Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The adherence of Bordetella pertussis to human respiratory cilia is critical to the pathogenesis of whooping cough but the significance of bacterial attachment to macrophages has not been determined. Adherence to cilia and macrophages is mediated by two large, nonfimbrial bacterial proteins, filamentous hemagglutinin (FHA), and pertussis toxin (PT). PT and FHA both recognize carbohydrates on cilia and macrophages; FHA also contains an Arg-Gly-Asp (RGD) sequence which promotes bacterial association with the macrophage integrin complement receptor 3 (CR3). We determined that virulent B. pertussis enter and survive in mammalian macrophages in vitro and that CR3 is important for this uptake process. We then determined the relative contribution of CR3 versus carbohydrate-dependent interactions to in vivo pulmonary colonization using a rabbit model. B. pertussis colonized the lung as two approximately equal populations, one extracellular population attached to ciliary and macrophage surface glycoconjugates and another population within pulmonary macrophages. Loss of the CR3 interaction, either by mutation of FHA or treatment with antibody to CR3, disrupted accumulation of viable intracellular bacteria but did not prevent lung pathology. In contrast, elimination of carbohydrate-bound bacteria, either by a competitive receptor analogue or an anti-receptor antibody, was sufficient to prevent pulmonary edema. We propose that CR3-dependent localization of B. pertussis within macrophages promotes persistence of bacteria in the lung without pulmonary injury. On the other hand, the presence of extracellular bacteria adherent to cilia and macrophages in carbohydrate-dependent interactions is associated with pulmonary pathology.
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PMID:Integrin-mediated localization of Bordetella pertussis within macrophages: role in pulmonary colonization. 202 24

To demonstrate the liver profile abnormalities in jaundiced falciparum malaria patients and to determine whether jaundice was associated with other complications in falciparum malaria, 390 patients with acute falciparum malaria were studied. 124 patients were jaundiced and the others were non-jaundiced. Hyperbilirubinemia (total serum bilirubin 3 to 64 mg/dl) was found in jaundiced patients predominantly as unconjugated bilirubin. Asparatate amino-transferase and alanine minotransferase were significantly higher in jaundiced patients (p < 0.01). There was a slight decrease of serum albumin in jaundiced malaria. The complications in jaundiced patients included cerebral malaria (n = 10), acute renal failure (n = 12), pulmonary edema (n = 3), shock (n = 3), and other severe malarial complications (n = 43). Jaundice was associated with cerebral malaria (p < 0.05), acute renal failure (p < 0.01), and hyperparasitemia (p < 0.01). After successful treatment, liver profile returned to normal within a few weeks. We found that jaundiced malaria patients had transient liver profile impairment which indicated predominantly hemolysis rather than liver damage; complications were more frequent in jaundiced patients.
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PMID:Liver profile changes and complications in jaundiced patients with falciparum malaria. 771 91

The intrathecal (i.t.) injection of endothelins to conscious rats was found to cause respiratory arrest. To gain some insights into this central phenomenon, peripheral vascular permeability and lung oedema were measured after i.t. and i.v. injections of these peptides. When injected at T-8 spinal cord level, endothelin-1 (65 and 650 pmol) and endothelin-3 (650 pmol) enhanced vascular permeability in the lungs by 22-fold and 7-fold, respectively, and caused sudden death at the highest dose. Less prominent increases (between 1.4- and 2.2-fold) of vascular permeability were observed in other tissues (trachea, kidney, ears, skin of hind paws and back skin) with endothelin-1. Endothelin-1 (650 pmol) caused a similar increase (27-fold) in lung vascular permeability when injected at T-2, although the response was significantly less (P < 0.05) if injected at the L-4 (15-fold) spinal cord level. Only endothelin-1 produced lung oedema when injected at the T-2 or T-8 level. In contrast, intravenous injection of endothelins-1 and -3 (650 pmol) did not produce lung oedema and the lung vascular permeability was increased by only 1.4-1.6-fold and all rats survived. The prior i.t. injection of 6.5 nmol BQ-123 (cyclo[D-Trp, D-Asp, L-Pro, D-Val, L-Leu]), a selective endothelin ET(A) receptor antagonist, prevented the increases of lung vascular permeability and oedema and the mortality induced by i.t. endothelin-1 (650 pmol). Whereas i.v. treatment with phentolamine (2 mg/kg) or pentolinium (25 mg/kg + 50 mg/kg per h x 15 min) abolished the lung vascular permeability changes evoked by endothelin-1 (650) pmol), atropine (1 mg/kg), NG-nitro-L-arginine (50 mg/kg) or indomethacin (5 mg/kg) had no effect. Moreover, the effects of endothelin-1 were attenuated in capsaicin pretreated rats (125 mg/kg, 10 days earlier) and almost abolished in rats subjected to sympathectomy with 6-hydroxydopamine (100 mg/kg, 24-48 h earlier). All these treatments except atropine and NG-nitro-L-arginine prevented the endothelin-1-induced lung oedema and reduced the lethality by around 50%. These results suggest that the increases of pulmonary vascular permeability and oedema induced by i.t. endothelin-1 are due to an intense pulmonary vasoconstriction mediated by alpha-adrenoceptors following the release of catecholamines in response to the activation of endothelin ET(A) receptor in the spinal cord. This central phenomenon seems to be reflexogenic, including the involvement of primary afferent C-fibers and spinal cord ascending fibers to the brain. Thus, endothelin-1 could play a role in neurogenic pulmonary oedema through a central mechanism.
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PMID:Increased pulmonary vascular permeability and oedema induced by intrathecally injected endothelins in rat. 960 Jun 61

Three sows were fed a diet mixed with Fusarium moniliforme fungal culture from the 107th day of pregnancy until parturition. Fumonisin B(1) toxin was administered to two sows (sows 1 and 2) in a daily dose of 300 mg for an additional 7 days subsequent to parturition, i.e., for a total of 14-16 days. The third sow (No. 3) was given the toxin in the same daily dose only until parturition, i.e., for 7 days in total. There were no symptoms observed in any of the sows. Two piglets were taken from each of the three sows and sacrificed immediately after parturition, i.e., prior to the first suckling. After 24 h, two additional piglets were taken for slaughter from each of the litters, which by then had access to colostrum. Finally, on the 7th day postparturition another two piglets per litter were sacrificed and material obtained from them was processed for examination. It was established that fumonisin B(1) present in the Fusarium moniliforme culture resulted in damage to the fetuses in utero. Of the changes indicating toxic effect, intraalveolar, subpleural, and interstitial pulmonary edema of various degrees of severity could be detected in the piglets sacrificed immediately following parturition and before the first suckling. Pathological changes were observed in the histopathological sections of the liver, and increases in the activities of plasma aspartic acid transaminase (AST), gamma glutamyl transferase (GGT) and alkaline phosphatase (AKLP), higher than physiological levels were detected. The serum-free sphinganine/sphingosine ratio, considered a bioindicator of fumonisin B(1) toxicosis, varied in accordance with the degree of severity of the changes which occurred. The values obtained were found to be between 0.29 and 0.36 in the cases of severe pulmonary edema, and between 0.20 and 0.24 for the cases of mild pulmonary edema. In the piglets of the sows fed the toxin for an additional 7 days subsequent to parturition and which were born with severe pulmonary edema, mild pulmonary edema could be detected after colostrum suckling, 24 h, and 7 days after parturition. The SA/SO value of the serum in these two piglets was 0.19 and 0.20, while at the same time AST, GGT, and ALKP values higher than physiological levels were measured. In the milk samples taken from sows 1 and 2 and examined after 24 h and after 7 days FB(1) was detected in quantities of 18.0-27.5 ppb. There were no changes observed on the seventh day in the piglets of the third sow, the diet of which contained no toxin after parturition. However, as the piglets of the third sow demonstrated only mild effects of pulmonary edema it is not possible to establish with certainty a postpartum cause-effect relationship between fumonisin in colostrum and pulmonary edema.
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PMID:Preliminary communication: examination of the harmful effect to fetuses of fumonisin B(1) in pregnant sows. 1099 76