thiry-Vella loops for daily biopsies. The survival rate of group 2 was significantly longer than that of group 1 (P < 0.05). One best survivor in group 2 was killed at postoperative day (POD) 365. Treatment by FK506 prevented rejection, but most of the pigs died of pneumonia. In group 1, rejection began on POD 3 and progressed to severe rejection rapidly within 7 days. In group 2, rejection began from POD 6 to POD 8, but either remained mild or spontaneously improved. The differences in the routine laboratory data and the tumor necrosis factor-alpha level were not evident between the groups. Histological studies of repeated graft biopsies are thus considered to be essential for detecting signs of graft rejection.
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PMID:Allograft rejection of small bowel transplantation in pigs. 985 21

Circulating interleukin (IL)-1 beta, IL-6, and tumor necrosis factor (TNF)-alpha were examined in 42 febrile children with fever lasting more than 4 days. Their diagnosis were probable viral syndrome in 22, urinary tract infection (UTI) in 10, and probable bacterial pneumonia in 10. None of our study patients had detectable serum IL-1 beta. TNF-alpha levels were significantly higher in children with pneumonia than in those with viral syndrome (p < 0.01). Children with UTI and pneumonia had significantly higher IL-6 and CRP, compared to those with probable viral syndrome (p < 0.01 for both IL-6 and CRP). When appropriate cutoff values are chosen, IL-6 had greatly improved specificity (86.4%, > 20 pg/ml) to demonstrate UTI and pneumonia, as compared to that using CRP (48%, > 40 mg/l). After three days' antibiotic treatment, IL-6 fell to control levels in children with UTI and pneumonia, while CRP remained elevated. There was no difference in TNF-alpha values before and after treatment. Thus, IL-6, rather than IL-1 beta and TNF-alpha, may be a helpful diagnostic tool for evaluation of pediatric febrile infection. Sequential studies involving more patients are needed to determine whether IL-6 is better than CRP in this clinical setting.
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PMID:Circulating interleukin (IL)-1 beta, IL-6 and tumor necrosis factor-alpha in children with febrile infection--a comparison with C-reactive protein. 987 48

Resistance to Pneumocystis carinii is achieved through cell-mediated and humoral immunity, but the interplay between these two systems in the immunocompetent host is not fully understood. TCRbetaxdelta-/- double-mutant mice deficient of all T cell populations naturally acquired P. carinii pneumonia with lethal consequences. Moribund mutants displayed numbers of pulmonary pathogens comparable to RAG-1-/- mice lacking all functional T and B lymphocytes. Pulmonary lavage cells of diseased TCRbetaxdelta-/- mutants secreted proinflammatory cytokines tumor necrosis factor-alpha, interleukin (IL)-12, and interferon-gamma, but not IL-4, -5, or -10. Serum immunoglobulin levels of both healthy and diseased mice were significantly reduced compared with immunocompetent animals. Secreted antibodies were mainly IgM, which also bound P. carinii. Mutants completely lacked IgG1, emphasizing strict T cell dependence of immunoglobulin switching to this isotype. Other IgG subclasses were strongly reduced and did not bind P. carinii. These results suggest that T cells are crucial for generation of antibodies against P. carinii relevant to resistance.
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PMID:Pneumocystis carinii pneumonia in mutant mice deficient in both TCRalphabeta and TCRgammadelta cells: cytokine and antibody responses. 987 31

In rat models of Gram-negative pneumonia, pulmonary emigration of neutrophils (polymorphonuclear leukocytes [PMNs]) is blocked when rats are made endotoxemic by an intravenous administration of endotoxin (lipopolysaccharide [LPS]). To test whether dysfunctional PMN migratory responses in the endotoxemic rat are specific for airway endotoxin, we gave rats intrapulmonary stimuli known to elicit different adhesion pathways for pulmonary PMN migration. Sprague-Dawley rats were treated intravenously with either saline or LPS and then instilled intratracheally with either sterile saline, LPS from Escherichia coli, interleukin (IL)-1, hydrochloric acid (HCl), zymosan-activated serum (ZAS), or lipoteichoic acid (LTA). Three hours later, accumulation of PMNs and protein in bronchoalveolar lavage fluid (BALF) were assessed. BALF PMN accumulation in response to intratracheal treatment with LPS (100%), IL-1 (100%), ZAS (40%), and LTA (58%) was inhibited by endotoxemia. In rats given intratracheal HCl, BALF PMN numbers were unaffected by intravenous LPS. The pattern of inhibition of migration suggests that intravenous LPS only inhibits migration in response to stimuli for which migration is CD18-dependent. In contrast to PMN migration, BALF protein accumulation was inhibited by intravenous LPS only when IL-1 or LPS was used as the intratracheal stimulus. To characterize further the differential responses to the various airway stimuli, the appearance in BALF of tumor necrosis factor-alpha (TNF-alpha) and the PMN chemokine macrophage inflammatory protein (MIP)-2 was measured. Accumulation of PMNs in BALF correlated with the BALF concentrations of MIP-2 (r = 0.846, P < 0.05) and TNF (r = 0.911; P < 0.05). The ability of intravenous LPS to inhibit pulmonary PMN migration correlated weakly with MIP-2 (r = 0.659; P < 0.05) and with TNF (r = 0.413; P > 0.05) concentrations in BALF. However, this correlation was strengthened for TNF (r = 0.752; P < 0.05) when data from IL-1-treated animals were excluded. Thus, the presence in BALF of inflammatory mediators that are known to promote CD18-mediated migration correlates with endotoxemia-related inhibition of PMN migration. Furthermore, the pattern of inhibition of pulmonary PMN migration during endotoxemia is consistent with the CD18 requirement of each migratory stimulus.
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PMID:Inhibition of pulmonary neutrophil trafficking during endotoxemia is dependent on the stimulus for migration. 1010 Oct 10


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