{'fraction_non_alphanumeric': 0.018226002430133656, 'fraction_numerical': 0.028554070473876064, 'mean_word_length': 4.903225806451613, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Changes of expression of complement 3bi receptors on granulocytes after physical exercise in rats.

OBJECTIVE
The purpose of this study was to examine the effects of physical exercise on the expression of clusters of differentiation (CD)11b, CD18 and CD 54 on granulocytes and complement 3bi (C3bi)-dependent functions in rats.


EXPERIMENTAL DESIGN
The rats were separated into two groups: the control group (n = 21) and the training group (n = 14). The rats in the training group were subjected to a program that consisted of swimming 6 days in a week for 7 weeks.


MEASURES
The phagocytic and hydrogen peroxide (H2O2) generating activities and the expression of receptors on granulocytes were measured using flow cytometric techniques.


RESULTS
The acute swimming and the 7 weeks of swim training caused high C3bi-dependent phagocytic activity of granulocytes. Swim training led to an increase of H2O2 generating activity together with C3bi-dependent phagocytosis both immediately after and 24 hrs after the 120 min swimming. The 24 hrs recovery from the 120 min swimming in trained and untrained rats caused an increase of H2O2 generating activity of granulocytes. In the training group, an increase in this activity could be observed immediately after the 120 min swimming exercise. The upregulation of the CI1b on granulocytes was induced by the 120 min of swimming regardless of swim training.


CONCLUSIONS
These results suggest that the increase of C3bi receptor-dependent phagocytosis and H2O2 generating activities induced by the physical exercise might depend on the upregulation of the CD11b that is the component of C3bi receptor.