Effects of concanavalin a and pokeweed mitogen in vivo on mouse peritoneal macrophages

Untreated mouse peritoneal macrophages as well as macrophages treated with concanavalin A (ConA) were incubated in the presence of untreated or ConA-treated epimastigotes and trypomastigotes of Trypanosoma cruzi. Treatment of epimastigotes or trypomastigotes with ConA increased or decreased their uptake by macrophages, respectively. Treatment of their macrophages with ConA reduced by 70% and increased by five times the ingestion of epimastigotes and trypomastigotes, respectively. These results are discussed in relation to previous studies on the mobility of ConA receptors in the membrane of the parasite. Using fluorescein- or ferritin-labelled ConA we observed that ConA binding sites located on the plasma membrane of macrophages are internalized during endocytosis of T. cruzi, and observed in association with the membrane of the endocytic vacuole. Vacuoles without parasites showed a uniform distribution of ConA binding sites, while these sites were distributed in patches in vacuoles containing parasites. These results, in association with others previously reported, suggest the involvement of glycoproteins and/or glycolipids localized on the cell surface of T. cruzi and macrophages during the T. cruzi-macrophage interaction.

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In vitro and in vivo interaction between sporocysts of Sarcocystis muris and mouse peritoneal macrophages

Veterinary Parasitology ◽

10.1016/0304-4017(89)90044-7 ◽

1989 ◽

Vol 32 (4) ◽

pp. 341-347 ◽

Cited By ~ 1

Author(s):

H.S. Gill ◽

K.M. Moriarty ◽

W.A.G. Charleston

Keyword(s):

Peritoneal Macrophages ◽

Mouse Peritoneal Macrophages

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Mycoplasma pneumoniae-Derived Lipopeptides Induce Acute Inflammatory Responses in the Lungs of Mice

Infection and Immunity ◽

10.1128/iai.00955-07 ◽

2007 ◽

Vol 76 (1) ◽

pp. 270-277 ◽

Cited By ~ 40

Author(s):

Takashi Shimizu ◽

Yutaka Kida ◽

Koichi Kuwano

Keyword(s):

Mycoplasma Pneumoniae ◽

Inflammatory Responses ◽

Lavage Fluid ◽

Peritoneal Macrophages ◽

Necrosis Factor Alpha ◽

Chemokine Production ◽

Cytokines And Chemokines ◽

Tnf Α ◽

Mouse Peritoneal Macrophages

ABSTRACT The pathogenesis of Mycoplasma pneumoniae infection is considered to be in part attributable to excessive immune responses. In this study, we investigated whether synthetic lipopeptides of subunit b of F0F1-type ATPase (F0F1-ATPase), NF-κB-activating lipoprotein 1 (N-ALP1), and N-ALP2 (named FAM20, sN-ALP1, and sN-ALP2, respectively) derived from M. pneumoniae induce cytokine and chemokine production and leukocyte infiltration in vivo. Intranasal administration of FAM20 and sN-ALP2 induced infiltration of leukocyte cells and production of chemokines and cytokines in bronchoalveolar lavage fluid, but sN-ALP1 failed to do so. The activity of FAM20 was notably higher than that of sN-ALP2. FAM20 and sN-ALP2 induced tumor necrosis factor alpha (TNF-α) through Toll-like receptor 2 in mouse peritoneal macrophages. Moreover, in the range of low concentrations of lipopeptides, FAM20 showed relatively high activity of inducing TNF-α in mouse peritoneal macrophages compared to synthetic lipopeptides such as MALP-2 and FSL-1, derived from Mycoplasma fermentans and Mycoplasma salivarium, respectively. These findings indicate that the F0F1-ATPase might be a key molecule in inducing cytokines and chemokines contributing to inflammatory responses during M. pneumoniae infection in vivo.

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Constitutive secretion of cystatin C (gamma-trace) by monocytes and macrophages and its downregulation after stimulation.

Journal of Experimental Medicine ◽

10.1084/jem.166.6.1912 ◽

1987 ◽

Vol 166 (6) ◽

pp. 1912-1917 ◽

Cited By ~ 89

Author(s):

A H Warfel ◽

D Zucker-Franklin ◽

B Frangione ◽

J Ghiso

Keyword(s):

Cell Lines ◽

Cystatin C ◽

Peritoneal Macrophages ◽

Inflammatory Conditions ◽

Monocytes And Macrophages ◽

Constitutive Secretion ◽

Established Cell ◽

Mouse Peritoneal Macrophages

Cystatin C (gamma-trace) was found to be a constitutively secreted protein of isolated human monocytes and mouse peritoneal macrophages, as well as the histiocytic lymphoma cell lines U937, P388D.1, and J774. This proteinase inhibitor is not uniquely secreted by monocytes/macrophages, but was also identified in the conditioned media from several primary cells, including brain cells, and diverse established cell lines. In vitro treatment of resident mouse peritoneal macrophages with either LPS or IFN-gamma caused a downregulation in cystatin C secretion. Elaboration of this protein was also diminished by macrophages that had been stimulated by thioglycollate in vivo, and treatment of these cells with LPS led to further decline. It is suggested that, under some inflammatory conditions, downregulation of cystatin C may contribute to tissue pathology.

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Activin A down-regulates the phagocytosis of lipopolysaccharide-activated mouse peritoneal macrophages in vitro and in vivo

Cellular Immunology ◽

10.1016/j.cellimm.2008.11.001 ◽

2009 ◽

Vol 255 (1-2) ◽

pp. 69-75 ◽

Cited By ~ 27

Author(s):

Jing Zhou ◽

Guixiang Tai ◽

Haiyan Liu ◽

Jingyan Ge ◽

Ye Feng ◽

...

Keyword(s):

Peritoneal Macrophages ◽

Activin A ◽

Mouse Peritoneal Macrophages

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EFFECTS OF CONCANAVALIN A ON MOUSE PERITONEAL MACROPHAGES

Journal of Experimental Medicine ◽

10.1084/jem.140.5.1364 ◽

1974 ◽

Vol 140 (5) ◽

pp. 1364-1386 ◽

Cited By ~ 128

Author(s):

Paul J. Edelson ◽

Zanvil A. Cohn

Keyword(s):

Concanavalin A ◽

Peritoneal Macrophages ◽

Surface Marker ◽

Marker Enzyme ◽

Apparent Effect ◽

Con A ◽

Cytoplasmic Vesicles ◽

Secondary Lysosomes ◽

Mouse Peritoneal Macrophages ◽

Pinocytic Vesicles

Concanavalin A (Con A) binds to saccharide residues on the mouse peritoneal macrophage plasma membrane and stimulates extensive pinocytic interiorization of the membrane. The overall pinocytic rate is increased 3.5–4.5 times by the addition of Con A, and the surface marker enzyme adenosine triphosphatase can be identified histochemically in association with the cytoplasmic vesicles generated after exposure of the cells to Con A. Once formed, these pinocytic vesicles may persist for several days and fail to show morphologic evidence of fusion with primary or preformed secondary lysosomes. There is no apparent effect on the capacity of the macrophage to ingest either latex particles or IgG-coated SRBC administered either simultaneously with or subsequent to the Con A.

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Increased production of superoxide anion by macrophages exposed in vitro to muramyl dipeptide or lipopolysaccharide.

Journal of Experimental Medicine ◽

10.1084/jem.151.1.101 ◽

1980 ◽

Vol 151 (1) ◽

pp. 101-114 ◽

Cited By ~ 229

Author(s):

M J Pabst ◽

R B Johnston

Keyword(s):

Superoxide Anion ◽

Muramyl Dipeptide ◽

Peritoneal Macrophages ◽

Generating Capacity ◽

Nonadherent Cell ◽

Mouse Peritoneal Macrophages ◽

Nonadherent Cells ◽

Oxygen Metabolites

After in vitro exposure to lipopolysaccharide (LPS) or muramyl dipeptide (MDP), cultured resident mouse peritoneal macrophages were primed to display enhanced generation of superoxide anion (O2-) in response to stimulation by phorbol myristate acetate (PMA) or opsonized zymosan. Priming with LPS (1 microgram/ml) produced a sevenfold enhancement of PMA-stimulated O2- generation; priming was detected within 30 min and persisted for at least 4 d. Exposure to MDP (1 muM) primed the macrophages to double their O2- release; the response was first observed after 4 h and persisted for at least 3 d. The priming response was not observed with stereoisomers of MDP, which are inactive as adjuvants. LPS and MDP appeared to work directly on the macrophages rather than indirectly by interacting with adherent lymphocytes: (a) Addition of nonadherent cell populations that contained lymphocytes had no effect on the response. (b) The response was normal with cells from nude mice, which lack mature T lymphocytes. (c) Macrophages from C3H/HeJ mice, whose B lymphocytes fail to respond to LPS, were weak in their response to priming LPS; the addition of normal (C3Heb/FeJ) nonadherent cells had no effect on this weak response. (d) The macrophage-like cell line J774.1 also showed enhanced O2--generating capacity after a 4-h exposure to LPS or MDP. The O2--generating capacity of macrophages primed with LPS in vitro was equivalent to that previously observed with cells elicited in vivo by injection of LPS or activated by infection with Bacille Calmette-Guérin. The data suggest that previous exposure to bacterial products could prime macrophages to respond with increased production of toxic oxygen metabolites on contact with invading microorganisms or tumor cells.

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