Growth hormone activation of human monocytes for superoxide production but not tumor necrosis factor production, cell adherence, or action against Mycobacterium tuberculosis

Warwick-Davies, Jan; Lowrie, Douglas B.; Cole, Peter

doi:10.1128/iai.63.11.4312-4316.1995

Cited by 31 publications

(9 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies have indicated that ROI are insufficient alone for effective killing or inhibition of mycobacterial pathogens [ 6, 15, 17, 30, 31]. We also found that a xathine oxidase‐acetaldehyde system, which enzymatically generates ROI, was unable to kill mycobacteria [ 32], suggesting that ROI alone are not sufficient for macrophage anti‐mycobacterial activity.…”

Section: Discussionmentioning

confidence: 62%

Differential potentiation of anti-mycobacterial activity and reactive nitrogen intermediate-producing ability of murine peritoneal macrophages activated by interferon-gamma (IFN-γ) and tumour necrosis factor-alpha (TNF-α)

Sato¹,

Akaki

Tomioka³

1998

Clinical and Experimental Immunology

View full text Add to dashboard Cite

SUMMARYThe anti-mycobacterial activities of IFN-g and TNF-a-treated murine peritoneal macrophages were determined. Resident macrophages pretreated with IFN-g or TNF-a for 2 days were infected with test organisms and subsequently cultured for up to 7 days. First, the early-phase growth of Mycobacterium tuberculosis (days 0-3) was strongly suppressed in IFN-g-treated macrophages, and progressive bacterial elimination was subsequently observed. Although TNF-a treatment of macrophages did not affect the early phase growth of organisms, bacterial killing was observed in the later phase of cultivation. Second, although IFN-g-treated macrophages killed M. avium during the first 3 days of culture, regrowth of the intracellular organisms was subsequently observed. TNF-a treatment of macrophages did not influence the mode of intracellular growth of M. avium. Third, IFN-g but not TNF-a enhanced production of reactive nitrogen intermediates (RNI) by macrophages infected with M. tuberculosis or M. avium, whereas both cytokines increased macrophage release of reactive oxygen intermediates (ROI). The present findings therefore show that IFN-g and TNF-a potentiated the anti-mycobacterial activity of murine peritoneal macrophages in different fashions. They also suggest that RNI played more important roles than did ROI in the expression of macrophage anti-mycobacterial, particularly anti-M. avium, activity.

show abstract

Section: Discussionmentioning

confidence: 62%

Differential potentiation of anti-mycobacterial activity and reactive nitrogen intermediate-producing ability of murine peritoneal macrophages activated by interferon-gamma (IFN-γ) and tumour necrosis factor-alpha (TNF-α)

Sato¹,

Akaki

Tomioka³

1998

Clinical and Experimental Immunology

View full text Add to dashboard Cite

show abstract

“…21 Mycobacteria are intracellular pathogens which survive and grow in host macrophages, whereas activated macrophages are presumed to eliminate the bacteria effectively. 22 My c o ba cte riu m tu be rcu lo s is bacilli enter the macrophage via binding to several distinct cell surface molecules. Following phagocytosis, sustained intracellular bacterial growth depends on the ability to avoid destruction by macrophagemediated host defences such as lysosomal enzymes, reactive oxygen and reactive nitrogen intermediates.…”

Section: Discussionmentioning

confidence: 99%

Role of cytokines and nitric oxide in the induction of tuberculostatic macrophage functions

Petricevich

Alves²

2000

Mediators of Inflammation

View full text Add to dashboard Cite

The aim of this study was to determine phenotypic differences when BCG invades macrophages. Bacilli prepared from the same BCG primary seed, but produced in different culture media, were analysed with respect to the ability to stimulate macrophages and the susceptibility to treatment with cytokines and nitric oxide (NO). Tumour necrosis factor (TNF) activity was assayed by measuring its cytotoxic activity on L-929 cells, interleukin-6 (IL-6) and interferon-gamma (IFN-gamma) were assayed by enzyme-linked immunosorbent assay (ELISA), whereas NO levels were detected by Griess colorimetric reactions in the culture supernatant of macrophages incubated with IFN-gamma, TNF or NO and subsequently exposed to either BCG-I or BCG-S. We found that BCG-I and BCG-S bacilli showed different ability to simulate peritoneal macrophages. Similar levels of IL-6 were detected in stimulated macrophages with lysate from two BCG samples. The highest levels of TNF and IFN-gamma were observed in macrophages treated with BCG-S and BCG-I, respectively. The highest levels of NO were observed in cultures stimulated for 48 h with BCG-S. We also found a different susceptibility of the bacilli to exogenous treatment with IFN-gamma and TNF which were capable of killing 60 and 70% of both bacilli, whereas NO was capable of killing about 98 and 47% of BCG-I and BCG-S, respectively. The amount of bacilli proportionally decreased with IFN-gamma and TNF, suggesting a cytokine-related cytotoxic effect. Moreover, NO also decreased the viable number of bacilli. Interestingly, NO levels of peritoneal macrophages were significantly increased after cytokine treatment. This indicates that the treatment of macrophages with cytokines markedly reduced bacilli number and presented effects on NO production. The results obtained here emphasize the importance of adequate stimulation for guaranteeing efficient killing of bacilli. In this particular case, the IFN-gamma and TNF were involved in the activation of macrophage bactericidal activity.

show abstract

“…First, concerning reactive oxygen intermediates (ROI), a well known effect of macrophage antimicrobial activity against Listeria monocytogenes and Salmonella typhimurium [5,6], their participation in killing and growth inhibition of mycobacteria, including M. tuberculosis and MAC, is reported to be relatively small [7][8][9][10][11]. Indeed, a xanthine oxidase-acetaldehyde system which enzymatically generates ROI molecules (O 2 ¹ , H 2 O 2 , .…”

Section: Introductionmentioning

confidence: 99%

Effector molecules of the host defence mechanism against Mycobacterium avium complex: the evidence showing that reactive oxygen intermediates, reactive nitrogen intermediates, and free fatty acids each alone are not decisive in expression of macrophage antimicrobial activity against the parasites

Tomioka

Sato

Sano

et al. 1997

Clinical and Experimental Immunology

View full text Add to dashboard Cite

SUMMARYIn this study, we evaluated the roles of reactive oxygen intermediates (ROI), reactive nitrogen intermediates (RNI), and free fatty acids (FFA) as effectors of the macrophage-mediated host defence mechanism against Mycobacterium avium complex (MAC). First, M. avium (three strains) and M. intracellulare (two strains) were treated with the H 2 O 2 -Fe 2þ -mediated halogenation system, acidified NaNO 2 -derived RNI, or FFA (linolenic acid) in sodium acetate buffer pH 5 . 5, and then counted for the number of residual colony-forming units (CFU) of organisms. Although these effectors exerted strong bactericidal activity against the MAC, the susceptibility of test organisms markedly varied from strain to strain. There was no significant relationship between the degree of resistance of a given MAC strain to these effectors and its virulence in mice, indicating that ROI, RNI, and FFA each alone are not decisive as the effector components of the host defence mechanism against the MAC. Second, the increase in ROI-producing ability in murine peritoneal macrophages due to tumour necrosis factor-alpha (TNF-a) treatment was not accompanied by parallel potentiation of anti-MAC activity of the same macrophage population. This excludes the possibility that ROI play a central role in macrophage-mediated killing and inhibition of MAC organisms. Third, anti-MAC activity of BAM3 macrophage cell line was not significantly attenuated by N G -monomethyl-L-arginine (NO synthaseinhibitor causing reduction of RNI production) or by quinacrine (phospholipase A 2 -inhibitor causing reduction of FFA release), indicating that RNI and FFA each alone do not play crucial roles in the expression of macrophage antimicrobial activity against the MAC. The present findings suggest important roles of collaborating actions of various antimicrobial effectors and/or the participation of other kinds of effectors in macrophage-mediated killing and inhibition of MAC organisms.

show abstract

Growth hormone activation of human monocytes for superoxide production but not tumor necrosis factor production, cell adherence, or action against Mycobacterium tuberculosis

Cited by 31 publications

References 36 publications

Differential potentiation of anti-mycobacterial activity and reactive nitrogen intermediate-producing ability of murine peritoneal macrophages activated by interferon-gamma (IFN-γ) and tumour necrosis factor-alpha (TNF-α)

Differential potentiation of anti-mycobacterial activity and reactive nitrogen intermediate-producing ability of murine peritoneal macrophages activated by interferon-gamma (IFN-γ) and tumour necrosis factor-alpha (TNF-α)

Role of cytokines and nitric oxide in the induction of tuberculostatic macrophage functions

Effector molecules of the host defence mechanism against Mycobacterium avium complex: the evidence showing that reactive oxygen intermediates, reactive nitrogen intermediates, and free fatty acids each alone are not decisive in expression of macrophage antimicrobial activity against the parasites

Contact Info

Product

Resources

About