Phagocyte

Long rod-shaped bacteria, one of which has been partially engulfed by a larger blob-shaped white blood cell. The shape of the cell is distorted by undigested bacterium inside it.
Scanning electron micrograph of a neutrophil phagocytosing anthrax bacilli (orange)

Phagocytes are cells that protect the body by ingesting harmful foreign particles, bacteria, and dead or dying cells. Their name comes from the Greek phagein, "to eat" or "devour", and "-cyte", the suffix in biology denoting "cell", from the Greek kutos, "hollow vessel". They are essential for fighting infections and for subsequent immunity. Phagocytes are important throughout the animal kingdom[1] and are highly developed within vertebrates.[2] One litre of human blood contains about six billion phagocytes.[3] They were discovered in 1882 by Ilya Ilyich Mechnikov while he was studying starfish larvae.[4] Mechnikov was awarded the 1908 Nobel Prize in Physiology or Medicine for his discovery.[5] Phagocytes occur in many species; some amoebae behave like macrophage phagocytes, which suggests that phagocytes appeared early in the evolution of life.[6]

Phagocytes of humans and other animals are called "professional" or "non-professional" depending on how effective they are at phagocytosis.[7] The professional phagocytes include many types of white blood cells (such as neutrophils, monocytes, macrophages, mast cells, and dendritic cells).[8] The main difference between professional and non-professional phagocytes is that the professional phagocytes have molecules called receptors on their surfaces that can detect harmful objects, such as bacteria, that are not normally found in the body. Non-professional phagocytes do not have efficient phagocytic receptors, such as those for opsonins.[9] Phagocytes are crucial in fighting infections, as well as in maintaining healthy tissues by removing dead and dying cells that have reached the end of their lifespan.[10]

During an infection, chemical signals attract phagocytes to places where the pathogen has invaded the body. These chemicals may come from bacteria or from other phagocytes already present. The phagocytes move by a method called chemotaxis. When phagocytes come into contact with bacteria, the receptors on the phagocyte's surface will bind to them. This binding will lead to the engulfing of the bacteria by the phagocyte.[11] Some phagocytes kill the ingested pathogen with oxidants and nitric oxide.[12] After phagocytosis, macrophages and dendritic cells can also participate in antigen presentation, a process in which a phagocyte moves parts of the ingested material back to its surface. This material is then displayed to other cells of the immune system. Some phagocytes then travel to the body's lymph nodes and display the material to white blood cells called lymphocytes. This process is important in building immunity,[13] and many pathogens have evolved methods to evade attacks by phagocytes.[14]

  1. ^ Delves et al. 2006, p. 250
  2. ^ Delves et al. 2006, p. 251
  3. ^ Hoffbrand, Pettit & Moss 2005, p. 331
  4. ^ Ilya Mechnikov, retrieved on November 28, 2008. From Nobel Lectures, Physiology or Medicine 1901–1921, Elsevier Publishing Company, Amsterdam, 1967. Archived August 22, 2008, at the Wayback Machine
  5. ^ Schmalstieg, FC; AS Goldman (2008). "Ilya Ilich Metchnikoff (1845–1915) and Paul Ehrlich (1854–1915): the centennial of the 1908 Nobel Prize in Physiology or Medicine". Journal of Medical Biography. 16 (2): 96–103. doi:10.1258/jmb.2008.008006. PMID 18463079. S2CID 25063709.
  6. ^ Janeway, Chapter: Evolution of the innate immune system. retrieved on March 20, 2009
  7. ^ Ernst & Stendahl 2006, p. 186
  8. ^ Robinson & Babcock 1998, p. 187 and Ernst & Stendahl 2006, pp. 7–10
  9. ^ Ernst & Stendahl 2006, p. 10
  10. ^ Cite error: The named reference pathogenesis was invoked but never defined (see the help page).
  11. ^ Cite error: The named reference money was invoked but never defined (see the help page).
  12. ^ Fang FC (October 2004). "Antimicrobial reactive oxygen and nitrogen species: concepts and controversies". Nat. Rev. Microbiol. 2 (10): 820–32. doi:10.1038/nrmicro1004. PMID 15378046. S2CID 11063073.
  13. ^ Delves et al. 2006, pp. 172–84
  14. ^ Delves et al. 2006, pp. 2–10