Stimulatory and inhibitory guanine‐nucleotide‐binding regulatory protein involvement in stimulation of arachidonic‐acid release by <i>N</i>‐formyl‐methionyl‐leucyl‐phenylalanine and platelet‐activating factor from guinea‐pig alveolar macrophages

Levistre, Romuald; Masliah, J.; Béréziat, G.

doi:10.1111/j.1432-1033.1993.tb17762.x

Cited by 12 publications

(9 citation statements)

References 53 publications

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“…Previous work by other groups established that murine peritoneal macrophages express G␣ i1 and/or G␣ i2 as well as G␣ i3 (26), and guinea pig AMs express G␣ i1 and/or G␣ i2 , but not G␣ i3 (24). However, these studies were limited by the use of reagents that could not discriminate between G␣ i1 and G␣ i2 .…”

Section: Discussionmentioning

confidence: 99%

Specific Leukotriene Receptors Couple to Distinct G Proteins to Effect Stimulation of Alveolar Macrophage Host Defense Functions

Peres

Aronoff

Serezani

et al. 2007

The Journal of Immunology

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Leukotrienes (LTs) are lipid mediators implicated in asthma and other inflammatory diseases. LTB4 and LTD4 also participate in antimicrobial defense by stimulating phagocyte functions via ligation of B leukotriene type 1 (BLT1) receptor and cysteinyl LT type 1 (cysLT1) receptor, respectively. Although both Gαi and Gαq proteins have been shown to be coupled to both BLT1 and cysLT1 receptors in transfected cell systems, there is little known about specific G protein subunit coupling to LT receptors, or to other G protein-coupled receptors, in primary cells. In this study we sought to define the role of specific G proteins in pulmonary alveolar macrophage (AM) innate immune responses to LTB4 and LTD4. LTB4 but not LTD4 reduced cAMP levels in rat AM by a pertussis toxin (PTX)-sensitive mechanism. Enhancement of FcγR-mediated phagocytosis and bacterial killing by LTB4 was also PTX-sensitive, whereas that induced by LTD4 was not. LTD4 and LTB4 induced Ca2+ and intracellular inositol monophosphate accumulation, respectively, highlighting the role of Gαq protein in mediating PTX-insensitive LTD4 enhancement of phagocytosis and microbicidal activity. Studies with liposome-delivered G protein blocking Abs indicated a dependency on specific Gαq/11 and Gαi3 subunits, but not Gαi2 or Gβγ, in LTB4-enhanced phagocytosis. The selective importance of Gαq/11 protein was also demonstrated in LTD4-enhanced phagocytosis. The present investigation identifies differences in specific G protein subunit coupling to LT receptors in antimicrobial responses and highlights the importance of defining the specific G proteins coupled to heptahelical receptors in primary cells, rather than simply using heterologous expression systems.

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Section: Discussionmentioning

confidence: 99%

Specific Leukotriene Receptors Couple to Distinct G Proteins to Effect Stimulation of Alveolar Macrophage Host Defense Functions

Peres

Aronoff

Serezani

et al. 2007

The Journal of Immunology

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“…Besides, the adenosine diphosphate (ADP)-ribosylating PT promotes inflammation and leukocytosis in vivo (Gierschik, 1992;Hewlett, 1997). Nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase, phospholipases A and C activities (Gierschik and Jakobs, 1987;Levistre et al, 1993), and Fc-mediated phagocytosis (Hamilton and Adams, 1987;Gierschik, 1992) are among the signaling pathways affected by PT.…”

mentioning

confidence: 99%

Adaptive responses of human monocytes infected byBordetella pertussis: The role of adenylate cyclase hemolysin

et al. 2000

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The activation/adaptive responses of human monocytes exposed to Bordetella pertussis parental or mutant strains were evaluated and correlated to the expression of two bacterial toxins: adenylate cyclase-hemolysin and pertussis toxin. The marked rise in intracellular cyclic adenosine monophosphate (cAMP) observed in monocytes infected by B. pertussis parental strain, inversely correlated with (1) the production of tumor necrosis factor alpha; (2) the release of superoxide anion; and (3) the expression of the 72-kDa heat shock/stress protein, Hsp70. Experiments performed with mutants deficient in adenylate cyclase-hemolysin or with purified bacterial toxins confirmed the key role of adenylate cyclase-hemolysin in the control of monocytes' response to infection by B. pertussis. This bacterial strategy primarily involves evasion from antimicrobial defenses and, eventually, the sacrifice of the host cell.

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“…We had shown that pretreatment of guinea-pig alveolar macrophages with cholera toxin increases ADP-ribosylation of G,protein by cholera or pertussis toxin in vitro [15]. This effect of cholera toxin was mimicked by a cAMP analogue, suggesting that it was mediated by a cAMP-dependent mechanism ( Figure 1, lane d versus lanes b and a).…”

Section: Resultsmentioning

confidence: 86%

“…The procedure for activating the toxin and incubating membranes with cholera toxin and [32P]NAD+ is described in [15]. Briefly of the Gpa2 subunit [17].…”

Section: Macrophage Culture Membrane Preparationmentioning

confidence: 99%

“…We have previously shown that pretreating alveolar macrophages with cholera toxin induces ADP-ribosylation of G.proteins. G,-proteins from cholera toxin-treated ceUs appear to be more heavily labelled by ADP-ribosylation with pertussis toxin than are control cells [15]. Therefore, the aim of this study was to demonstrate that the target of the cross-regulation of arachidonic acid release by cholera toxin could be the G,-protein itself.…”

Section: Introductionmentioning

confidence: 98%

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The cross-regulation of Gi-protein by cholera toxin involves a phosphorylation by protein kinase A

Levistre

Berguerand

Béréziat

et al. 1995

Biochemical Journal

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Pretreatment of alveolar macrophages with cholera toxin inhibits the release of arachidonic acid induced by the chemotactic peptide N-formylmethionyl-leucyl-phenylalanine. The results presented here show that cholera toxin might exert its inhibitory effect through the phosphorylation of Gi alpha by protein kinase A (PKA). (1) Gi-proteins from cells pretreated with cholera toxin showed parallel increases in their sensitivity to ADP-ribosylation by toxins in vitro and in Gi alpha phosphorylation. By contrast, the Gi alpha concentration was unchanged. (2) Cholera toxin pretreatment also decreased the functional activity of Gi, as assessed by the inhibition (80%) of agonist-induced binding of guanosine-5'-[gamma-thio]triphosphate (GTP[gamma S]). (3) These effects of cholera toxin were blocked by a specific PKA inhibitor, N-(2-[methyl-amino]ethyl)-3-isoquinolinesulphonamide dihydrochloride (H8) and mimicked by a cyclic AMP (cAMP) analogue and a phosphatase inhibitor. (4) Gi alpha was also phosphorylated in vitro by the catalytic subunit of PKA. In contrast with other cell systems, the stimulation of protein kinase C seems to have no effect on the sensitivity of Gi to ADP-ribosylation or on its phosphorylation. Therefore, the phosphorylation of Gi-proteins by PKA seems to be the actual target of the negative control of arachidonic acid release via the cAMP-mediated pathway.

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Stimulatory and inhibitory guanine‐nucleotide‐binding regulatory protein involvement in stimulation of arachidonic‐acid release by N‐formyl‐methionyl‐leucyl‐phenylalanine and platelet‐activating factor from guinea‐pig alveolar macrophages

Cited by 12 publications

References 53 publications

Specific Leukotriene Receptors Couple to Distinct G Proteins to Effect Stimulation of Alveolar Macrophage Host Defense Functions

Specific Leukotriene Receptors Couple to Distinct G Proteins to Effect Stimulation of Alveolar Macrophage Host Defense Functions

Adaptive responses of human monocytes infected byBordetella pertussis: The role of adenylate cyclase hemolysin

The cross-regulation of Gi-protein by cholera toxin involves a phosphorylation by protein kinase A

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