Cargando…

A Comparison between SARS-CoV-2 and Gram-Negative Bacteria-Induced Hyperinflammation and Sepsis

Sepsis is a life-threatening condition caused by the body’s overwhelming response to an infection, such as pneumonia or urinary tract infection. It occurs when the immune system releases cytokines into the bloodstream, triggering widespread inflammation. If not treated, it can lead to organ failure...

Descripción completa

Detalles Bibliográficos
Autores principales: Brandenburg, Klaus, Ferrer-Espada, Raquel, Martinez-de-Tejada, Guillermo, Nehls, Christian, Fukuoka, Satoshi, Mauss, Karl, Weindl, Günther, Garidel, Patrick
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10607443/
https://www.ncbi.nlm.nih.gov/pubmed/37894850
http://dx.doi.org/10.3390/ijms242015169
_version_ 1785127542769844224
author Brandenburg, Klaus
Ferrer-Espada, Raquel
Martinez-de-Tejada, Guillermo
Nehls, Christian
Fukuoka, Satoshi
Mauss, Karl
Weindl, Günther
Garidel, Patrick
author_facet Brandenburg, Klaus
Ferrer-Espada, Raquel
Martinez-de-Tejada, Guillermo
Nehls, Christian
Fukuoka, Satoshi
Mauss, Karl
Weindl, Günther
Garidel, Patrick
author_sort Brandenburg, Klaus
collection PubMed
description Sepsis is a life-threatening condition caused by the body’s overwhelming response to an infection, such as pneumonia or urinary tract infection. It occurs when the immune system releases cytokines into the bloodstream, triggering widespread inflammation. If not treated, it can lead to organ failure and death. Unfortunately, sepsis has a high mortality rate, with studies reporting rates ranging from 20% to over 50%, depending on the severity and promptness of treatment. According to the World Health Organization (WHO), the annual death toll in the world is about 11 million. One of the main toxins responsible for inflammation induction are lipopolysaccharides (LPS, endotoxin) from Gram-negative bacteria, which rank among the most potent immunostimulants found in nature. Antibiotics are consistently prescribed as a part of anti-sepsis-therapy. However, antibiotic therapy (i) is increasingly ineffective due to resistance development and (ii) most antibiotics are unable to bind and neutralize LPS, a prerequisite to inhibit the interaction of endotoxin with its cellular receptor complex, namely Toll-like receptor 4 (TLR4)/MD-2, responsible for the intracellular cascade leading to pro-inflammatory cytokine secretion. The pandemic virus SARS-CoV-2 has infected hundreds of millions of humans worldwide since its emergence in 2019. The COVID-19 (Coronavirus disease-19) caused by this virus is associated with high lethality, particularly for elderly and immunocompromised people. As of August 2023, nearly 7 million deaths were reported worldwide due to this disease. According to some reported studies, upregulation of TLR4 and the subsequent inflammatory signaling detected in COVID-19 patients “mimics bacterial sepsis”. Furthermore, the immune response to SARS-CoV-2 was described by others as “mirror image of sepsis”. Similarly, the cytokine profile in sera from severe COVID-19 patients was very similar to those suffering from the acute respiratory distress syndrome (ARDS) and sepsis. Finally, the severe COVID-19 infection is frequently accompanied by bacterial co-infections, as well as by the presence of significant LPS concentrations. In the present review, we will analyze similarities and differences between COVID-19 and sepsis at the pathophysiological, epidemiological, and molecular levels.
format Online
Article
Text
id pubmed-10607443
institution National Center for Biotechnology Information
language English
publishDate 2023
publisher MDPI
record_format MEDLINE/PubMed
spelling pubmed-106074432023-10-28 A Comparison between SARS-CoV-2 and Gram-Negative Bacteria-Induced Hyperinflammation and Sepsis Brandenburg, Klaus Ferrer-Espada, Raquel Martinez-de-Tejada, Guillermo Nehls, Christian Fukuoka, Satoshi Mauss, Karl Weindl, Günther Garidel, Patrick Int J Mol Sci Review Sepsis is a life-threatening condition caused by the body’s overwhelming response to an infection, such as pneumonia or urinary tract infection. It occurs when the immune system releases cytokines into the bloodstream, triggering widespread inflammation. If not treated, it can lead to organ failure and death. Unfortunately, sepsis has a high mortality rate, with studies reporting rates ranging from 20% to over 50%, depending on the severity and promptness of treatment. According to the World Health Organization (WHO), the annual death toll in the world is about 11 million. One of the main toxins responsible for inflammation induction are lipopolysaccharides (LPS, endotoxin) from Gram-negative bacteria, which rank among the most potent immunostimulants found in nature. Antibiotics are consistently prescribed as a part of anti-sepsis-therapy. However, antibiotic therapy (i) is increasingly ineffective due to resistance development and (ii) most antibiotics are unable to bind and neutralize LPS, a prerequisite to inhibit the interaction of endotoxin with its cellular receptor complex, namely Toll-like receptor 4 (TLR4)/MD-2, responsible for the intracellular cascade leading to pro-inflammatory cytokine secretion. The pandemic virus SARS-CoV-2 has infected hundreds of millions of humans worldwide since its emergence in 2019. The COVID-19 (Coronavirus disease-19) caused by this virus is associated with high lethality, particularly for elderly and immunocompromised people. As of August 2023, nearly 7 million deaths were reported worldwide due to this disease. According to some reported studies, upregulation of TLR4 and the subsequent inflammatory signaling detected in COVID-19 patients “mimics bacterial sepsis”. Furthermore, the immune response to SARS-CoV-2 was described by others as “mirror image of sepsis”. Similarly, the cytokine profile in sera from severe COVID-19 patients was very similar to those suffering from the acute respiratory distress syndrome (ARDS) and sepsis. Finally, the severe COVID-19 infection is frequently accompanied by bacterial co-infections, as well as by the presence of significant LPS concentrations. In the present review, we will analyze similarities and differences between COVID-19 and sepsis at the pathophysiological, epidemiological, and molecular levels. MDPI 2023-10-14 /pmc/articles/PMC10607443/ /pubmed/37894850 http://dx.doi.org/10.3390/ijms242015169 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Brandenburg, Klaus
Ferrer-Espada, Raquel
Martinez-de-Tejada, Guillermo
Nehls, Christian
Fukuoka, Satoshi
Mauss, Karl
Weindl, Günther
Garidel, Patrick
A Comparison between SARS-CoV-2 and Gram-Negative Bacteria-Induced Hyperinflammation and Sepsis
title A Comparison between SARS-CoV-2 and Gram-Negative Bacteria-Induced Hyperinflammation and Sepsis
title_full A Comparison between SARS-CoV-2 and Gram-Negative Bacteria-Induced Hyperinflammation and Sepsis
title_fullStr A Comparison between SARS-CoV-2 and Gram-Negative Bacteria-Induced Hyperinflammation and Sepsis
title_full_unstemmed A Comparison between SARS-CoV-2 and Gram-Negative Bacteria-Induced Hyperinflammation and Sepsis
title_short A Comparison between SARS-CoV-2 and Gram-Negative Bacteria-Induced Hyperinflammation and Sepsis
title_sort comparison between sars-cov-2 and gram-negative bacteria-induced hyperinflammation and sepsis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10607443/
https://www.ncbi.nlm.nih.gov/pubmed/37894850
http://dx.doi.org/10.3390/ijms242015169
work_keys_str_mv AT brandenburgklaus acomparisonbetweensarscov2andgramnegativebacteriainducedhyperinflammationandsepsis
AT ferrerespadaraquel acomparisonbetweensarscov2andgramnegativebacteriainducedhyperinflammationandsepsis
AT martinezdetejadaguillermo acomparisonbetweensarscov2andgramnegativebacteriainducedhyperinflammationandsepsis
AT nehlschristian acomparisonbetweensarscov2andgramnegativebacteriainducedhyperinflammationandsepsis
AT fukuokasatoshi acomparisonbetweensarscov2andgramnegativebacteriainducedhyperinflammationandsepsis
AT mausskarl acomparisonbetweensarscov2andgramnegativebacteriainducedhyperinflammationandsepsis
AT weindlgunther acomparisonbetweensarscov2andgramnegativebacteriainducedhyperinflammationandsepsis
AT garidelpatrick acomparisonbetweensarscov2andgramnegativebacteriainducedhyperinflammationandsepsis
AT brandenburgklaus comparisonbetweensarscov2andgramnegativebacteriainducedhyperinflammationandsepsis
AT ferrerespadaraquel comparisonbetweensarscov2andgramnegativebacteriainducedhyperinflammationandsepsis
AT martinezdetejadaguillermo comparisonbetweensarscov2andgramnegativebacteriainducedhyperinflammationandsepsis
AT nehlschristian comparisonbetweensarscov2andgramnegativebacteriainducedhyperinflammationandsepsis
AT fukuokasatoshi comparisonbetweensarscov2andgramnegativebacteriainducedhyperinflammationandsepsis
AT mausskarl comparisonbetweensarscov2andgramnegativebacteriainducedhyperinflammationandsepsis
AT weindlgunther comparisonbetweensarscov2andgramnegativebacteriainducedhyperinflammationandsepsis
AT garidelpatrick comparisonbetweensarscov2andgramnegativebacteriainducedhyperinflammationandsepsis