Macrophages: Current Views on Their Differentiation, Structure, and Function

Papadimitriou, J. M.; Ashman, R. B.

doi:10.3109/01913128909048488

Cited by 108 publications

(55 citation statements)

References 126 publications

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“…One marker of macrophage activation is cell size (Papadimitriou and Ashman, 1989). In crushed nerves undergoing WD we found a significant difference in macrophage morphology and size between control and complement-depleted animals (see Fig.…”

Section: The Role Of Complement In Macrophage Activationmentioning

confidence: 67%

Complement Depletion Reduces Macrophage Infiltration and Activation during Wallerian Degeneration and Axonal Regeneration

et al. 1998

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After peripheral nerve injury, macrophages infiltrate the degenerating nerve and participate in the removal of myelin and axonal debris, in Schwann cell proliferation, and in axonal regeneration. In vitro studies have demonstrated the role serum complement plays in both macrophage invasion and activation during Wallerian degeneration of peripheral nerve. To determine its role in vivo, we depleted serum complement for 1 week in adult Lewis rats, using intravenously administered cobra venom factor. At 1 d after complement depletion the right sciatic nerve was crushed, and the animals were sacrificed 4 and 7 d later. Macrophage identification with ED-1 and CD11a monoclonal antibodies revealed a significant reduction in their recruitment into distal degenerating nerve in complement-depleted animals. Complement depletion also decreased macrophage activation, as indicated by their failure to become large and multivacuolated and their reduced capacity to clear myelin, which was evident at both light and electron microscopic levels. Axonal regeneration was delayed in complement-depleted animals. These findings support a role for serum complement in both the recruitment and activation of macrophages during peripheral nerve degeneration as well as a role for macrophages in promoting axonal regeneration.

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Section: The Role Of Complement In Macrophage Activationmentioning

confidence: 67%

Complement Depletion Reduces Macrophage Infiltration and Activation during Wallerian Degeneration and Axonal Regeneration

et al. 1998

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“…Infection percentages were higher in J774 cells compared to Lulo cells, due to the former presenting macrophage characteristics with cells of phagocytic ability (Ralph et al 1975, Papadimitriou & Ashman 1989. These cells were also physiologically adapted as parasite host cells.…”

Section: Discussionmentioning

confidence: 99%

Experimental infection of Leishmania (L.) chagasi in a cell line derived from Lutzomyia longipalpis (Diptera:Psychodidae)

Bello

Mejía

Corena

et al. 2005

Mem. Inst. Oswaldo Cruz

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The present work describes the in vitro infection of a cell line Lulo, derived fromLeishmania chagasi is a causative protozoan parasite of American visceral leishmaniasis (Grimaldi & Tesh 1993). The disease is endemic in some regions of Colombia (Corredor et al. 1989(Corredor et al. , 1990 and throughout all the South and Central America (Grimaldi & Tesh 1993, Tanner 1996; the parasite has been isolated from hosts, reservoirs and sand fly vectors. This species, as well as other species belonging to the Leishmania genus, develops through a digenetic life cycle consisting of an extracellular promastigote form that develops and multiplies in the alimentary tract of the sand fly vector and an intracellular amastigote form that resides and multiplies inside the infected mammal host's macrophages. Clinical and experimental evidence indicates that vector, parasite, and host factors influence the evolution and outcome of the infection caused by Leishmania parasites (Grimaldi &Tesh 1993).Promastigotes are routinely cultured in vitro using cell free medium; such easily obtained media have also been used to induce promastigote transformation to amastigotelike forms in response to elevated temperature and acid pH (Hendrick et al. 1978, Hunter et al. 1982, Pan 1984, Zilberstein et al. 1991, Bates et al. 1992, Bates & Tetley 1993, Zilberstein & Sahapira 1994, Bates 1994 , Hodgkinson 1996, Saar et al. 1998. It has been shown that these axenic amastigotes closely resemble animal-derived amastigotes. Leishmania in vitro differentiation, maturation, and replication has also been achieved in both macrophage cell cultures (Chang & Dwyer 1978, Chang 1979, Pearson et al. 1981, Aikawa et al. 1982 and non-macrophage cell lines, mainly in fibroblast cultures (Mattock & Petters 1975, Chang 1978, Dedet et al. 1983, Schwartzman & Pearson 1985, Corte-Real et al. 1995, Hervás Rodrigues et al. 1996, Pessotti et al. 2004. However, in spite of current support, cell lines and cell free media being available for transforming the life cycle of diferent Leishmania species, there is no information available regarding this process in cell cultures obtained from phlebotomine sand fly vectors.The present study describes the in vitro infection of Lulo cell line (Rey et al. 2000) by L. chagasi promastigotes and some ultrastructural characteristics regarding the parasite's interaction with these cells were determined. This cell line was derived from L. longipalpis embryonic tissue, which is the main vector of L. chagasi in its natural environment. The experimental infection of Lulo cell line was compared to infection of J774 cell (Ralph et al. 1975). MATERIALS AND METHODSParasites -The strain of L. chagasi, MH/CO/84/ Cl-044B, was isolated from a human case of visceral leishmaniasis in Quipile, Cundinamarca, Colombia. This strain has been maintained by periodic inoculations of promastigotes in Syrian golden hamsters (Mesocricetus auratus) in the parasitology laboratory at the National Institute of Health in Colombia. L. chagasi amastigotes were recovered...

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“…Evidence from bone-marrow irradiation studies supports the hypothesis that blood-borne macrophages and nonresident macrophages play a vital role in phagocytosis of tissue debris. 36 Activated macrophages at the site of muscle injury also facilitate myofiber repair by producing cytokines and growth factors, such as fibroblast growth factor (FGF) 32 which are chemotactic for muscle precursor cells and other leukocytes, 37 and stimulate proliferation and differentiation of vascular endothelial cells and muscle precursors (reviewed in Refs. 13,16).…”

mentioning

confidence: 99%

Macrophages and dendritic cells in normal and regenerating murine skeletal muscle

1997

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Mononuclear phagocytes and MHC class II + dendritic cells (DC) were identified in frozen sections of skeletal muscle using a panel of pan-specific antimacrophage (MOMA-2, SER-4, Mac-1, F4/80), anti-major histocompatibility complex (MHC) class II (M5/114) and anti-DC (NLDC-145, N418, M342) monoclonal antibodies. Uninjured and regenerating skeletal muscle were investigated in SJL/J and BALB/c mice, strains with known differences in muscle regenerative capacity. Resident tissue macrophages and MHC class II + DC were present within uninjured mouse muscle. A subpopulation of DC were positive for the pan-DC markers, N418 and M342, and negative for the lymphoid DC marker NLDC-145. Following crush injury, the macrophage population increased by day 2, became marked by day 3, and had decreased by day 6. In contrast, the number of MHC class II + cells around the injury site increased steadily after injury and remained high at day 6. The numbers of macrophages and DC detected by immunohistochemical staining were consistently higher in SJL/J than BALB/c muscles. This study confirms that macrophages are a significant component of normal murine skeletal muscle and that these cells increase dramatically after injury. Furthermore the data also reveal for the first time that DC are present in normal skeletal muscle and that MHC class II + cells, including DC, increase after injury. The presence of DC in muscle has important implications for the understanding of the immunobiology of muscle and immune-mediated processes such as the host versus graft responses following muscle transplants and autoimmune diseases affecting this tissue.

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Macrophages: Current Views on Their Differentiation, Structure, and Function

Cited by 108 publications

References 126 publications

Complement Depletion Reduces Macrophage Infiltration and Activation during Wallerian Degeneration and Axonal Regeneration

Complement Depletion Reduces Macrophage Infiltration and Activation during Wallerian Degeneration and Axonal Regeneration

Experimental infection of Leishmania (L.) chagasi in a cell line derived from Lutzomyia longipalpis (Diptera:Psychodidae)

Macrophages and dendritic cells in normal and regenerating murine skeletal muscle

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