Effects of Chlorella vulgaris on bone marrow progenitor cells of mice infected with Listeria monocytogenes

Citation
Dcm. Dantas et Mls. Queiroz, Effects of Chlorella vulgaris on bone marrow progenitor cells of mice infected with Listeria monocytogenes, INT J IMMUN, 21(8), 1999, pp. 499-508
Citations number
30
Categorie Soggetti
Immunology
Journal title
INTERNATIONAL JOURNAL OF IMMUNOPHARMACOLOGY
ISSN journal
01920561 → ACNP
Volume
21
Issue
8
Year of publication
1999
Pages
499 - 508
Database
ISI
SICI code
0192-0561(199908)21:8<499:EOCVOB>2.0.ZU;2-2
Abstract
In this study we investigated the effects of the treatment with Chlorella v ulgaris extract (CVE) on the hematopoietic response of granulocyte-macropha ge colony-forming unit (CFU-GM) of mice infected with a sublethal dose of L isteria monocytogenes (1 x 10(4) organisms/animal). CVE was given orally as 50 mg/kg/day for 5 days. In the CVE treated/infected groups L. monocytogen es was administered at the end of CVE treatment. The colony stimulating act ivity of the serum (CSA) was also studied in all groups. Although no effect s on CFU-GM, as compared to controls, were observed in the groups receiving CVE alone, the extract produced an increase in CSA levels as compared to c ontrols. On the other hand, the presence of the infection led to a signific ant reduction in the numbers of CFU-GM as observed at 48 and 72 h after the infection, in spite of the significant increase in serum CSA activity. CVE treatment of infected animals restored the numbers of CFU-GM to control le vels. In the treated/ infected group the increased serum CSA was significan tly higher than that observed in the only infected group. The CVE treatment (50 and 500 mg/kg) of mice infected with a dose of 3 x 10(5) bacteria/anim al, which was lethal for all the non-treated controls, produced a dose-resp onse protection which led to a 20 and 52% survival, respectively. These res ults demonstrated that CVE produces a significant increase in the resistanc e of the animals infected with L, monocytogenes, and that this protection i s due, at least in part, to increased CFU-GM in the bone marrow of infected animals. (C) 1999 International Society for Immunopharmacology. Published by Elsevier Science Ltd. All rights reserved.