These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Growth inhibition of Cryptococcus neoformans by human alveolar macrophages. Author: Weinberg PB, Becker S, Granger DL, Koren HS. Journal: Am Rev Respir Dis; 1987 Nov; 136(5):1242-7. PubMed ID: 3314617. Abstract: Macrophage cytotoxicity for Cryptococcus neoformans was investigated by culturing human alveolar macrophage (AM) with a thin-capsuled clone of C. neoformans in a polypropylene culture tube assay system. Yeast replication was quantitated by electronic particle counting after detergent lysis of AM and viability by quantitative plate counts. Under appropriate conditions, fungal replication was inhibited in the presence of human AM. This effect persisted over the 48-h time course that was evaluated. During this period, organisms in medium alone proliferated rapidly, doubling their number every 4 h. Human AM did not require endotoxin, fetal calf serum, or specific rabbit anticryptococcal antibody for fungistasis. Under these conditions, microscopic evaluation of a cytocentrifuge preparation of AM-yeast cocultures, stained by a modified Giemsa technique, revealed all the fungi to be extracellular. In the presence of 10% fresh human serum, AM phagocytized C. neoformans and exhibited fungicidal activity. Tumor necrosis factor did not affect the replication rate of the yeast. These findings suggest that there may be at least 2 mechanisms by which human AM protect against C. neoformans. One is serum-independent and extracellular and results in fungistasis, and the other is dependent on a serum factor and leads to intracellular inhibition of growth and possibly killing of the organism.[Abstract] [Full Text] [Related] [New Search]