Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.5 (5'-nucleotidase)
 3,167 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alveolar macrophages (AM) are highly suppressive of the in vitro plaque-forming cell (PFC) response of spleen cells obtained from mice primed with sheep erythrocytes. Comparison of macrophage populations obtained from disparate anatomical sites revealed that although in both cases there was a cell-concentration-dependent suppression of the PFC response, resident AM or AM activated as a result of intravenous injection of Mycobacterium bovis BCG were equally suppressive at the doses examined. Although there was a similar dose-dependent suppression with peritoneal macrophages, BCG-activated cells were more suppressive of the PFC response than were resident cells. In contrast, splenic macrophages at comparable concentrations were not at all suppressive. Resident AM exhibited significantly lower levels of 5'-nucleotidase activity than did resident peritoneal macrophages. Macrophage-mediated suppression of the in vitro PFC response could not be attributed to the release of toxic oxygen metabolites (H2O2, O2- ,and .OH) or prostaglandins, since the addition of catalase, superoxide dismutase, 2-mercaptoethanol, or indomethacin did not completely reverse suppression. These results suggest that the lung microenvironment may maintain AM in an activated state which contributes to their potential immunoregulatory functions.
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PMID:Role of activation in alveolar macrophage-mediated suppression of the plaque-forming cell response. 283 Jan 91

The kinetics of induction of the bronchoalveolar cell population (i.e., alveolar macrophages [AM], lymphocytes, and polymorphonuclear leukocytes) was studied in mice inoculated intravenously with heat-killed Mycobacterium bovis BCG. Injection of BCG at 100 and 500 micrograms but not at 10 micrograms per mouse resulted in an increase in the total number of bronchoalveolar cells (threefold) and in the number of AM (sixfold) recovered by bronchoalveolar lavage in a time-dependent manner, as compared with control mice. A significant increase in the number of lymphocytes was also observed between days 2 and 4 after injection, but this number returned to normal levels by day 8, whereas the number of polymorphonuclear leukocytes was not significantly altered. AM were characteristically phagocytic and stained positively for nonspecific esterase. AM recruited in response to BCG injection were activated, as indicated by elevated levels of acid phosphatase activity and decreased levels of membrane 5'-nucleotidase activity. However, both resident and BCG-induced AM suppressed the in vitro plaque-forming cell response of sheep erythrocyte-primed mice to the same extent. These results indicate that injection of heat-killed BCG induced increased numbers of activated AM, which appeared to be functionally similar to resident AM in their ability to phagocytize and modulate in vitro immune responses.
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PMID:Enhanced recovery of murine alveolar macrophages: morphological and functional characteristics following intravenous injection of heat-killed Mycobacterium bovis BCG. 351 Sep 78

A decline in 5'-nucleotidase production was observed in short-term tissue culture of guinea pig alveolar, peritoneal, splenic, and liver macrophages during exposure to 10(2) microM rifampicin, 1 microM levamisole, or 10 micrograms of cytoplasmic protein antigen extracted from Mycobacterium microti. Liver macrophage 5'-nucleotidase production was more significantly inhibited by the three agents. Cytoplasmic protein antigen from M. microti was the most potent inhibitor of 5'-nucleotidase production.
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PMID:Effect of rifampin, levamisole, and cytoplasmic protein antigen from Mycobacterium microti on 5'-nucleotidase production by guinea pig macrophages. 628 May 98

Activation of alveolar, peritoneal, liver, and spleen macrophages was measured by decreased 5'-nucleotidase and elevated alkaline phosphodiesterase I activities in newborn and juvenile guinea pigs for up to 48 days after intracardiac or intranasal infection with Mycobacterium microti. Increased AP and reduced 5'-nucleotidase activity in cell lysates of macrophages appeared to be related to the carrier state during infection. Intranasal infection of 8-week-old guinea pigs with M. microti produced decreases of 5'-nucleotidase activity in alveolar macrophages during 1-8 weeks post infection and in macrophages from all four sources from 4-8 weeks.
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PMID:Macrophage activation measured by changes in 5'-nucleotidase and alkaline phosphodiesterase I activities after infection of newborn and juvenile guinea pigs with mycobacterium microti. 632 4