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Open Access March 01, 2022

Nicotinic agonists promoted the activation of nicotinic acetylcholine α7 receptors (α7 nAChR) in neurons, but failed to activate these receptors in mouse peritoneal macrophages

Abstract Nicotinic acetylcholine receptor (nAChR) of subtypes said "neuronal" are expressed in epithelial and immune system cells and participate in acetylcholine signaling by neural or non-neural pathways. It has been shown in macrophages that activation of type α7 nAChRs inhibits the release of pro-inflammatory cytokines, but the ion channel function has not been recorded in these cells. The objective of [...] Read more.
Nicotinic acetylcholine receptor (nAChR) of subtypes said "neuronal" are expressed in epithelial and immune system cells and participate in acetylcholine signaling by neural or non-neural pathways. It has been shown in macrophages that activation of type α7 nAChRs inhibits the release of pro-inflammatory cytokines, but the ion channel function has not been recorded in these cells. The objective of this work was to clarify what are the molecular mechanisms of transduction of α7 nAChRs in macrophages. To this end, RAW 264.7 cells, mouse peritoneal macrophages and rat hippocampal neurons were used. Cells were submitted to electrophysiological studies and stimulated with brief applications of the agonists acetylcholine, choline and nicotine, associated or not with the allosteric modulator PNU-120596. Responses to ATP were recorded as a reference. Furthermore, macrophages were submitted to cytokine quantitation. The electrophysiological results showed that macrophages responded to ATP but did not show whole-cell current by stimulation with nicotinic agonists. However, hippocampal neurons stimulated in the same pharmacological conditions of the macrophages showed ionic currents typical of the α7 nicotinic receptors. No effect of nicotine was observed in the lipopolysaccharide-induced TNF-α release. These results suggest that the α7 nAChR in macrophages do not work as ion channels similar to those expressed in neurons.
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Open Access June 21, 2021

COVID-19 and Human Immune Response: A Literature Based Review

Abstract Currently, the world is facing the COVID-19 epidemic, a disease caused by SARS-CoV-2. Emerging body of molecular evidences suggested a similar path to SARS and MERS viruses. A viral particles cascade enters into the human body through eyes, nose, and mouth, few of these viral particles reaches to the lower respiratory tract through breathing and here their spike protein act like a key and lock [...] Read more.
Currently, the world is facing the COVID-19 epidemic, a disease caused by SARS-CoV-2. Emerging body of molecular evidences suggested a similar path to SARS and MERS viruses. A viral particles cascade enters into the human body through eyes, nose, and mouth, few of these viral particles reaches to the lower respiratory tract through breathing and here their spike protein act like a key and lock into epithelial cells which are the air sacs in lungs. SARS-CoV-2 is undetectable for a longer period of time than many other flu and coronaviruses. Once they entered inside body, they overtake the cell’s machinery, replicate, multiply and infect the adjoining cells. All the viruses have a tell-tale signature on the surface known as antigens, identifying these antigens is what activate the immune system by producing the antibodies. Researchers have shown that a wide range of immune cells that react to SARS-CoV-2 and helps in recovery could be helpful in the development of potential vaccines.
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Keyword:  Immune cells

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