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  • 1
    ISSN: 1573-0832
    Keywords: lung ; macrophage ; neutrophil ; Candida albicans ; cyclophosphamide ; cortisone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Cortisone (CA) or cyclophosphamide (Cy) treatment of mice was used to investigate the relative contributions of pulmonary alveolar macrophages (PAM) and inflammatory neutrophils (PMN) in the initial defense against intratracheal challenge (IT) with Candida albicans. Mice treated with either CA or Cy were susceptible to IT challenge with 10–100 x less C. albicans than were untreated mice. Untreated mice rapidly eliminated C. albicans from their lungs with the majority of the organisms being cleared within three hours of challenge. Mice treated with CA initially cleared some of the C. albicans but were unable to clear all the C. albicans as did the untreated mice. Mice treated with Cy were unable to clear C. albicans from their lungs. Candida albicans did not disseminate from the lungs of untreated mice, while in both of the treated groups, C. albicans disseminated to the liver, spleen, brain and kidneys, rapidly killing the treated hosts. Analysis of the changes in cells in lung lavage fluids collected at various times after C. albicans challenge, revealed that large numbers of PMN accumulated in the lungs of both untreated and CA-treated mice, whereas PMN were virtually undetectable in lavage fluids from Cy-treated mice. Resident PAM from untreated mice were able to kill approximately 70 % of 105 C. albicans in a 3 hr in vitro killing assay. By contrast, at similar effector: target ratios, resident PAM from Cy-treated mice killed only about 20% of the inoculum and resident PAM from CA-treated mice were unable to kill C. albicans. PMNs from both untreated and CA-treated mice killed approximately 70% of 105 C. albicans in vitro. The data indicates that both PAM and PMN were critical to the initial clearance of C. albicans from pulmonary tissue. The accumulation of PMN in the lungs appeared to be required for the complete clearance of C. albicans from the lungs yet was not sufficient to inhibit dissemination of C. albicans from the lungs in CA-treated mice. The presence of PAM with in vitro candidacidal abilities appeared to be required for both the clearance of C. albicans and inhibition of dissemination of C. albicans from the lungs. Compromise of either PAM or PMN function can lead to increased pulmonary susceptibility to C. albicans.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Mycopathologia 104 (1988), S. 81-85 
    ISSN: 1573-0832
    Keywords: Candida albicans ; hepatic trapping ; monosaccharides ; adherence
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The initial clearance of Candida albicans in situ by hepatic tissue was investigated using the isolated perfused mouse liver model in combination with various monosaccharides. When 106 yeasts were infused into untreated ICR mouse livers, approximately 61±2% (X + SEM) were recovered from the liver and 13±2% in the effluent for a total recovery of 74±2%. This suggests that 26±2% of the infused yeasts were eliminated within the liver and that a total of 87±1% were trapped (% in the liver + % killed) by the liver. In contrast, when either D-mannose or alpha-methyl-D-mannoside, but not glucose, sucrose, lactose or mannitol, were added to perfusion media (1% w/v) the ability of hepatic tissue to trap C. albicans decreased, in a dose-dependent manner, with increasing concentrations of monosaccharide. Decreased trapping was due to the interaction of these monosaccharides with hepatic tissue and not directly with yeasts. The data suggest that one component of in situ hepatic clearance of C. albicans was the binding of mannose containing structures on the surface of yeasts, most probably by hepatic mannose receptors.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Mycopathologia 109 (1990), S. 99-109 
    ISSN: 1573-0832
    Keywords: Candida albicans ; pulmonary alveolar macrophage ; host-parasite interaction ; pulmonary infection ; phagocytosis and killing
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The initial interaction of Candida albicans with pulmonary tissue of B6D2/F1 mice was investigated. The LD50 for mice challenged intravenously (IV) was approximately 3 × 105 yeasts, whereas the LD50 by the intratracheal (IT) route was in excess of 108 yeasts. Mice challenged IV died of progressive yeast growth in the kidneys. In contrast, mice challenged IT rapidly eliminated the entire inoculum by the first day after challenge. Resident pulmonary alveolar macrophages (PAM) killed upwards of 70% of C. albicans in an in vitro killing assay. At effector: target ratios favoring the effector cell population resident PAM were able to restrict the formation of yeast germ tubes to only 30% of the yeasts, whereas at equivalent ratios virtually all of the intracellular yeasts produced germ tubes. Evaluation of the ability of PAM, harvested from genetically different strains of inbred mice, to kill C. albicans in vitro showed that killing ability was a property of resident PAM from mice with the black 6 background. It was discovered that during the initial stages of infection in vivo, the expression of the F4/80 surface molecule was down regulated, and the expression of the Mac 1 surface molecule upregulated. There were no quantitative changes in expression of either Mac 2, Mac 3, Ly 5 or the 5C6 surface epitopes. Taken together, the data show that pulmonary tissue is quantitatively very resistant to C. albicans infection, because of the ability of resident PAM to rapidly phagocytize and kill yeasts. Killing of C. albicans by resident PAM may be a property of a subset of this mononuclear phagocyte population and was accompanied by alterations in the expression of surface molecules.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation 17 (1993), S. 273-281 
    ISSN: 1573-2576
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The purpose of this study was to evaluate the ability of intravenous zymosan-A (ZyA) challenge to induce an alveolar inflammatory response as indicated by inflammatory changes among lung lavage cells. The organ distribution of 1 mg of [51ZyA revealed that immediately following intravenous challenge of female ICR mice approximately 81 % of the total cpm injected was associated with pulmonary tissue. Approximately 15% of the injected cpm was associated with the peripheral blood, liver, andspleen. ZyA translocated from the vascular compartment into pulmonary alveoli and was detected within polymorphonuclear neutrophils (PMN) and alveolar macrophages (AM) 18 h after intravenous challenge. PMN numbers among lung lavage cells increased beginning one day after challenge to a peak of approximately 5 × 105 PMNs by day 3 after challenge. The PMN response subsided by day 5 after challenge. There was no significant increase in the numbers of AM during the first week after intravenous ZyA; however, the number of AM increased from approximately 5 × 1C5 AM on day 1 after challenge to approximately 1.1 × 106 AM by day 5 after challenge. Within 24 h of intravenous ZyA, the number of AM in S phase of the cell cycle increased from approximately 2.5 × 104 AM one day after challenge to 1.1 × 105 AM in S phase five days after challenge. The data suggest that intravenous ZyA localized within pulmonary tissue immediately following intravenous challenge and translocated into the alveolar compartment where ZyA particles were found within phagocytes. This process was accompanied by an acute PMN inflammation, an acute increase in the proliferation of mononuclear phagocytes within the alveoli, and a significant increase in AM numbers by one week after intravenous ZyA. Intravenous ZyA challenge may be used to explore acute and chronic inflammatory responses within pulmonary alveoli without the need for intratracheal challenge.
    Type of Medium: Electronic Resource
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