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Protein PGLYRP1/Tag7 Peptides Decrease the Proinflammatory Response in Human Blood Cells and Mouse Model of Diffuse
Tatiana N Sharapova1, Elena A Romanova1, Aleksandr S Chernov2
1Laboratory of Molecular Immunogenetics of Cancer, Institute of Gene Biology RAS, Vavilova 34/5, 111394 Moscow, Russia.
Abstract:
Infection caused by the severe acute respiratory syndrome coronavirus (SARS-CoV-2) in many cases is accompanied by the release of a large amount of proinflammatory cytokines in an event known as "cytokine storm", which is associated with severe coronavirus disease 2019 (COVID-19) cases and high mortality. The excessive production of proinflammatory cytokines is linked, inter alia, to the enhanced activity of receptors capable of recognizing the conservative regions of pathogens and cell debris, namely TLRs, TREM-1 and TNFR1. Here we report that peptides derived from innate immunity protein Tag7 inhibit activation of TREM-1 and TNFR1 receptors during acute inflammation. Peptides from the N-terminal fragment of Tag7 bind only to TREM-1, while peptides from the C-terminal fragment interact solely with TNFR1. Selected peptides are capable of inhibiting the production of proinflammatory cytokines both in peripheral blood mononuclear cells (PBMCs) from healthy donors and in vivo in the mouse model of acute lung injury (ALI) by diffuse alveolar damage (DAD). Treatment with peptides significantly decreases the infiltration of mononuclear cells to lungs in animals with DAD. Our findings suggest that Tag7-derived peptides might be beneficial in terms of the therapy or prevention of acute lung injury, e.g., for treating COVID-19 patients with severe pulmonary lesions.
Insights
New peptides from the Tag7 protein can inhibit key receptors involved in severe inflammation, potentially offering a novel therapy for acute lung injury and COVID-19 complications.
Area of Science:
- Immunology
- Molecular Biology
- Pathology
Background:
- Severe acute respiratory syndrome coronavirus (SARS-CoV-2) infections can trigger a
- cytokine storm
- leading to severe coronavirus disease 2019 (COVID-19) and high mortality.
- This excessive inflammation is linked to overactive receptors like TREM-1 and TNFR1.
- Innate immunity protein Tag7 plays a role in regulating immune responses.
Purpose of the Study:
- To investigate the potential of Tag7-derived peptides in modulating inflammatory responses.
- To determine if these peptides can inhibit TREM-1 and TNFR1 activation.
- To evaluate the therapeutic potential of Tag7 peptides in acute lung injury (ALI) models.
Main Methods:
- Peptide synthesis from N-terminal and C-terminal fragments of Tag7.
- Assays using peripheral blood mononuclear cells (PBMCs) from healthy donors.
- In vivo studies using a mouse model of acute lung injury (ALI) with diffuse alveolar damage (DAD).
Main Results:
- Tag7-derived peptides selectively inhibit TREM-1 (N-terminal) and TNFR1 (C-terminal) receptors.
- Peptides reduced proinflammatory cytokine production in PBMCs and in the ALI mouse model.
- Treatment decreased mononuclear cell infiltration into the lungs of DAD model animals.
Conclusions:
- Tag7-derived peptides demonstrate potent anti-inflammatory properties by targeting TREM-1 and TNFR1.
- These peptides show promise for preventing or treating acute lung injury, including severe pulmonary manifestations of COVID-19.
- Further research into Tag7 peptides could lead to novel therapeutic strategies for inflammatory lung diseases.
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