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Phagosomes (goblets from the Greek "phagein" = to eat) are large organelles inside phagocytes (macrophages, neutrophilic granulocytes and dendritic cells), which belong to the group of phagocytes . Phagosomes are the place where some particles (e.g. bacteria or small eukaryotic parasites ) are killed and enzymatically broken down after phagocytosis and they therefore play a crucial role in the immune defense of eukaryotes .


Phagosomes are intracellular compartments with a diameter of over 500 nm, surrounded by a lipid bilayer (double lipid membrane).

Formation of phagosomes

As soon as the immune defense detects an intruder within the system, the process of phagocytosis is initiated in which the macrophages bind the exogenous particle to themselves. This happens either directly via microbial ligands that bind to mammalian cell receptors or via the fact that the microbes are "opsonized". During opsonization, mammalian proteins (e.g. immunoglobulins, complement factors) bind to the microbes in order to identify them as foreign and thus promote their subsequent uptake.

For phagocytosis, scavenger cells enclose the foreign body with part of their cell membrane and tie off a vesicle called a phagosome inside the macrophage. The process of constriction and formation of the vesicle is called phagocytosis , a special case of endocytosis (into the cell / opposite of exocytosis ) .


The phagosome can be flooded with acid and reactive oxygen and nitrogen species (ROS, RNS) after formation if the receiving cell is a polymorphonuclear granulocyte or an activated macrophage. In most cases, the death of the microbe will be initiated after the phagosome has fused with lysosomes in the cell , which also provide the necessary enzymes to break down the phagosomal contents. The fusion product of phagosome and lysosome is called phagolysosome.

Pathogen-containing phagosomes


Infection with the tuberculosis pathogen Mycobacterium tuberculosis and many other "intracellular" pathogens associated with phagocytosis does not go according to plan .

Mycobacterium tuberculosis has evolved several mechanisms that allow it to survive in the phagosome: it initially has a waxy, fat-rich cell wall that enables it to protect itself against its destruction within the immune system. The enzymes contained in the phagosome are unable to break down the outer layer of the pathogen's cell wall. In addition, the outer wax layer contains lipoarabinomannan (LAM), a glycolipid that, together with a protein phosphatase, disrupts the signal transduction of the phagosome so that it does not go through the full program of destruction. Furthermore, several enzymes ( catalase , superoxide dismutase and others) are excreted by the bacterium , which eliminate any danger from reactive oxygen and nitrogen species. Finally, the bacterium brings itself into a hibernation-like state in which no transcription or translation takes place and the organism lives on the back burner from its own fat layer. This renders ineffective many antibiotics that otherwise interfere with normal cell processes.

The immune system binds the Mycobacterium tuberculosis in so-called granulomas , whereby the pathogen is not eliminated, but only encapsulated. The infection remains lifelong and can trigger an outbreak of the disease at any time, even after several years. About a third of the world's population is infected with the bacterial pathogen Mycobacterium tuberculosis .

See also

Individual evidence

  1. ^ Briken V, Porcelli SA, Besra GS, Kremer L: Mycobacterial lipoarabinomannan and related lipoglycans: from biogenesis to modulation of the immune response . In: Mol. Microbiol. . 53, No. 2, July 2004, pp. 391-403. doi : 10.1111 / j.1365-2958.2004.04183.x . PMID 15228522 .
  2. Hestvik AL, Hmama Z, Av-Gay Y: Mycobacterial manipulation of the host cell . In: FEMS Microbiol. Rev. . 29, No. 5, November 2005, pp. 1041-50. doi : 10.1016 / j.femsre.2005.04.013 . PMID 16040149 .
  3. Deretic V, Singh S, Master S, et al. : Mycobacterium tuberculosis inhibition of phagolysosome biogenesis and autophagy as a host defense mechanism . In: Cell. Microbiol. . 8, No. 5, May 2006, pp. 719-27. doi : 10.1111 / j.1462-5822.2006.00705.x . PMID 16611222 .