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)

Mycoplasma bovis is a causative agent of bovine mastitis, arthritis, and pneumonia. Six monoclonal antibodies (MAbs) against M. bovis were prepared and used to characterize specific antigens of the mycoplasma. Reactivity of the MAbs to six M. bovis strains was tested by IFA, ELISA, and immunoblotting. The specificity of these MAbs was tested by the same methods against 8 other species of bovine mycoplasmas and 1 mycoplasma species of sheep and goats (Mycoplasma agalactiae) that is highly cross-reactive with M. bovis. Three of the MAbs were used on Western blots of trypsin-treated whole organisms to determine if the antigens were exposed on the surface of M. bovis By isotyping, MAbs were identified as kappa chain IgG1 (3 MAbs), and IgM (3MAbs). The MAbs reacted with all six M. bovis strains in IFA, ELISA, and Western blots. Four of the antigens recognized were highly specific for M. bovis in ELISA, and 3 were cross-reactive with M. agalactiae or other bovine mycoplasmas in Western blots. One MAb reacted with multiple bands with all M. bovis strains, indicating recognition of a size-variant antigen. The size-variant antigen and one of the M. bovis-specific antigens were recognized as surface proteins. A large M. bovis-specific antigen was a conserved cytosolic protein. The M. bovis antigens discovered may be used for specific detection of the organism or measurement of antibody responses, particularly if used in tests with nondenatured alkali-treated antigen, such as ELISA.
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PMID:Membrane-associated and cytosolic species-specific antigens of Mycoplasma bovis recognized by monoclonal antibodies. 857 97

Neonatal infections caused by Group B streptococci (GBS) may lead to pneumonia, sepsis, or meningitis indicating that GBS are able to invade tissues and enter the bloodstream from infected sites. In this study, we showed that the tissue invasiveness of GBS may be related to their ability to invade epithelial cells in vitro by correlating the degree of GBS invasion of cultured human respiratory epithelial cells with the clinical source of isolation. Among 77 isolates tested, those from invasive infections of neonates and adults were significantly (P < 0.001) more invasive than those from vaginal carriers and colonised neonates without clinical symptoms. Furthermore, isolates from the blood were more invasive (P < 0.05) than those from other sites. GBS invasion seemed to be mediated by bacterial surface proteins since trypsin treatments of streptococci significantly reduced their invasion into epithelial cells and invasiveness was not limited to a certain capsular serotype. The two major GBS surface protein antigens c and R, however, were not involved in the invasion process. These results indicate that in vitro invasion of cultured human cells reflects the in vivo invasive property of GBS and involves bacterial surface components different from known virulence factors such as capsule or protein antigens c and R.
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PMID:Correlation of epithelial cell invasiveness of group B streptococci with clinical source of isolation. 857 38

Idiopathic bronchiolitis obliterans organizing pneumonia (BOOP) is characterized by air space inflammation and fibrosis of unknown origin. The pathogenesis of the inflammatory reaction and fibrosis in fibrotic lung disorders remains unclear; however, recent attention has focused on the potential role of the mast cell in the genesis of fibrosis. To determine whether mast cells are implicated in the pathogenesis of BOOP, mast cells were identified in BAL fluid and in transbronchial lung biopsy specimens from 11 patients affected by BOOP and 17 control subjects. Mast cells and tryptase were significantly increased in BAL fluid of patients with BOOP (p = 0.001 and p = 0.03, respectively). In lung tissue of patients with BOOP, there was an increased number of mast cells per square millimeter of lung tissue with respect to control group (p = 0.001). Seventy-three percent of mast cells were found in the alveolar septa, 18% within alveoli often plunged in organizing pneumonia, 4% among alveolar lining cells, and 6% along blood vessels. No mast cells were located within alveoli in control subjects. Mast cell degranulation was evident in lung tissue specimens of patients with BOOP but not in those of control subjects (p = 0.01). This study shows the importance of mast cells and mast cell activation in the pathogenesis of BOOP.
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PMID:Mast cells in bronchiolitis obliterans organizing pneumonia. Mast cell hyperplasia and evidence for extracellular release of tryptase. 869 38

Although Streptococcus pneumoniae is the leading cause of community-acquired pneumonia in humans, the mechanism whereby the organism penetrates lung tissue is poorly understood. In the present study we have examined the capacity of pneumococci to penetrate A549 cells, a human lung alveolar carcinoma (type II pneumocyte) cell line. Not all clinical S. pneumoniae isolates initially tested were capable of penetration of the cells, as judged by resistance to extracellular antibiotics. The presence of a polysaccharide capsule also significantly reduced the capacity to both adhere to and penetrate A549 cells. Electron micrographs showed the presence of pneumococci enclosed within vacuoles of intact A549 cells, but bacteria were also seen free in the cytoplasm of damaged cells. Ongoing bacterial DNA, RNA, or protein synthesis was not essential for uptake of pneumococci by A549 cells, and uptake was not diminished by pretreatment of the pneumococci with trypsin. However, inhibition of A549 microfilament assembly with cytochalasin D abolished the phenomenon.
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PMID:Uptake of Streptococcus pneumoniae by respiratory epithelial cells. 875 28

During lower respiratory tract infection, massive influx and activation of phagocytes is observed. Reactive oxygen species (ROS) released by macrophages and polymorphonuclear neutrophils (PMNs) kill microorganisms and cause damage to host tissues. One feature of this damage may be enhanced lipid peroxidation. Therefore, the aim of this study was to estimate the serum concentration of lipid peroxidation products in combination with clinical and biochemical indicators of inflammation in 32 patients with pneumonia. Serum concentration of lipid peroxides (CLP) and malondialdehyde (CMDA) was measured at Day 1, 4, 10 and 14 of observation, whilst chest radiography and routine blood analysis were performed at Day 1 and 14 during a 2 week treatment of lower airway infection. The CLP decreased during treatment (p < 0.05) from 0.059 +/- 0.024 to 0.043 +/- 0.017 (A532 nm) and the CMDA (p < 0.05) from 3.5 +/- 1.4 to 2.8 +/- 1.3 nmol.mL-1. A negative correlation between CLP and radiological regression (r = 0.49) and a drop in white blood cell count (WBC) (r = 0.39) was observed during the treatment. A positive correlation between CMDA and serum trypsin inhibitory capacity (STIC) (r = 0.47) and erythrocyte sedimentation rate (ESR) (r = 0.43) was found. Our data indicate that an enhanced process of lipid peroxidation occurs during pneumonia and that serum concentration of lipid peroxides returns to normal values quicker than the concentration of malondialdehyde during recovery. The use of antioxidants is suggested as an adjuvant treatment in patients with pneumonia.
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PMID:Changes of serum concentration of lipid peroxidation products in patients with pneumonia. 876 91

Intranasal infection of rats with active (infectious) Sendai virus enhances secretion of tryptase Clara, a Sendai virus-activating protease, into the bronchial lumen by Clara cells of the bronchial epitheliums, and inversely suppresses secretion of pulmonary surfactant, an inhibitor of the protease, into the lumen [Kido H et al. (1993) FEBS Lett 322: 115-119]. A trypsin-resistant mutant, TR-2, showed similar effects, although its replication was restricted to a single cycle in the lungs. In contrast, neither nonactive (noninfectious) wild-type virus possessing receptor-binding activity and lacking envelope fusion activity nor UV-inactivated virus retaining receptor binding and envelope fusion activities altered the mode of secretions. These results indicate that viral replication is required for producing a condition in the bronchial lumen for proteolytic activation of progeny virus, thereby infection is extended to a fatal pneumonia. On the other hand, intranasal administration of infected rats with pulmonary surfactant suppressed activation of progeny virus and pathological changes in the lungs, suggesting a therapeutic use of pulmonary surfactant for influenza pneumonia.
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PMID:Inhibitory effect of pulmonary surfactant on Sendai virus infection in rat lungs. 885 34

In order to analyze the protective role that IgA may play in a chlamydial infection two IgA monoclonal antibodies (mAb), MoPn 4-2 and MoPn 13-2, were raised against the major outer membrane protein (MOMP) of the Chlamydia trachomatis mouse pneumonitis (MoPn) biovar. mAb MoPn 4-2 was found to be serovar specific while mAb MoPn 13-2 was species specific. mAb MoPn 4-2 recognized a surface exposed conformational epitope as shown by its ability to bind to native EBs and nonreduced MOMP while failing to bind to heat and trypsin treated EBs, to reduced MOMP and to synthetic MOMP peptides. In contrast, mAb MoPn 13-2 recognized a nonconformational epitope since it was able to bind treated EBs, to reduced MOMP and to the synthetic peptide MTTWNPTISGSGI located in variable domain 4 of the MOMP. Both mAbs agglutinated intact EBs and had in vitro neutralizing activity. However, mAb MoPn 4-2 had a 20-fold higher in vitro neutralizing ability when compared to mAb MoPn 13-2 (50% neutralization at 5 micrograms ml-1 vs 100 micrograms ml-1). In an in vitro in vivo infectivity assay, mAb MoPn 4-2 protected mice against infertility when C. trachomatis MoPn elementary bodies were preincubated with the mAb before inoculation. In addition, passive transfer of mAb MoPn 4-2 resulted in significant protection as measured by a decrease in the number of mice infected, and in the intensity and duration of vaginal shedding. These results support previous findings suggesting that IgA antibodies can play a role in protection against a chlamydial infection, and further encourage work to develop vaccination strategies that elicit mucosal immunity.
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PMID:Monoclonal immunoglobulin A antibody to the major outer membrane protein of the Chlamydia trachomatis mouse pneumonitis biovar protects mice against a chlamydial genital challenge. 916 May 28

Mycoplasma bovis is responsible for considerable economic losses in cattle due to pneumonia, arthritis and mastitis. As the agent was shown to be capable of adhering to neutrophils and embryonic bovine lung (EBL) cells and invading the respiratory epithelium it is highly desirable to improve our understanding of cytadherence processes. Although several surface proteins likely to be directly involved in this initial stage of interaction between pathogen and host cells have been identified, these findings mainly referred to type strain PG45 adhering to the continuous EBL cell line. The present study provides new and complementary data about cytadherence of M. bovis based on adherence of various radiolabeled strains to a primary culture of bovine bronchial epithelial (BBE) cells using a standardized adherence assay. M. bovis was shown to adhere specifically to the primary culture of BBE cells. Inhibition of adherence was observed upon addition of monoclonal antibodies (MAbs), trypsin treatment of mycoplasmas, and competition with non-radiolabeled mycoplasma cells. Interestingly, three MAbs against proteins involved in adherence to EBL cells failed to inhibit significantly the adherence to BBE cells. On the other hand, significant reduction of adherence rates by MAbs 2A8 and 9F1 directed against epitopes of variable surface lipoproteins VspC and VspF, respectively, demonstrated the involvement of these proteins in adherence of M. bovis to primary culture of BBE cells.
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PMID:Adherence of Mycoplasma bovis to bovine bronchial epithelial cells. 1263 75

Recruitment of neutrophils into the alveoli plays a major role in the pathogenesis of acid-induced pneumonitis. Preliminary data suggest that alteration in the expression of cellular adhesion molecules on the airway epithelial cells may play an important role in the recruitment of neutrophils following acid-induced lung injury. The aim of this study was to evaluate the change in the surface expression of intercellular adhesion molecule-1 (ICAM-1), E-cadherin, and vascular cell adhesion molecule -1 (VCAM-1) on acid-exposed A549 alveolar lining epithelial cells by flow cytometry and confocal laser microscopy. Acid exposure changed cell morphology, increased cell adhesion after trypsin-EDTA treatment, and up-regulated the expression of ICAM-1 and E-cadherin but not of VCAM-1. The up-regulation of ICAM-1 expression will induce the dysfunction of epithelial cells with or without accumulation of neutrophils in air spaces. Because the distribution of E-cadherin in acid-exposed A549 cells was at the sites where the cells attached to culture dish but not at the intercellular junctions between adjoining cells, up-regulated expression of E-cadherin will rather result in alterations of epithelial morphology and function of epithelial barrier. In addition, pentoxifylline suppressed the up-regulation of ICAM-1 and E-cadherin expression and may therefore attenuated the airway inflammation in acid-induced pneumonitis.
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PMID:Acid exposure potentiates intercellular adhesion molecule-1 and e-cadherin expression on A549 alveolar lining epithelial cells. 1288 51

Streptococcus pneumoniae is the major pathogen of community-acquired pneumonia and one of the most common causes of death due to infectious diseases in industrialized countries. Lung epithelium lines the airways and constitutes the first line of innate defense against respiratory pathogens. Little is known about the molecular interaction of pneumococci with lung epithelial cells. Apoptosis of lung epithelium is involved in some bacterial lung infections. In this study different pneumococcal strains specifically induced either apoptotic or necrotic death of human alveolar and bronchial epithelial cells. Pneumococcus-induced apoptosis did not depend on the virulence factors pneumolysin and H(2)O(2). Apoptotic cells showed increased activity of caspases 6, 8, and 9 but not increased activity of caspase 3. Moreover, programmed cell death could be strongly reduced by a caspase 6 inhibitor and a pan-caspase inhibitor. Inhibitors of calpain and chymotrypsin- and trypsin-like proteases also reduced pneumococcus-induced apoptosis. Furthermore, pneumococcus-infected human alveolar epithelial cells showed Bid cleavage and reduced levels of Bcl2 and Bax. Overexpression of Bcl2 in these cells reduced apoptosis significantly. Thus, pneumococci induced apoptosis of human alveolar and bronchial epithelial cells. Programmed cell death was executed by caspase 6 and noncaspase proteases, but not by caspase 3, and could be blocked by overexpression of Bcl2.
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PMID:Streptococcus pneumoniae-induced caspase 6-dependent apoptosis in lung epithelium. 1532 85


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