Phagocytosis

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Phagocytosis in three steps:
1. Unbound phagocyte surface receptors do not trigger phagocytosis.
2. Binding of receptors causes them to cluster.
3. Phagocytosis is triggered and the particle is taken up by the phagocyte.

In cell biology, phagocytosis is the process of engulfing a solid particle by a phagocyte or a protist to form an internal phagosome (from Ancient Greek φαγεῖν (phagein) , meaning "to devour", κύτος, (kytos) , meaning "cell", and -osis, meaning "process"). Phagocytosis was revealed by Élie Metchnikoff in 1882. Phagocytosis is a specific form of endocytosis involving the vesicular internalization of solids such as bacteria, and is, therefore, distinct from other forms of endocytosis such as the vesicular internalization of various liquids. Phagocytosis is involved in the acquisition of nutrients for some cells, and, in the immune system, it is a major mechanism used to remove pathogens and cell debris. Bacteria, dead tissue cells, and small mineral particles are all examples of objects that may be phagocytized.

The process is homologous to eating at the level of single-celled organisms; in multicellular animals, the process has been adapted to eliminate debris and pathogens, as opposed to taking in fuel for cellular processes, except in the case of the animal Trichoplax.

In immune system[edit]

Scanning electron micrograph of a phagocyte (yellow, right) phagocytosing anthrax bacilli (orange, left)

Phagocytosis in mammalian immune cells is activated by attachment to Pathogen-associated molecular patterns (PAMPS), which leads to NF-κB activation. Opsonins such as C3b and antibodies can act as attachment sites and aid phagocytosis of pathogens.[1]

Engulfment of material is facilitated by the actin-myosin contractile system. The phagosome of ingested material is then fused with the lysosome, leading to degradation.

Degradation can be oxygen-dependent or oxygen-independent.

It is possible for cells other than dedicated phagocytes (such as dendritic cells) to engage in phagocytosis.[3]

In apoptosis[edit]

Following apoptosis, the dying cells need to be taken up into the surrounding tissues by macrophages in a process called efferocytosis. One of the features of an apoptotic cell is the presentation of a variety of intracellular molecules on the cell surface, such as calreticulin, phosphatidylserine (From the inner layer of the plasma membrane), annexin A1, and oxidised LDL. These molecules are recognised by receptors on the cell surface of the macrophage such as the phosphatidylserine receptor or by soluble (free floating) receptors such as thrombospondin 1, Gas-6, and MFG-E8, which themselves then bind to other receptors on the macrophage such as CD36 and alpha-v beta-3 integrin. Defects in apoptotic cell clearance is usually associated with impaired phagocytosis of macropghages. Accumulation of apoptotic cell remnants often causes autoimmune disorders, thus pharmacological potentiation of phagocytosis has a medical potential in treatment of certain forms of autoimmune disorders.[4][5][6][7]

Additional information on phagocytosis of apoptotic cells could be found in the book: “Phagocytosis of dying cells: from molecular mechanisms to human diseases” (Eds DV Krysko and P Vandenabeele, 2009, Springer).

In protists[edit]

Trophozoites of Entamoeba histolytica with ingested erythrocytes

In many protists, phagocytosis is used as a means of feeding, providing part or all of their nourishment. This is called phagotrophic nutrition, as distinguished from osmotrophic nutrition, which takes place by absorption.

The resulting phagosome may be merged with lysosomes containing digestive enzymes, forming a phagolysosome. The food particles will then be digested, and the released nutrients are diffused or transported into the cytosol for use in other metabolic processes.

Mixotrophy can involve phagotrophic nutrition and phototrophic nutrition.[11]

See also[edit]

References[edit]

  1. ^ The Immune System, Peter Parham, Garland Science, 2nd edition
  2. ^ http://www.colorado.edu/intphys/iphy3700/vitCHemila92.pdf
  3. ^ Ishimoto, H; Yanagihara, K; Araki, N; Mukae, H; Sakamoto, N; Izumikawa, K; Seki, M; Miyazaki, Y et al. (July 2008). "Single-cell observation of phagocytosis by human blood dendritic cells". Jpn. J. Infect. Dis. 61 (4): 294–7. PMID 18653972. 
  4. ^ Mukundan, Lata; Odegaard, Justin I; Morel, Christine R; Heredia, Jose E; Mwangi, Julia W; Ricardo-Gonzalez, Roberto R; Goh, Y P Sharon; Eagle, Alex Red; Dunn, Shannon E; Awakuni, Jennifer U H; Nguyen, Khoa D; Steinman, Lawrence; Michie, Sara A; Chawla, Ajay (18 October 2009). "PPAR-δ senses and orchestrates clearance of apoptotic cells to promote tolerance". Nature Medicine 15 (11): 1266–1272. doi:10.1038/nm.2048. PMC 2783696. PMID 19838202. 
  5. ^ Roszer, T; Menéndez-Gutiérrez, MP; Lefterova, MI; Alameda, D; Núñez, V; Lazar, MA; Fischer, T; Ricote, M (2011 Jan 1). "Autoimmune kidney disease and impaired engulfment of apoptotic cells in mice with macrophage peroxisome proliferator-activated receptor gamma or retinoid X receptor alpha deficiency". Journal of immunology (Baltimore, Md. : 1950) 186 (1): 621–31. doi:10.4049/jimmunol.1002230. PMID 21135166. 
  6. ^ Kruse, K; Janko, C; Urbonaviciute, V; Mierke, CT; Winkler, TH; Voll, RE; Schett, G; Muñoz, LE; Herrmann, M (2010 Sep). "Inefficient clearance of dying cells in patients with SLE: anti-dsDNA autoantibodies, MFG-E8, HMGB-1 and other players". Apoptosis : an international journal on programmed cell death 15 (9): 1098–113. doi:10.1007/s10495-010-0478-8. PMID 20198437. 
  7. ^ Han, CZ; Ravichandran, KS (2011 Dec 23). "Metabolic connections during apoptotic cell engulfment". Cell 147 (7): 1442–5. doi:10.1016/j.cell.2011.12.006. PMC 3254670. PMID 22196723. 
  8. ^ Boettner DR, Huston CD, Linford AS, et al. (January 2008). "Entamoeba histolytica phagocytosis of human erythrocytes involves PATMK, a member of the transmembrane kinase family". PLoS Pathog. 4 (1): e8. doi:10.1371/journal.ppat.0040008. PMC 2211552. PMID 18208324. 
  9. ^ "DPDx - Amebiasis". Retrieved 2008-12-30. 
  10. ^ Grønlien HK, Berg T, Løvlie AM (July 2002). "In the polymorphic ciliate Tetrahymena vorax, the non-selective phagocytosis seen in microstomes changes to a highly selective process in macrostomes". J. Exp. Biol. 205 (Pt 14): 2089–97. PMID 12089212. 
  11. ^ Stibor H, Sommer U (April 2003). "Mixotrophy of a photosynthetic flagellate viewed from an optimal foraging perspective". Protist 154 (1): 91–8. doi:10.1078/143446103764928512. PMID 12812372. 

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