Effects of latrunculin A on immunological phagocytosis and macrophage spreading-associated changes in the F-actin/G-actin content of the cells

Oliveira, Carlos Alberto de; Kashman, Yoel; Mantovani, Bernardo

doi:10.1016/0009-2797(96)03695-2

Cited by 39 publications

(30 citation statements)

References 30 publications

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“…For the experiments, corticosterone was first dissolved in DMSO; the final concentration of DMSO in the experiments was less than 0.05% (v/v). We have found, in accordance with other observations [5] , that concentrations less than 0.1% DMSO have no effect on phagocytosis.…”

Section: In Vitro Effect Of Corticosterone Epinephrine and Norepinepsupporting

confidence: 81%

“…However, macrophages also deserve attention because they are one of the first cell types involved in the immune reaction, and they help to orchestrate immune events. Phagocytosis, the internalization of particles larger than 0.5 m by a mechanism dependent on actin polymerization [4,5] , is among the most important functions of macrophages due to the role of this process in the elimination of foreign particles and microorganisms.…”

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confidence: 99%

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Effects of Cold Stress, Corticosterone and Catecholamines on Phagocytosis in Mice: Differences between Resting and Activated Macrophages

Baccan

Sesti-Costa

Chedraoui-Silva

et al. 2010

Neuroimmunomodulation

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Objective: We subjected mice to acute cold stress and studied the effect on phagocytosis by peritoneal macrophages mediated by 3 types of phagocytic receptors: Fcγ, complement receptors 3 (CR3) and mannose and β-glucan receptors. Methods: Mice were subjected to a cold stress condition (4°C for 4 h), and then peritoneal macrophages were harvested and phagocytosis assays performed in vitro. Results: We found a striking difference between resting and lipopolysaccharide (LPS)-activated macrophages (by intraperitoneal injection of LPS 4 days before the stress experiment): for resting macrophages cold stress caused a decrease in phagocytosis mediated by Fcγ or mannose receptors, while for activated macrophages we observed an increase in phagocytosis by the 3 types of receptors. These effects were associated with an increase in plasma concentrations of corticosterone and catecholamines following the cold stress. In order to verify whether these hormone changes could account for the observed effects on phagocytosis, we performed in vitro assays by incubating macrophages harvested from nonstressed animals with these hormones for 4 h at 37°C and measuring their phagocytic capacity. The following experiments were done: (a) with resting (nonactivated) macrophages; (b) with macrophages previously activated in vitro by incubation with LPS; (c) with macrophages previously activated in vivo by intraperitoneal injection of mice with LPS, 4 days before harvesting the cells. We found that for resting macrophages, corticosterone decreased phagocytosis mediated by Fcγ and mannose and β-glucan receptors, but catecholamines had no effect. For macrophages activated either in vivo or in vitro, catecholamines caused an increase in phagocytosis (excluding mannose receptors) while corticosterone had no effect. Conclusion: The above findings suggest that stress can regulate phagocytosis in different ways, depending on the kind of phagocytic receptor involved, the level of stress hormones and the physiological state of the macrophages.

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Section: In Vitro Effect Of Corticosterone Epinephrine and Norepinepsupporting

confidence: 81%

mentioning

confidence: 99%

Effects of Cold Stress, Corticosterone and Catecholamines on Phagocytosis in Mice: Differences between Resting and Activated Macrophages

Baccan

Sesti-Costa

Chedraoui-Silva

et al. 2010

Neuroimmunomodulation

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“…PKC Interacted with RGC-32 and Mediated RGC-32 Function in Phagocytosis-F-actin assembly during phagocytosis is regulated at different levels (32,34,35). PKC pathway has been reported to regulate F-actin assembly (36 -38).…”

Section: Rgc-32 Co-localized With F-actin and Was Essential For F-actmentioning

confidence: 99%

Response Gene to Complement 32 Protein Promotes Macrophage Phagocytosis via Activation of Protein Kinase C Pathway

Tang

Gui

Chen

2014

Journal of Biological Chemistry

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Background: Response gene to complement 32 (RGC-32) was initially identified in oligodendrocytes, suggesting an immune-related function. Results: RGC-32 deficiency did not affect macrophage differentiation but attenuated macrophage phagocytosis by reducing protein kinase C activity and F-actin formation. Conclusion: RGC-32 is a novel regulator for macrophage phagocytosis. Significance: RGC-32 may serve as a novel target for modulating immune function.

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“…If different receptors can trigger phagocytosis it is reasonable to suppose that there should be convergent biochemical pathways leading to the final reaction of polymerization of G-actin to F-actin which is an essential component for engulfment (2,3). The activation of tyrosine protein kinases could represent one of the points of convergence, although possibly different sets of enzymes and protein phosphorylations might be in- Macrophages activated in vivo with LPS were preincubated at 37ºC for 10 min with tyrosine kinase inhibitors.…”

Section: % Interactionmentioning

confidence: 99%

“…Phagocytosis is usually defined as the uptake by cells of particles visible under the light microscope (<~0.5 µm) and their internalization into vacuoles -a process that requires structural modifications of the cytoskeleton, including actin polymerization (1)(2)(3). In mammals the chief phagocytes are polymorphonuclear leukocytes, monocytes and macrophages.…”

Section: Introductionmentioning

confidence: 99%

Phagocytosis by macrophages mediated by receptors for denatured proteins - dependence on tyrosine protein kinases

Hespanhol

Mantovani

2002

Braz J Med Biol Res

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Previous studies have demonstrated that some components of the leukocyte cell membrane, CR3 (Mac-1, CD11b/CD18) and p150/95, are able to bind to denatured proteins. Thus, it is of interest to know which effector functions of these cells can be triggered by these receptors when they interact with particles or surfaces covered with denatured proteins. In the present study we analyzed their possible role as mediators of phagocytosis of red cells covered with denatured bovine serum albumin (BSA) by mouse peritoneal macrophages. We observed that a) macrophages are able to recognize (bind to) these red cells, b) this interaction can be inhibited by denatured BSA in the fluid phase, c) there is no phagocytosis of these particles by normal macrophages, d) phagocytosis mediated by denatured BSA can be, however, effectively triggered in inflammatory macrophages induced by glycogen or in macrophages activated in vivo with LPS, and e) this phagocytic capacity is strongly dependent on the activity of tyrosine protein kinases in its signal transduction pathway, as demonstrated by using three kinds of enzyme inhibitors (genistein, quercetin and herbimycin A).

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Effects of latrunculin A on immunological phagocytosis and macrophage spreading-associated changes in the F-actin/G-actin content of the cells

Cited by 39 publications

References 30 publications

Effects of Cold Stress, Corticosterone and Catecholamines on Phagocytosis in Mice: Differences between Resting and Activated Macrophages

Effects of Cold Stress, Corticosterone and Catecholamines on Phagocytosis in Mice: Differences between Resting and Activated Macrophages

Response Gene to Complement 32 Protein Promotes Macrophage Phagocytosis via Activation of Protein Kinase C Pathway

Phagocytosis by macrophages mediated by receptors for denatured proteins - dependence on tyrosine protein kinases

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