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However, macrophages, especially alveolar macrophages, usually produce far lower levels of ROS than neutrophils, and may require activation for their bactericidal properties. Instead, their transient oxidative burst regulates the inflammatory response by inducing cytokine synthesis for redox signalling, resulting in an influx of neutrophils and ...
The C3a, C4a and C5a components are referred to as anaphylatoxins: [4] [5] they cause smooth muscle contraction, vasodilation, histamine release from mast cells, and enhanced vascular permeability. [5] They also mediate chemotaxis, inflammation, and generation of cytotoxic oxygen radicals. [5]
The binding of bacterial molecules to receptors on the surface of a macrophage triggers it to engulf and destroy the bacteria through the generation of a "respiratory burst", causing the release of reactive oxygen species. Pathogens also stimulate the macrophage to produce chemokines, which summon other cells to the site of infection. [2]
Beyond increasing inflammation and stimulating the immune system, macrophages also play an important anti-inflammatory role and can decrease immune reactions through the release of cytokines. Macrophages that encourage inflammation are called M1 macrophages, whereas those that decrease inflammation and encourage tissue repair are called M2 ...
Some inflammatory cytokines have additional roles such as acting as growth factors. [5] Pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α also trigger pathological pain. [1] While IL-1β is released by monocytes and macrophages, it is also present in nociceptive DRG neurons. IL-6 plays a role in neuronal reaction to an injury.
Macrophages have been classified as M1 or M2 depending on the adaptive immune response that elicited the phenotype: Th1 or Th2 respectively. [2] [4] [5] The phrase 'alternatively activated macrophage' is used to refer to M2 macrophages. [2] Regulatory macrophages do not fit into the M1/M2 classification system, and they display different ...
Cytokinins can also be produced by recycled tRNAs in plants and bacteria. [20] [21] tRNAs with anticodons that start with a uridine and carrying an already-prenylated adenosine adjacent to the anticodon release on degradation the adenosine as a cytokinin. [20] The prenylation of these adenines is carried out by tRNA-isopentenyltransferase. [21]
In macrophages, it has also been shown to signal via STAT3. The cytokine activates macrophages to inhibit fungal survival. It induces deprivation in intracellular free zinc and increases production of reactive oxygen species that culminate in fungal zinc starvation and toxicity. [9]