Research Article
NF-KB: A Key Transcription Factor in Cytokine Storm of Patients with COVID
Shrihari T G*
Corresponding Author: Shrihari T G, Assistant Professor, Department of Oral Medicine and Oral Oncology, Krishna Devaraya College of Dental Sciences and Hospital, Bangalore -562157, Karnataka, India
Received: September 05, 2022; Revised: October 09, 2022; Accepted: October 12, 2022 Available Online: November 4 , 2022
Citation: Shrihari TG. (2023) NF-KB: A Key Transcription Factor in Cytokine Storm of Patients with COVID. J Microbiol Microb Infect, 5(1): 157-158.
Copyrights: ©2023 Shrihari TG. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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SARS- COVID2 is a current global pandemic infectious disease caused by corona virus affecting mankind worldwide. Surface antigenic glycoprotein present on the virus recognized by PRR(Pattern recognition receptors) belongs to TLR activate NF-KB a key transcription factor, deregulated NF-KB, a key transcription factor involved in activation of inflammatory mediators responsible for cytokine storm involved in lung damage, pulmonary thrombosis, pulmonary fibrosis, and severe acute respiratory distress syndrome, later leads to death. This article brief about the role of NF-KB, a key transcription factor in cytokine storm of patients with SARS-COVID 2.

Keywords: IL-1, IL-6, TNF-α, ikB, SARS, UPA, Mmp’s

SARS-COVID2 is a global pandemic infectious disease caused by corona virus has an affinity to bind to ACE receptors present on the lungs. NF-KB is a ubiquitous transcription factor present in cytosol of every cell. NF-KB a key transcription factor controls more than 500 genes. NF-KB a key transcription factor normally in an inactive state byIkb (inhibitory kappa beta) factor, when activation degradation of IKB occurs [1-6].


Activation of NF-KB by surface antigenic glycoprotein of corona virus results in NF-KB binding to DNA by shifting the NF-KB a key transcription factor from cytosol to nucleus leads to transcription of inflammatory mediators [7-9]. Deregulated NF-KB activation results in release of inflammatory mediators responsible for cytokine storm from chronic inflammatory cells such as neutrophils, macrophages, and mast cells release cytokines (IL-1,TNF-α,IL-6,TGF-β), free radicals (ROS,RNS), proteolytic enzymes (UPA, Mmp’s2,9),chronic inflammation (IL-1,TNF-α,IL-6), angiogenesis (IL-8,COX-2,HIF-1α), immune modulation by (IL10,IL-4,IL-5,IL-13)  involved in lung damage, pulmonary fibrosis, pneumonia, pulmonary thrombosis, and Severe Acute respiratory distress syndrome(SARS) then later death. Cytokine storm in SARS-COVID patients is mainly by NF-KB key transcription factor activation is graded in to mild, moderate, and severe responsible for disease severity causes lung alveoli damage, pneumonia, severe acute respiratory disease, acts as a therapeutic target and prognostic marker [10-16].


NF-KB, a key transcription factors a ubiquitous transcription factor activated by surface glycoprotein present on the corona virus. NF-KB, a key transcription factor activates inflammatory mediators such as cytokines, growth factors, and proteolytic enzymes involved in lung damage. Thorough understanding of NF-KB transcription factor activation and it’s mechanisms of actions in patients with SARS-COVID2 helpful for therapeutic target and prognostic marker.
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