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Phagocyte Intro edit
Phagocytes (from the Greek words phagein, meaning 'to eat or devour', and kutos, meaning 'hollow vessel')[1][2] are cells that are found in the blood, bone marrow and other tissues of vertebrates.[3] Phagocytes ingest pathogenic and infectious agents in the body.[4] Like all cells involved in the immune system, they originate in the bone marrow. Phagocytes derive from a group of stem cells in the bone marrow called myeloid progenitor cells. Phagocytes are the basis of defense in the innate immune system; these cells ingest pathogens and often take part in antigen presentation.[5] Phagocytes were first discovered in 1882 by Ilya Ilyich Mechnikov while he was studying the larvae of starfishes.[6] For his findings Mechnikov was awarded the 1908 Nobel Prize in Physiology or Medicine along with with Paul Ehrlich.[7] The professional phagocytes include neutrophils,monocytes, tissue macrophages, dendritic cells, and possibly mast cells. [8] The main distinguishing factor between professional and non-professional phagocytes is that professional phagocytes have receptors that aid in phagocytosis while non-professional phagocytes do not. [9] Of the professional phagocytes two are known to be professional antigen presenting cells: macrophages and dendritic cells.[10]
During an infection signals are given off that attract phagocytes to the site of infection. These signals may come from bacteria, complement factors, or tissue macrophages (already at the site of infection).[5] The phagocytes going to the site of infection must also be able to cross endothelial barriers. The signals given off that attract the phagocytes also promote a series of binding reactions that enable the phagocytes to cross the endothelial cell barrier.[11] Once across the cell barrier, the phagocytes follow the signal to the cite of infection through a process called chemotaxis.[5] When the phagocyte comes in contact with infectious agents, the foreign body binds to the receptors on the phagocyte's surface. After the agent is bound to the receptors the phagocyte extends its pseudopodium around the agent and engulfs it through the process of phagocytosis.[5] Once the agent is englufed the phagocyte can use methods to kill it that depend on reactive oxygen compunds that kill the bacteria because of their toxicity. In neutrophils and monocytes an enzyme called myeloperoxidase is used to further advance the use of toxic substances to kill the infectious agent.[12] The phagocyte can also use methods of killing without using oxygen. These methods involve using enzymes to destroy certain parts of the bacteria and using a substance called lactoferrin that deprives the bacteria of iron.[5] Macrophages also participate in extra-cellular killing of microbes by releasing nitric oxide.[13] After phagocytosis macrophages and dendritic cells may participate in antigen presentation. During this process antigens are taken from the pathogen or its by-products. These antigens are then converted into peptides and taken to the surface of the cell. Once at the surface the peptides are recognized by T cells.[14]
- The types of phagocytes include neutrophils, macrophages, and monocytes.[15] Dendritic cells also participate in phagocytosis and presentation of antigens to other cells that are important in the immune response.[16]
Host damage by phagocytes edit
Acute lung injury edit
Neutrophils are a main component of many acute lung injury (ALI) cases; experiments have shown that a reduction in the number of neutrophils lessens the effects of ALI.[17] The steps to lung damage by neutrophils start with the neutrophil migration through pulmonary microvasculature (this includes the adhesion process). Then neutrophils are activated and begin to fight microbes (with reactive oxygen compunds and proteolytic enzymes).[18] When neutrophils respond to infection they phagocytise the invader and then release granule contents into the phagosome. However, sometimes the granule contents are released outside the cell (this occurs when the release of these substances is unregulated). The microbicidal substances that were released now damage surrounding host tissue. Other compunds (elastase for example) change the pulmonary cells by combining to surface receptors and through signal transduction. These changes may have positive or negative results.[19]
Septic shock edit
TNF-alpha is an important chemical that is released by macrophages: it causes the blood in small vessels to clot (this keeps an infection from spreading). However if an infection spreads to the blood, this helpful chemical can then produce negative results. If the infection has spread to the blood stream TNF-alpha will be released in vital organs (the liver, for example) and can cause vasodilation along with a decrease in plasma volume; this in turn will be followed by shock. Also during septic shock, because TNF-alpha causes clotting, small vessels will be blocked off and many vital organs may fail. Septic shock may lead to death.[11]
Granulocyte Types edit
Basophil edit
Basophils are one of the least abundant cells in bone marrow and blood (ocurring at less than two percent of all cells). Like neutrophils and eosinophils they have lobed nuclei; however they only have two lobes and the chromatin filaments that connect them are not very visible. Basophils have receptors that can bind to IgE, IgG, complement, and histamine. The cytoplasm of basophils contains a varied amount of granules; these granules are usually numerous enough to partially conceal the nucleus. Granule contents of basophils are abundant with histamine, heparin, chondroitin sulfate, peroxidase, platelet activating factor, and other substances. When an infection occurs mature basophils will be released from the bone marrow and travel to the site of infection. [20]
Degranulation edit
Compunds stored in granules are released through three different ways: classical exocytosis, piecemeal degranulation, and cytolysis. Eosinophils are capable of all three of these processes. Basophils are capable of classical eoxcytosis (called anaphylactic degranulation in basophils) and piecemeal degranulation. Neutrophils are capable of classical exocytosis.
Classical exocytosis edit
Piecemeal degranulation edit
Cytolysis edit
- ^ "phago-". Dictionary.com. Retrieved 2008-11-12.
- ^ "-cyte". Dictionary.com. Retrieved 2008-11-13.
- ^ Van Ginderachter JA, Movahedi K, Hassanzadeh Ghassabeh G; et al. (2006). "Classical and alternative activation of mononuclear phagocytes: picking the best of both worlds for tumor promotion". Immunobiology. 211 (6–8): 487–501. doi:10.1016/j.imbio.2006.06.002. PMID 16920488. Retrieved 2008-11-01.
{{cite journal}}: Explicit use of et al. in:|author=(help)CS1 maint: multiple names: authors list (link) - ^ Langermans, JA (1994-09-14). "Antimicrobial functions of mononuclear phagocytes". Journal of Immunological Methods. 174 (1–2): 185–94. PMID 8083520. Retrieved 2008-11-13.
{{cite journal}}: Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ a b c d e Mayer, Gene (2006). "Immunology — Chapter One: Innate (non-specific) Immunity". Microbiology and Immunology On-Line Textbook. USC School of Medicine. Retrieved 2008-11-12.
- ^ "Ilya Mechnikov". The Nobel Foundation. Retrieved 2008-11-28.
- ^ Schmalstieg, FC (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. PMID 18463079. Retrieved 2008-11-28.
{{cite journal}}: Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ Robinson p. 187 and Ernst pp. 7–10
- ^ Ernst p. 10
- ^ "Antigen Presenting Cells (APC)". Dalhousie University. Retrieved 2008-11-13.
- ^ a b Janeway, Charles A. Induced innate responses to infection. ISBN 978-0-8153-4123-9.
{{cite book}}: Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ Klebenoff, SJ (1999). "Myeloperoxidase". Proceedings of the Association of American Physicians. 111 (5): 383–9. PMID 10519157. Retrieved 2008-12-30.
{{cite journal}}: Cite has empty unknown parameter:|coauthors=(help) - ^ Masek, Katherine S. (2007). Eurekah Bioscience Collection: Macrophage Effector Functions. Landes Bioscience.
{{cite book}}: Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ Janeway, Charles A. (2007). Immunobiology: Antigen Presentation to T Lymphocytes. Garland Science. ISBN 978-0-8153-4123-9.
{{cite book}}: Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ Miyasaki, Ken. "Phagocytes-Neutrophils". Retrieved 2008-11-13.
- ^ Guermonprez, P (2002). "Antigen presentation and T cell stimulation by dendritic cells". Annual Review of Immunology. 20: 621–67. PMID 11861614. Retrieved 2008-11-12.
{{cite journal}}: Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ Abraham E (2003). "Neutrophils and acute lung injury". Crit. Care Med. 31 (4 Suppl): S195–9. doi:10.1097/01.CCM.0000057843.47705.E8. PMID 12682440. Retrieved 2009-01-20.
{{cite journal}}: Unknown parameter|month=ignored (help) - ^ Lee WL, Downey GP (2001). "Neutrophil activation and acute lung injury". Curr Opin Crit Care. 7 (1): 1–7. PMID 11373504. Retrieved 2009-01-20.
{{cite journal}}: Unknown parameter|month=ignored (help) - ^ Moraes TJ, Zurawska JH, Downey GP (2006). "Neutrophil granule contents in the pathogenesis of lung injury". Curr. Opin. Hematol. 13 (1): 21–7. PMID 16319683.
{{cite journal}}:|access-date=requires|url=(help); Unknown parameter|month=ignored (help)CS1 maint: multiple names: authors list (link) - ^ Hess, Charles E. "Mature Basophil". University of Virginia Health System. Retrieved 2009-04-10.