Macrophages are a critical factor within the immune response. Their ability to engulf and degrade target molecules is a main component of the innate immune response. Modulation to the site of tissue damage (inflammation), occurs through the process of signaling via cytokines. In addition, structural changes are induced through triggering the macrophage via trans-membrane protein responses
Introduction – Macrophage Overview
Macrophages are integral factors in the human immunological system. These cells typically referred to by the layperson as “white blood cells”, engulf foreign moieties that enter into the human body. Macrophages have major roles in the non-specific innate immune system and the specific adaptive immune system, either by direct participation to remove the foreign particle or by triggering the appropriate cellular response that will execute the given task (Elhelu, 1983). The primary mechanisms of action include the ingestion of cell components, viral particles, and foreign protein through phagocytosis. Macrophages may also act as antigen-presenting cells (APCs) for triggering the cascade leading to a T-cell mediated (secondary) immune response. Macrophages are derived from bone marrow-based mononuclear cells and inherently respond within the immune system during periods of inflammation (COPE, 2015). The structure of macrophages is optimal for the designated mechanisms of action. Hence macrophages are composed of actin filaments within their cytoskeleton, which allow for the cell to under-go unique conformational changes (Elhelu, 1983). This report will focus primarily on the cytoskeleton of the macrophage with respect to extracellular signaling.
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"Macrophages Cytoskeletal Considerations".
Extracellular Signaling (Migration) of Macrophage Phenotypes
Extracellular signaling impacts the modulation for different phenotypes and alters the behavior of the macrophage cytoskeleton. These behavioral changes contribute to the in-vivo inflammatory response. Subsequently, the inflammatory response is a highly regulated process involving process of signaling for initiating the inflammatory response and for halting the response, when it is no longer required (Fujiwara et.al, 2005). During the initiation of the immune response inflammation may be required and consists of cells such as eosinophils, neutrophils, basophils and mast cells (COPE, 2015). The observation of these cells localized within a particular area of the human body corresponds to tissue damage and/or infection with foreign moieties (COPE, 2015). Extracellular signals that are classified within the cytokine and interleukin family are responsible for triggering the movement of macrophages from their location of origin to the area requiring an innate or adaptive immune response (Fujiwara, 2005). Activation signals include the following cytokines: Interferon-gamma, granulocyte-monocyte colony stimulating factor and tumor necrosis factors (Fujiwara, 2005).
Structural Changes of Macrophage Phenotypes (Myocardiac Tissue Models)
A great example of macrophage modulation is observed in various myopathies of the heart. Hence, cardiac macrophages are typically abundant in the myocardial tissue after a patient has undergone an infraction (Franz, 2014). New research shows that the leucocytes of the heart play host to many different types of macrophages and that these varying phenotypes are critical for maintaining what is referred to as the “steady state:” (Franz, 2014).
These macrophages function to ingest degrading tissue, which may cause blockage in and/or around myocardial tissue, by ingesting cellular parts. After migration to the troubled area, these macrophages initiate changes in their structure by movement of the actin filament framework. The macrophage begins conformational changes after identifying a foreign entity or cell part requiring removal through a trans-membrane receptor. Subsequently, molecular identification must occur prior to initiating structural changes. Once the protein has bound to the macrophage the macrophage engulfs the molecule, generating a lysosome within said macrophage. Microfilaments move the lysosome to the phagosome where fusion of the phagosome and lysosome occur to generate the phagolysosome complex. Within the phagolysosome, the molecule is exposed to unfavorable conditions that normally lead to the death and/or degradation of the molecule. The contents are then transported by microfilaments to the edge of the cell wall where the phagolysosome fuses with the cell membrane and contents are then expelled from the macrophage (COPE, 2015)
Conclusion
Macrophages vary vastly in phenotypes, however, most share identical mechanisms of actions. Furthermore, the conformational changes that lead to the degradation of target molecules is highly conserved among various phenotypes (Franz, 2014). Modulation occurs by cell signaling to the site of inflammation and for initiating the induced ingestion processes. Various cardiomyopathies are impacted by macrophages, which may contribute to the maintenance of the steady state and in some cases yield serious negative impacts triggering a disease state.
