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)

Pneumonia and lung injury are hallmarks of early-onset neonatal group B streptococcal (GBS) infections. Production of a beta-hemolysin/cytolysin (beta-h/c) encoded by the cylE gene is associated with GBS virulence in vivo. To elucidate the contribution of the beta-h/c toxin to lung injury, the interactions of GBS wild-type strains and isogenic cylE mutants with A549 lung epithelial cells were examined. Compared with wild-type GBS strains, cylE mutants did not produce cytolytic injury, even at high inocula, and exhibited decreased cellular invasion. Additionally, cylE mutants induced less A549 cell release of the neutrophil chemoattractant interleukin (IL)-8. GBS invasion and IL-8 induction were significantly reduced in the presence of dipalmotyl phosphatidylcholine, a major constituent of lung surfactant and a known inhibitor of beta-h/c activity. These data indicate that the GBS beta-h/c contributes to invasion and immune activation of lung epithelial cells and may represent a multifunctional virulence factor in the early pulmonary stages of GBS infection.
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PMID:Group B streptococcal beta-hemolysin/cytolysin promotes invasion of human lung epithelial cells and the release of interleukin-8. 1180 93

A porcine Pasteurella multocida (P. m.) infection model was established to study the spatial distribution of cytokine mRNA-expressing cells in lung tissue during acute pneumonia. The mRNA detection was performed by non-radioactive, formamide-free in situ hybridization (ISH) using oligonucleotides against the porcine interleukins (IL): IL-1 beta, IL-2, IL-4, IL-6, IL-8, TNF alpha and TGF beta. Cytokine mRNA-expressing macrophages were demonstrated by a double staining procedure combining immunohistochemistry (IH) using the primary antibody 2G6 with IL-1 beta, IL-6 and TGF beta ISH. With the exception of some stained TNF alpha-expressing cells, no IL mRNA was detectable in the lung of unaffected animals. The experimental P. m. pneumonia was characterized by a predominant, exudative and an additional proliferative interstitial component as well as abscess formation in the lung. Many cells of the region between the abscess membrane and the affected lung area showed high IL-6, IL-1 beta, IL-4 as well as TGF beta and few cells low IL-8 mRNA expression with characteristic distribution patterns. The ISH/IH double staining procedure revealed that at least some of the IL-6 or TGF beta-producing cells belonged to the 2G6-positive macrophages.
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PMID:Cytokine mRNA expression in experimental porcine pneumonia. 1199 74

The incidence of nosocomial pneumonia (NP) among injured patients is substantial. We hypothesize that traumatic injury induces alterations in local organ effector cell function that may predispose the lungs of injured patients to infection. It is the objective of this study to compare the systemic and alveolar effector cell response to injury and assess the relationship these have to the development of NP. Peripheral blood and bronchoalveolar lavage fluid (BAL) were collected from 10 elective surgery patients (controls) and 16 multitrauma patients at 12, 36, and 60 h post-injury. Systemic and alveolar levels of IL-8 and IL-10 were measured. CD11b expression on peripheral blood neutrophils (PBN) and alveolar neutrophils (AN) and HLA-DR expression on peripheral blood monocytes (PBM) and alveolar macrophages (AM) were measured. Alveolar levels of IL-8 and IL-10 were significantly higher than systemic levels after injury. HLA-DR expression was reduced on both PBM and AM after injury but was lowest on the AM. Six of 16 patients (38%) developed NP (NP+). There were no differences in cytokine levels (IL-8 and IL-10) or effector cell phenotype (CD11b and HLA-DR expression) within the systemic circulation of NP+ and NP- patients. In contrast, NP+ and NP- patients differed significantly in alveolar cytokine levels and alveolar effector cell phenotype. IL-8 was significantly higher in BAL form NP+ patients at all time points after injury. Furthermore, alveolar levels of IL-10 decreased in NP- patients but increased in NP+ patients. In all patients, AM HLA-DR expression was significantly reduced from normal controls 12 h post-injury. In NP-patients, AM HLA-DR expression returned to normal 60 h post-injury, whereas in NP+ patients, expression remained suppressed. These findings identify distinct trends in local organ cytokine production and alterations in effector cell phenotype that precede NP. The persistence of reduced HLA-DR expression amidst increasing levels of IL-10 in NP+ patients suggest that cell-mediated immune function is being suppressed. As such, local organ immunosuppression may be responsible for the development of nosocomial pneumonia in injured patients.
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PMID:Increased IL-10 production and HLA-DR suppression in the lungs of injured patients precede the development of nosocomial pneumonia. 1206 78

Sputum and serum from patients with active pulmonary tuberculosis (TB), healthy purified protein derivative-positive adults, and patients with bacterial pneumonia were collected to simultaneously assess local immunity in the lungs and peripheral blood. To determine whether cytokine profiles in sputum from TB patients and control subjects were a reflection of its cellular composition, cytospin slides were prepared in parallel and assessed for the presence of relative proportions of epithelial cells, neutrophils, macrophages, and T cells. Gamma interferon (IFN-gamma) in sputum from TB patients was markedly elevated over levels for both control groups. With anti-TB therapy, IFN-gamma levels in sputum from TB patients decreased rapidly and by week 4 of treatment were comparable to those in sputum from controls. Further, IFN-gamma levels in sputum closely followed mycobacterial clearance. Although detected at fourfold-lower levels, IFN-gamma immunoreactivities in serum followed kinetics in sputum. TNF-alpha, interleukin 8 (IL-8) and IL-6 also were readily detected in sputum from TB patients at baseline and responded to anti-TB therapy. In contrast to IFN-gamma, however, TNF-alpha and IL-8 levels also were elevated in sputum from pneumonia controls. These data indicate that sputum cytokines correlate with disease activity during active TB of the lung and may serve as potential early markers for sputum conversion and response to anti-TB therapy.
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PMID:Sputum cytokine levels in patients with pulmonary tuberculosis as early markers of mycobacterial clearance. 1209 79

Recruitment of neutrophils into alveolar air spaces is an early event in the pathogenesis of pneumonia due to Streptococcus pneumoniae. This results from chemokines released by activated endothelial and epithelial cells and alveolar macrophages. Culture supernatants of 6 wild-type strains of S. pneumoniae, shown to contain choline-binding protein A (CbpA; clades A and B), induced release of chemokine CXCL8 from the human alveolar epithelial cell line A549, whereas a CbpA deletion mutant elicited significantly reduced CXCL8 release, compared with that of its isogenic parent (P<.01). Recombinant CbpA up-regulated expression of messenger RNA of CXCL8 and CCL2 but not of XCL1, CXCL10, CCL1, CCL3, CCL4, or CCL5 in A549 cells and induced increased secretion of CXCL8, CCL2, CXCL1, and CXCL5 in a dose- and time-dependent manner. CbpA also increased the expression of intercellular adhesion molecule 1 (CD54) by A549 cells. Thus, CbpA of S. pneumoniae induces the transcription and release of proinflammatory molecules by human alveolar epithelial cells.
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PMID:Choline-binding protein A of Streptococcus pneumoniae elicits chemokine production and expression of intercellular adhesion molecule 1 (CD54) by human alveolar epithelial cells. 1240 94

Smoking causes various changes in the lung. This report describes a case of cigarette smoke-induced acute eosinophilic pneumonia (CS-AEP) with neutrophilia in the blood. However, the precise mechanism is unknown, so we examined the effect of exposure to cigarette smoke extracts on the production of interleukin (IL)-4, IL-5, IL-8, IL-18, granulocyte macrophage-colony stimulating factor (GM-CSF), and vascular endothelial growth factor (VEGF) by human bronchial epithelial cells (HBECs) obtained from the patient. We found that IL-8 released from HBECs was involved in neutrophilia in the blood, and is a new factor in the development of AEP, especially in the early phase.
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PMID:Cigarette smoke-induced acute eosinophilic pneumonia accompanied with neutrophilia in the blood. 1248 58

Chlamydia pneumoniae is an obligate intracellular human pathogen that causes acute respiratory diseases such as pneumonia and bronchitis. Previous studies have established that C. pneumoniae can induce cytokines in mouse and/or human cells, but little information is available on the cytokine response of respiratory epithelial cells, a first line of infection. In this study, heparin treatment of C. pneumoniae significantly reduced its ability to induce interleukin 8 (IL-8) and tumor necrosis factor alpha (TNF-alpha) mRNA in human lung carcinoma cells, indicating that cytadherence is an important early stimulus for induction of proinflammatory mediators. Although the IL-8, gamma interferon, and TNF-alpha message was consistently induced by infection of A549 cells not treated with heparin, only an elevation of IL-8 protein was detected in A549 supernatants. A549 IL-beta and IL-6 mRNA and supernatant protein profiles were not significantly changed by infection. Heat or UV inactivation of C. pneumoniae only partially reduced the cytokine response, and inhibition of C. pneumoniae protein or DNA synthesis did not affect its ability to induce cytokine gene expression. To prevent stress-induced cytokine release by the A549 cells, centrifugation was not utilized for infection experiments. These experiments establish the importance of cytadherence in cytokine release by cells of respiratory epithelial origin and suggest that further work in the area of cytokine mediators is warranted to gain valuable pathogenic and therapeutic insights.
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PMID:Induction of proinflammatory cytokines in human lung epithelial cells during Chlamydia pneumoniae infection. 1254 May 37

Methotrexate-induced pneumonitis has been reported as an infrequent but potentially serious complication of therapy in a variety of malignant and benign conditions. Because inflammatory cell infiltration is concerned with the development of methotrexate-induced pneumoinitis, and because airway epithelial cells participate in the orchestration of lung inflammation, the authors determined whether methotrexate might stimulate airway epithelial cells (A549 cells) to release neutrophil, monocyte, and eosinophil chemotactic activities (NCA, MCA, and ECA). A549 cells released NCA, MCA, and ECA in a dose- and time-dependent manner in response to methotrexate. Partial characterization revealed the heterogeneity of NCA, MCA, and ECA. The release of chemotactic activity was blocked by lipoxygenase inhibitors and cycloheximide. NCA was inhibited by leukotriene (LT) B(4) receptor antagonist, and anti-interleukin (IL)-8 and granulocyte colony-stimulating factor (G-CSF) antibodies. MCA was attenuated by LTB(4) receptor antagonist, and anti-monocyte chemoattractant protein (MCP)-1 and granulocyte-macrophage CSF (GM-CSF) antibodies. ECA was attenuated by LTB(4) receptor antagonist, and anti-IL-8 and GM-CSF antibodies. The release of IL-8, G-CSF, MCP-1, GM-CSF, and LTB(4) from A549 cells significantly increased in response to methotrexate. The mRNA expression of IL-8 and MCP-1 was augmented by methotrexate stimulation. These data suggest that type II epithelial cells may modulate inflammatory cell recruitment into the lung by releasing NCA, MCA, and ECA in response to methotrexate.
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PMID:Methotrexate stimulates lung epithelial cells to release inflammatory cell chemotactic activities. 1255 56

We have studied the changes in the serum level of the following cytokines during the course of treatment of nosocomial pneumonia (NP): pro-inflammatory--IL-1alpha and IL-6, chemoattractive--IL-8, anti-inflammatory--IL-4 and IL-10, and differentiating-activating--IFN-gamma and TNF-alpha. It has been found that at the time of admission of the patients the clinical severity of their condition was correlated with increased levels of all circulating cytokines except for IFN-gamma, the level of which was low. An adequate ethiotropic therapy helped to clear the clinical symptoms of infection and intoxication in 1-2 weeks. The level of circulating pro- and anti-inflammatory cytokines, IL-8, and TNF-alpha was decreasing, however, the level of IFN-gamma did not change significantly during 15 days. The ratio IFN-gamma/IL-10 did not change much but was slightly low during the treatment of the severe form of NP. Radical positive changes in the cytokine dynamics were achieved after the addition of leukinferon to the ethiotropic therapy.
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PMID:Dynamics of cytokines and role of immunocorrection in nosocomial pneumonia. 1268 58

Lung tissue removed from neonatal calves with acute Mannheimia haemolytica pneumonia showed that rapid up-regulation of the basal mRNA expression of tracheal antimicrobial peptide (TAP), NF-kappa B, and intercellular adhesion molecule 1 occurred after infection; TAP and interleukin 8 expression were highly correlated. This work suggests that the coordinated expression of beta-defensin and inflammatory elements occurs during bacterial pneumonia.
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PMID:Coordinated expression of tracheal antimicrobial peptide and inflammatory-response elements in the lungs of neonatal calves with acute bacterial pneumonia. 1270 77


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