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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the involvement of oxygen free radicals and their scavenger systems in the defenses of compromised hosts against pulmonary infections, we determined superoxide anion (SOA) and superoxide dismutase (SOD; EC 1.15.1.1) concentrations in the blood of compromised hosts and noncompromised hosts, with or without pneumonia. In the compromised hosts without pneumonia (compromised controls), SOD concentrations were lower than in noncompromised hosts (healthy controls). However SOA values in compromised controls did not differ statistically from that in healthy controls. Similar changes were observed in noncompromised hosts with pneumonia. In compromised hosts with pneumonia, SOD concentrations were further decreased by pulmonary infections. By contrast, SOA values were increased in pneumonia. There were, however, no differences in the values for ceruloplasmin among all the groups. The values for alpha 2-macroglobulin and alpha1-antitrypsin were within normal limits in compromised controls but were greater in compromised hosts with pneumonia. These results suggest that a decreased activity concentration of SOD in compromised controls may be partly responsible for the depression of the host's immune defenses.
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PMID:Concentrations of superoxide dismutase and superoxide anion in blood of patients with respiratory infections and compromised immune systems. 244 6

The potential protective effects of ICRF 187, Didox, Amidox and VF 165 were investigated in models of bleomycin, or bleomycin and hyperoxia induced lung injury. ICRF 187, a bispiperazinedione compound, is a strong chelating agent which blocks a number of free radical mediated processes. The polyhydroxyphenyl derivatives, Didox, Amidox and VF 165, demonstrate degrees of Fe chelating activities and free radical scavenging abilities. Hamsters treated with 5.0 U/kg bleomycin followed by treatment with ICRF 187 or Didox exhibited similar mortality to the bleomycin alone treated group. In a second study, a low dose of bleomycin (1.2 U/kg) was used followed by exposure to 70% oxygen. Treatment with ICRF 187, Didox, Amidox, or VF 165 failed to protect against lung injury; with the ICRF 187 and Amidox groups exhibiting significantly increased rates of mortality over that seen in animals treated only with bleomycin and hyperoxia. No animals treated with the agents alone died. Histopathology documented that all bleomycin-treated hamsters died of severe pneumonitis. Additionally, in the agent-treated groups there was a prominent proliferation of type II pneumocytes, which demonstrated marked anaplasia, a feature not typical of early bleomycin and hyperoxia lung injury. In conclusion, ICRF 187 and the polyhydroxyphenyl derivative, Amidox, paradoxically increase bleomycin- and hyperoxia-induced lung injury. The possible mechanisms of this interaction include: (1) increased availability of Fe to bleomycin; (2) interference with the healing process; or (3) inhibition of endogenous protective effects of SOD.
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PMID:ICRF 187 and polyhydroxyphenyl derivatives fail to protect against bleomycin induced lung injury. 247 96

The preventive and therapeutic effect of the traditional Chinese compound medicine Feixiankang (FXK) on the mice pulmonary fibrosis formation have been studied with the mice model. The level of LPO and the activity of SOD in the mice lung showed that LPO increased remarkably (P < 0.01), while the activity of SOD decreased significantly (P < 0.01) during the alveolar pneumonia period, although the LPO content had no significant change (P < 0.01) during experimental pulmonary fibrosis formation. In addition, the effect of FXK on the reducing of LPO was much stronger than that of the antioxidative agent Vitamin E. Also, FXK could improve the activity of SOD.
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PMID:[Effect of promoting blood circulation to remove stasis and supplementing qi and nourishing yin on the lipid peroxide and superoxide dismutase during experimental pulmonary fibrosis]. 753 99

The pathogenesis of influenza virus infections of the lungs is in part mediated by oxidative stress. Such infections might therefore be expected to induce expression of stress-response genes and genes encoding antioxidant enzymes and to activate transcriptional regulatory proteins. Mice (C57B1/6 and C3H/HeJ) were infected intranasally with influenza virus A/PR/8/34 (H1N1). Expression of the genes encoding the antioxidant enzymes manganese superoxide dismutase (Mn- SOD), indoleamine-2, 3-dioxygenase (IDO), heme oxygenase-1, and glutathione peroxidase were increased in the lungs of virus-infected animals. Cu/ZnSOD and catalase mRNA were not induced by viral infection. Activation of the transcriptional regulatory proteins AP-1, C/EBP, and NF-kappa B (which are known to be affected by oxidant stress) was demonstrated by electrophoretic mobility shift assay after viral infection. In the case of MnSOD, despite increased gene expression enzyme activity was not increased. In contrast, for heme oxygenase-1 both mRNA and activity were increased. C3H/ HeJ and C57B1/6 mice, which are known to have different responses to other types of oxidant stress, also differed in their responses to viral infection. Induction of heme oxygenase-1 expression was greater in C57B1/6 mice than in C3H/ HeJ mice, although inhibiting this enzyme did not alter virus-induced mortality. In contrast, IDO was more strongly induced in C3H/HeJ mice. Activation of NF-kappa B was much more marked in C57B1/6 mice than in C3H/HeJ mice. Although virus replication and inflammatory responses were equivalent in the two strains, lung injury (as measured by wet-to-dry wt ratios) and mortality were greater in C3H/HeJ mice than in C57B1/6 mice, a difference that may be related to differing oxidant stress responses. Thus influenza pneumonia causes an oxidant stress response in the lungs, the nature of which is determined in part by the genetic background of the host.
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PMID:Oxidant stress responses in influenza virus pneumonia: gene expression and transcription factor activation. 884 86

The effects of a combined inoculation of gastric juice and Streptococcus pneumoniae on the lungs of mice was investigated. Survival rates of mice inoculated with bacteria alone, gastric juice alone, and both bacteria and gastric juice were compared over 18 days. Xanthine oxidase (XO) activities in the lung tissues of mice inoculated with bacteria and gastric juice were measured and injected with a free radical scavenger, pyran-superoxide dismutase (pyran-SOD). A high mortality rate was observed in mice inoculated with both gastric juice and Streptococcus pneumoniae (81%). Mice inoculated with either Streptococcus pneumoniae or gastric juice showed a separate mortality rate of up to 10% during 18 days after inoculation. XO activity in the lung tissue of the mice inoculated with both gastric juice and bacteria was higher than in mice inoculated with either of them separately. The high mortality rate in the group inoculated with both two agents was reduced to 25% by the administration of pyran-SOD. XO activity raised by Streptococcus pneumoniae and gastric juice was significantly reduced by pyran-SOD. Thus, we suggest an important role in the combined effects of gastric juice and bacteria on pneumonia.
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PMID:Combined effects of both bacteria and gastric juice on pneumonia in mice. 1048 4

Reactive oxygen and nitrogen species such as superoxide and nitric oxide are released into the extracellular spaces by inflammatory and airway epithelial cells. These molecules may exacerbate lung injury after influenza virus pneumonia. We hypothesized that enhanced expression of extracellular superoxide dismutase (EC SOD) in mouse airways would attenuate the pathological effects of influenza pneumonia. We compared the pathogenic effects of a nonlethal primary infection with mouse-adapted Hong Kong influenza A/68 virus in transgenic (TG) EC SOD mice versus non-TG (wild-type) littermates. Compared with wild-type mice, EC SOD TG mice showed less lung injury and inflammation as measured by significant blunting of interferon-gamma induction, reduced cell count and total protein in bronchoalveolar lavage fluid, reduced levels of lung nitrite/nitrate nitrotyrosine, and markedly reduced lung pathology. These results demonstrate that enhancing EC SOD in the conducting and distal airways of the lung minimizes influenza-induced lung injury by both ameliorating inflammation and attenuating oxidative stress.
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PMID:Prevention of influenza-induced lung injury in mice overexpressing extracellular superoxide dismutase. 1113 96

The functional condition of prooxidant--antioxidant system in rat blood plasma in acute pneumonia, on the 4th full day after intranasal animals' infectioning, by Staphylococcus Aureus culture depending on sex was studied. The investigation of PLO indexes and AOS activity on the 4th full-day after animals' contamination with St. aureus culture, in blood plasma, in acute pneumonia, showed the increase of DK and MDA content, and oppression of AOS-SOD ferments and catalase activity. In males these changes were more expressed indicating an exhaustion of functional reserves of antioxidant system.
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PMID:[State of lipid peroxidation and blood antioxidant system in rats with acute pneumonia]. 1517 14

The model process of acute pneumonia in rats, after 2 hours after intranasal infectioning by Staphylococcus aureus culture, is accompanied with DK and MDA level growth, and SOD and catalase activity increase in pulmonary tissue of males and females. Later, after 6 hours after contamination the growth of POL products content was observed, the SOD and catalase activity in lungs is lowered. At the same time, in females the PLO indexes and SOD activity continue to grow. This suggests that females have more AOS enzymatic reserves than males.
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PMID:[Level of lipid peroxides and activity of antioxidant system enzymes in pulmonary tissue of rats with acute pneumonia]. 1532 Apr 29

Pneumonia is a severe infection that causes high morbidity and mortality rate worldwide. It is caused by Klebsiella pneumoniae, which generally causes upper respiratory tract infection. In case of such type of infection, levels of oxidant and antioxidant become imbalanced, which may contribute to lung injury. The present study was planned to evaluate the status of oxidant and antioxidant enzyme activities in plasma and lung tissue of pneumonia-infected rats model. Animals were randomly distributed into 3 groups of 8 rats each: groups I (control, normal saline treated), II (infected group), and III (infected + treated group). The findings showed that there was significant increase (P < .001) in body temperature along with decreased body weight in the infected group as compared to the control group. Similarly, all the activities of antioxidant enzymes (superoxide dismutase [SOD], catalase) were significantly decreased along with increased malonaldialdehyde (MDA) levels in plasma and lung tissue of the infected group as compared to the control group. These enzyme activities along with MDA levels were improved and came back near to normal level after administration of cefepime plus amikacin (potentox) for 7 days in group III. These studies concluded that fixed-dose combination of potentox improved oxidant and antioxidant levels in pneumonia infection.
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PMID:Fixed-dose combination of cefepime plus amikacin (potentox) inhibits pneumonia infection. 1984 49

Pneumocystis jirovecii pneumonia (PcP) remains a major cause of respiratory illness among immunocompromised patients, especially patients infected with HIV, but it has also been isolated from immunocompetent persons. This article discusses the application of multilocus genotyping analysis to the study of the genetic diversity of P. jirovecii and its epidemiological and clinical parameters, and the important concepts achieved to date with these approaches. The multilocus typing studies performed until now have shown that there is an important genetic diversity of stable and ubiquitous P. jirovecii genotypes; infection with P. jirovecii is not necessarily clonal, recombination between some P. jirovecii multilocus genotypes has been suggested. P. jirovecii-specific multilocus genotypes can be associated with severity of PcP. Patients infected with P. jirovecii, regardless of the form of infection they present with, are part of a common human reservoir for future infections. The CYB, DHFR, DHPS, mtLSU rRNA, SOD and the ITS loci are suitable genetic targets to be used in further epidemiological studies focused on the identification and characterization of P. jirovecii haplotypes correlated with drug resistance and PcP outcome.
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PMID:Pneumocystis jirovecii multilocus gene sequencing: findings and implications. 2072 2


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