Enhancement of bactericidal capacity of alveolar macrophages by human alveolar lining material.

Juers, J A; Rogers, Robert M.; McCurdy, Justine; Cook, Wade

doi:10.1172/jci108468

Cited by 106 publications

(56 citation statements)

References 11 publications

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“…The inefficiency of AM from rabbits, rats, and hamsters to phagocytize nonopsonized staphylococci is in 72 Verbrugh, Hoidal, Nguyen, Verhoef, Quie, and Peterson agreement with previous work using these animal species (57)(58)(59)(60). These species' differences point out that functions of human macrophages cannot be directly inferred from studies using macrophages from other animals.…”

Section: Discussionsupporting

confidence: 81%

Human alveolar macrophage cytophilic immunoglobulin G-mediated phagocytosis of protein A-positive staphylococci.

et al. 1982

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Section: Discussionsupporting

confidence: 81%

Human alveolar macrophage cytophilic immunoglobulin G-mediated phagocytosis of protein A-positive staphylococci.

et al. 1982

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“…This is particularly relevant because, as noted above, viable spores disseminate even in normal mice, but germination and progression of mucormycosis occurred only in diabetic animals. Within the bronchoalveolar spaces, alveolarlining material may play a major role in antimicrobial defenses (27,38,39). However, in vitro germination assays using alveolarlining material from normal and diabetic mice indicated that, unlike the reported bactericidal effects (27,38,39), alveolarlining material had no fungicidal activity.…”

Section: Discussionmentioning

confidence: 99%

“…Within the bronchoalveolar spaces, alveolarlining material may play a major role in antimicrobial defenses (27,38,39). However, in vitro germination assays using alveolarlining material from normal and diabetic mice indicated that, unlike the reported bactericidal effects (27,38,39), alveolarlining material had no fungicidal activity. Additionally, there was neither increased attachment nor enhanced bronchoalveolar macrophage-mediated fungicidal activity against spores in the presence of alveolar-lining material.…”

Section: Discussionmentioning

confidence: 99%

Specific susceptibility to mucormycosis in murine diabetes and bronchoalveolar macrophage defense against Rhizopus.

Waldorf¹,

Ruderman²,

Diamond³

1984

J. Clin. Invest.

200

149

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Abstract. To assess the influence of diabetes mellitus in predisposing to pulmonary mucormycosis, a murine model of streptozotocin-induced diabetes was used. Intranasal inoculation of Rhizopus oryzae into diabetic mice resulted in mucormycotic infection with histopathology resembling pulmonary mucormycosis observed in humans. There was no mortality nor infection in inoculated normal mice. Diabetic mice had fatal infections caused by R. oryzae but significantly reduced mortality following inoculation with Aspergillus fumigatus. These findings reflect the specific enhanced susceptibility to mucormycosis observed in human diabetics.Normal bronchoalveolar macrophages formed part of an efficient defense against R. oryzae by inhibiting germination, the critical step in the conversion of R. oryzae to its tissue invasive phase. Bronchoalveolar macrophages inhibited spore germination in vitro and appeared to help prevent germination in vivo. In contrast, spore germination occurred in diabetic mice following intranasal inoculation. Diabetic bronchoalveolar macrophages had a decreased ability to attach to hyphae. In diabetic mice, bronchoalveolar macrophages could damage spores or hyphae of R. oryzae, but serum factors appeared to both promote spore germination and impair attachment of macrophages to spores. This murine model ofdiabetes mellitus provides an opportunity for evaluation of the relative importance of cell and serum-mediated host factors in the pathogenesis of mucormycosis.Portions of this work were presented at a meeting of the American

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“…This lining material may enhance the phagocytic function of alveolar macrophages (5,134,211), prevent autolysis of the macrophages (30,134,211), enhance macrophage migration (17,212), improve bactericidal activity (22,213,214) and increase macrophage adherence to glass (82,215). It is reasonable to assume that certain inhaled noxious chemicals would interact with this lining fluid, altering the above macrophage functions, thus making the lung more vulnerable to.…”

Section: Influence Of Surrounding Milieumentioning

confidence: 99%

Alterations in Macrophage Functions by Environmental Chemicals

Gardner¹

1984

Environmental Health Perspectives

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Enhancement of bactericidal capacity of alveolar macrophages by human alveolar lining material.

Cited by 106 publications

References 11 publications

Human alveolar macrophage cytophilic immunoglobulin G-mediated phagocytosis of protein A-positive staphylococci.

Human alveolar macrophage cytophilic immunoglobulin G-mediated phagocytosis of protein A-positive staphylococci.

Specific susceptibility to mucormycosis in murine diabetes and bronchoalveolar macrophage defense against Rhizopus.

Alterations in Macrophage Functions by Environmental Chemicals

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