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Altered alveolar macrophage function in calorie-restricted rats.

Authors
Dong-W; Selgrade-MK; Gilmour-MI; Lange-RW; Park-P; Luster-MI; Kari-FW
Source
Am J Respir Cell Mol Biol 1998 Sep; 19(3):462-469
NIOSHTIC No.
20025294
Abstract
Alveolar macrophage functions associated with clearance of bacteria from the lung were assessed in male Fischer 344 rats maintained on a 25% calorie-restricted diet. Calorie-restricted and ad libitum-fed (control) rats were exposed to concentrations of ozone known to compromise phagocytic function of alveolar macrophages. Ozone suppressed alveolar macrophage phagocytosis of latex beads in vitro in ad libitum-fed rats, but not in calorie-restricted rats. In fact, caloric restriction enhanced phagocytic function in both control and ozone-exposed animals. Ad libitum-fed rats exposed to ozone and challenged with Streptococcus zooepidemicus experienced a prolonged infection and influx of polymorphonuclear leukocytes (PMN), whereas calorie-restricted rats exposed to ozone cleared the bacteria in 24 h without an inflammatory response. Bacterial endotoxin-stimulated in vitro production of nitric oxide and tumor necrosis factor (TNF)-alpha as well as expression of TNF-alpha and interleukin-6 messenger RNAs were all lower in alveolar macrophages isolated from calorie-restricted rats. Together, the data suggest that caloric restriction enhances resistance to gram-positive bacteria, while lowering the production of proinflammatory mediators elicited by endotoxin, a component of gram-negative bacteria. Although increased bacterial resistance is considered beneficial, reduction in the lung's ability to induce inflammatory mediators can have both positive and pathophysiologic consequences.
Keywords
Alveolar-cells; Laboratory-animals; Animals; Animal-studies; Bacteria; Lung-disorders; Exposure-levels; Phagocytes; Phagocytic-activity; In-vitro-studies; Microorganisms
Contact
Frank W. Kari, Ph.D., NIEHS, M.D. B3-09, P.O. Box 12233, Research Triangle Park, NC 27709
CODEN
AJRBEL
CAS No.
10102-43-9
Publication Date
19980901
Document Type
Journal Article
Email Address
kari@niehs.nih.gov
Fiscal Year
1998
NTIS Accession No.
NTIS Price
Issue of Publication
3
ISSN
1044-1549
NIOSH Division
HELD
Source Name
American Journal of Respiratory Cell and Molecular Biology
State
WV; NC
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