The Immune Features of Neutrophil and Neutrophil Immune Deviation Induced by Human SARS-COV-2 Infections
Journal of Pharmaceutical Research International · pp. 1–6 · Published 16 Sep 2022
10.9734/jpri/2022/v34i50B36437Abstract
Current published scientific works on human neutrophils have shown them to be heterogeneous in their immune functions. Activated neutrophil perform both up regulation and down regulation processes on other immune cells finalized by either tissue protection or tissue damage in virus human diseases. The objectives of the present opinion were to; I - make a show case analysis for the immune activities of neutrophil compartment both in children and adults with coviod-19 illness and ii - to deduce the possible existence of immune deviation mechanisms in this disease .The absolute numbers of circulating neutrophils in childhood and adulthood patients with sars-cov-2 infection were correlated with the infection severity .It was apparent that there was inhibition of T cell mediated immune responses with an elevated sars-cov-2 anti-spike antibodies in continuum with activated immature neutrophil phenotypes that might be induced by the virus antigens and can either preserve or damage the affected tissue. The antibody may directly inhibit T cells or activate neutrophil phenotype to inhibit T cell responses. The features of this immune deviation are; i – Conditional, ii – reversible, iii – associated with active functional state, iv – the virus antigen induced chemokine that orchestrate neutrophil and induce hyper-cytokinemia, v – acquisition of molecular surface markers variation and appearance of inhibitory markers, vi – the neutrophil/lymphocyte ration dis-proportionated, vii – activation consequences leaves tissue pathology at most, and viii – The inflammatory circuit stages may serve drug target identification and development. Thus the opinion suggest that the absolute number of circulating neutrophils is correlated with disease severity and the existence of neutrophil immune deviation in covid-19 human disease.
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