A novel definition and treatment of hyperinflammation in COVID-19 based on purinergic signalling.
Adenosine Triphosphate
/ metabolism
Anti-Inflammatory Agents
/ therapeutic use
COVID-19
/ immunology
Critical Care
Cytokine Release Syndrome
/ drug therapy
Humans
Inflammation
/ drug therapy
Infusions, Subcutaneous
Lidocaine
/ administration & dosage
Lymph Nodes
/ immunology
Lymphatic System
/ immunology
Male
Maximum Tolerated Dose
Middle Aged
Models, Immunological
Purinergic P2X Receptor Antagonists
/ administration & dosage
Receptors, Purinergic
/ drug effects
Receptors, Purinergic P1
/ drug effects
Receptors, Purinergic P2X7
/ physiology
Respiratory Distress Syndrome
/ drug therapy
Signal Transduction
T-Lymphocytes, Regulatory
/ immunology
COVID-19
Cytokine storm
Hyperinflammation
Immune paralysis
Lidocaine base
P2X7 receptor antagonist
Journal
Purinergic signalling
ISSN: 1573-9546
Titre abrégé: Purinergic Signal
Pays: Netherlands
ID NLM: 101250499
Informations de publication
Date de publication:
03 2022
03 2022
Historique:
received:
20
01
2021
accepted:
18
07
2021
pubmed:
11
11
2021
medline:
26
2
2022
entrez:
10
11
2021
Statut:
ppublish
Résumé
Hyperinflammation plays an important role in severe and critical COVID-19. Using inconsistent criteria, many researchers define hyperinflammation as a form of very severe inflammation with cytokine storm. Therefore, COVID-19 patients are treated with anti-inflammatory drugs. These drugs appear to be less efficacious than expected and are sometimes accompanied by serious adverse effects. SARS-CoV-2 promotes cellular ATP release. Increased levels of extracellular ATP activate the purinergic receptors of the immune cells initiating the physiologic pro-inflammatory immune response. Persisting viral infection drives the ATP release even further leading to the activation of the P2X7 purinergic receptors (P2X7Rs) and a severe yet physiologic inflammation. Disease progression promotes prolonged vigorous activation of the P2X7R causing cell death and uncontrolled ATP release leading to cytokine storm and desensitisation of all other purinergic receptors of the immune cells. This results in immune paralysis with co-infections or secondary infections. We refer to this pathologic condition as hyperinflammation. The readily available and affordable P2X7R antagonist lidocaine can abrogate hyperinflammation and restore the normal immune function. The issue is that the half-maximal effective concentration for P2X7R inhibition of lidocaine is much higher than the maximal tolerable plasma concentration where adverse effects start to develop. To overcome this, we selectively inhibit the P2X7Rs of the immune cells of the lymphatic system inducing clonal expansion of Tregs in local lymph nodes. Subsequently, these Tregs migrate throughout the body exerting anti-inflammatory activities suppressing systemic and (distant) local hyperinflammation. We illustrate this with six critically ill COVID-19 patients treated with lidocaine.
Identifiants
pubmed: 34757513
doi: 10.1007/s11302-021-09814-6
pii: 10.1007/s11302-021-09814-6
pmc: PMC8578920
doi:
Substances chimiques
Anti-Inflammatory Agents
0
Purinergic P2X Receptor Antagonists
0
Receptors, Purinergic
0
Receptors, Purinergic P1
0
Receptors, Purinergic P2X7
0
Adenosine Triphosphate
8L70Q75FXE
Lidocaine
98PI200987
Types de publication
Case Reports
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
13-59Informations de copyright
© 2021. The Author(s).
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