Infiltration and survival: the behaviour of normal, invasive cells implanted to the developing chick wing

1979 ◽  
Vol 40 (1) ◽  
pp. 257-270
Author(s):  
C. Tickle ◽  
A. Crawley

The invasiveness of mouse lymphocytes and thymocytes, rabbit peritoneal neutrophil granulocytes (PMNs), mouse peritoneal macrophages (both activated and non-activated) and pig endothelial cells was assayed by implanting these cells to the chick wing bud. Cells of each type moved into the wing mesenchyme, although activated macrophages invaded poorly. PMNs were the most invasive cells and had moved well into the limb after only a few hours. PMNs, lymphocytes and thymocytes were ingested by wing mesenchyme cells. Endothelial cells, however, ingested chick blood cells. The implanted cells showed differences in ability to survive in the limb: PMNs disappeared rapidly, lymphocytes and thymocytes sometimes persisted for 24 h, while grafts of macrophages and endothelial cells were present at 24 h. Mechanisms which might be involved in the invasiveness of these cells, and also in their different abilities to survive in the chick wing, are discussed with particular reference to the production of plasminogen activator.

1973 ◽  
Vol 137 (3) ◽  
pp. 807-820 ◽  
Author(s):  
H. Melsom ◽  
R. Seljelid

A cytotoxic effect of mouse peritoneal macrophages against syngeneic and allogeneic erythrocytes was demonstrated by isotope release and release of hemoglobin. The cytotoxic effect was dependent on the contact between viable, activated macrophages and target cells. Activation was accomplished by prolonged cultivation of macrophages and by the presence of Zn++ and Con-A. Immunization did not prove necessary. Morphological observations as well as experiments with various salt concentrations indicate that the cytotoxic reaction may involve some kind of osmotic effect upon the target cells.


1980 ◽  
Vol 29 (2) ◽  
pp. 477-482 ◽  
Author(s):  
P K Maiti ◽  
R Kumar ◽  
L N Mohapatra

Mouse peritoneal macrophages were infected in vitro with Candida albicans, and the phagocytic and candidacidal activities were estimated by microscopic examination of Giemsa-stained cells. Activated macrophages obtained from either BCG-vaccinated animals or by in vitro exposure of normal macrophages to phytohemagglutinin-induced lymphokines exhibited higher phagocytic and candidacidal activities than did normal macrophages. However, activated macrophages obtained by in vitro exposure of macrophages to candida-induced lymphokines exhibited the highest phagocytic and candidacidal activities. The incorporation of immune mouse serum into the culture medium also enhanced the phagocytic and candidacidal activities of the normal macrophages but failed to improve the function of the activated macrophages. These results suggest that both activated macrophages and antibodies may be required for controlling candida infections in mice.


2021 ◽  
Vol 8 ◽  
Author(s):  
Jing Liu ◽  
Zhaoyun Zong ◽  
Wenhao Zhang ◽  
Yuling Chen ◽  
Xueying Wang ◽  
...  

Macrophage activation is an important process in controlling infection, but persistent macrophage activation leads to chronic inflammation and diseases, such as tumor progression, insulin resistance and atherosclerosis. Characterizing metabolic signatures of macrophage activation is important for developing new approaches for macrophage inactivation. Herein, we performed metabolomic analysis on lipopolysaccharide (LPS)-activated macrophages and identified the associated changes in metabolites. Notably, the cellular Nicotinamide adenine dinucleotide+ levels were decreased while NADPH was increased, proposing that NAD+ restoration can inhibit macrophage activation. Indeed, supplementation of nicotinamide mononucleotide (NMN) increased cellular NAD+ levels and decreased cytokine productions in LPS-activated cells. Quantitative proteomics identified that nicotinamide mononucleotide downregulated the expressions of LPS-responsive proteins, in which cyclooxygenase-2 (COX-2) expression was significantly decreased in NMN-treated cells. Consequently, the cellular levels of prostaglandin E2 (PGE2) was also decreased, indicating that NMN inactivated macrophages via COX-2-PGE2 pathway, which was validated in activated THP-1 cells and mouse peritoneal macrophages. In conclusion, the present study identified the metabolic characteristics of activated macrophages and revealed that NMN replenishment is an efficient approach for controlling macrophage activation.


1980 ◽  
Vol 152 (2) ◽  
pp. 447-451 ◽  
Author(s):  
N Nogueira ◽  
S Chaplan ◽  
Z Cohn

Blood form trypomastigotes of the Y and CL strains of Trypanosoma cruzi were tested for their ability to enter and infect mouse peritoneal macrophages. Both strains failed to enter macrophages in appreciable numbers, whereas metacyclic trypomastigotes purified from acellular cultures were ingested with ease. Macrophage parasitization was enhanced manyfold after the removal of an antiphagocytic substance by trypsinization. This occurred without modification of parasite viability. Opsonization with hyperimmune mouse serum also enhanced the uptake of blood form trypomastigotes by macrophages. This effect was mediated by the macrophage Fc receptor. The effects of serum and trypsinization were additive at high parasite:cell ratios. Neither trypsin-mediated nor antibody-dependent opsonization of the organisms modified the fate of either strain within resident macrophages. However, lymphokine-activated macrophages were capable of destroying both strains, and antibody opsonization further enhanced this process.


1986 ◽  
Vol 164 (4) ◽  
pp. 1362-1367 ◽  
Author(s):  
S R Behr ◽  
F B Kraemer

Lipoprotein lipase (LPL) activity was measured in the media of cultured mouse peritoneal macrophages that were isolated after the intraperitoneal injection of inflammatory agents in order to yield a variety of states of activation. Fully activated macrophages obtained from Corynebacterium parvum-injected mice secreted very low levels of LPL when compared to unstimulated macrophages, while inflammatory and primed macrophages had increased LPL secretion. When inflammatory macrophages were incubated with conditioned medium obtained from fully activated macrophages, LPL secretion decreased in a time- and dose-dependent fashion. The factor(s) secreted by fully activated macrophages that inhibited LPL secretion was shown to be thermolabile and distinct from tumor necrosis factor. These results demonstrate that activation dramatically alters macrophage LPL secretion.


Biochimie ◽  
1979 ◽  
Vol 61 (4) ◽  
pp. 463-471 ◽  
Author(s):  
Jean Claude Drapier ◽  
Jean Pierre Tenu ◽  
Geneviève Lemaire ◽  
Jean François Petit

1973 ◽  
Vol 57 (2) ◽  
pp. 289-305 ◽  
Author(s):  
Martha E. Fedorko ◽  
Nicholas L. Cross ◽  
James G. Hirsch

Mouse peritoneal macrophages have been studied in vitro after ingestion of treated rat, rabbit, or sheep erythrocytes. Under light microscopy, phagocytic vacuoles persist up to 24 h. Macrophages lose benzidine reactivity about 5 h after red cell ingestion, and they become prussian blue positive at 2 days. Ultrastructural studies show little or no ferritin in control macrophages not fed erythrocytes. In contrast, after red cell ingestion, ferritin is widely distributed in the cytoplasmic matrix and in some cytoplasmic granules by 48 h. The Golgi complex, pinocytic vacuoles, endoplasmic reticulum, nuclei, and mitochondria do not contain ferritin. Between 2 and 4 days, ferritin in cytoplasmic granules increases, concomitant with decrease in the ferritin in the cytoplasmic matrix. Evidence is presented suggesting that ferritin in the cytoplasmic matrix is translocated into cytoplasmic granules by autophagy. Polyacrylamide gel studies on macrophages after uptake of red blood cells labeled with radioiron confirm that macrophages produce radiolabeled ferritin by 4 days.


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