Studies of polymorphonuclear leukocyte (PMN) functions in small animals have primarily been limited to elicited peritoneal PMNs. We have developed a model of induced acute inflammation in rats that provides a means of studying the functions of circulating PMNs. Using this model, we studied the influence of zinc deficiency on the chemotactic and respiratory burst capabilities of circulating PMNs responding to an inflammatory stimuli. Male rats were fed a zinc deficient (Zn-D) diet (0.5 μg Zn/g) or a control diet (25 μg Zn/g) either ad libitum (C) or in restricted amounts (R-C) for 6 weeks. PMNs were elicited by an intraperitoneal injection of glycogen and the circulating PMN response monitored for 4 h. The kinetics of peripheral blood PMN response were similar in all the groups, with the peak response time (cell number) at 2 h post-stimulation. Zinc deficiency was associated with an elevated baseline PMN concentration, as well as, an increase in the total number of circulating PMN. PMN function studies were done on PMN isolated at the peak response time of 2 h post-stimulation. Chemotaxis to FMLP was significantly lower in PMN from the Zn-D group than in PMN from the C and R-C groups. Respiratory burst capacity (SOD-inhibitable reduction of cytochrome C) was significantly higher in PMN from the Zn-D group compared to the ad libitum fed C group. Latency to the onset of the production of O2 - was significantly shortened in PMN from the Zn-D group relative to the C group. Thus, zinc deficiency is associated with altered circulating PMN function in the rat with respect to number, chemotactic response, and superoxide production.
|Original language||English (US)|
|Number of pages||16|
|Journal||Journal of Nutritional Immunology|
|State||Published - 1995|
ASJC Scopus subject areas
- Nutrition and Dietetics