Silva, M. T. When two is better than one: macrophages and neutrophils work in concert in innate immunity as complementary and cooperative partners of a myeloid phagocyte system. J. Leukoc. Biol. 87, 93-106

Instituto de Biologia Molecular e Celular, Rua do Campo Alegre 823, Porto, Portugal.
Journal of leukocyte biology (Impact Factor: 4.29). 01/2010; 87(1):93-106. DOI: 10.1189/jlb.0809549
Source: PubMed


The antimicrobial effector activity of phagocytes is crucial in the host innate defense against infection, and the classic view is that the phagocytes operating against intracellular and extracellular microbial pathogens are,respectively, macrophages and neutrophils. As a result of the common origin of the two phagocytes, they share several functionalities, including avid phagocytosis,similar kinetic behavior under inflammatory/infectious conditions, and antimicrobial and immunomodulatory activities. However, consequent to specialization during their differentiation, macrophages and neutrophils acquire distinctive, complementary features that originate different levels of antimicrobial capacities and cytotoxicity and different tissue localization and lifespan.This review highlights data suggesting the perspective that the combination of overlapping and complementary characteristics of the two professional phagocytes promotes their cooperative participation as effectors and modulators in innate immunity against infection and as orchestrators of adaptive immunity. In the concerted activities operating in antimicrobial innate immunity, macrophages and neutrophils are not able to replace each other. The common and complementary developmental,kinetic, and functional properties of neutrophils and macrophages make them the effector arms of a myeloid phagocyte system that groups neutrophils with members of the old mononuclear phagocyte system. The use by mammals of a system with two dedicated phagocytic cells working cooperatively represents an advantageous innate immune attack strategy that allows the efficient and safe use of powerful but dangerous microbicidal molecules.This crucial strategy is a target of key virulence mechanisms of successful pathogens.

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    • "Macrophages and neutrophils are central mediators of the innate immune system that act at early stages of bacterial infection and have the ability to clear the pathogen through phagocytosis and subsequent digestion (Mantovani et al., 2011; Wynn et al., 2013). Besides their overlapping functional properties, macrophages, and neutrophils also display distinct and specialized features allowing their concerted and cooperative action against pathogens (Appelberg, 2007; Silva, 2010; Silva and Correia-Neves, 2012). Accordingly to their antimicrobial capacity, toxicity, and lifespan, macrophages and neutrophils have different localizations. "

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    • "However, Mtb that escape the granuloma enter into the bloodstream and will encounter neutrophils as the dominant phagocytic cell[4,5]. Neutrophils express myeloperoxidase (MPO), and monocytes can be induced to express MPO during infection[6]. MPO is an enzyme that shares some catalytic resemblance to Mtb catalase-peroxidase (KatG) to produce reactive metabolites (through the peroxidation cycle)[7], but additionally generates hypochlorous acid (HOCl, through the chlorination cycle)[8]. "
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    • "After karyorrhexis extensive plasma membrane blebbing occurs forming apoptotic bodies which contains organelle and nuclear fragments in their cytoplasm (Elmore, 2007). Cells of myeloid series i.e., macrophages are main cells involved in apoptotic cells phagocytosis and thus can result in passive necrosis (hetrophagic necrosis) of phagocytized apoptotic cells (Silva, 2010; Henson and Hume, 2006; He et al., 2009; Odaka and Mizuochi, 1999; McIlroy et al., 2000). Apoptotic cells does not involve any inflammatory reaction as involved by necrotic cells because their plasma membrane remains intact and apoptotic cells are immediately engulfed by macrophages called as " Tingible body macrophages " so that not getting enough time to release their anti-inflammatory cytokines into the interstitial tissues (Elmore, 2007). "

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