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. 2023 Apr 28;2(3):202-211.
doi: 10.1016/j.imj.2023.04.006. eCollection 2023 Sep.

The role of SARS-COV-2 infection in promoting abnormal immune response and sepsis: A comparison between SARS-COV-2-related sepsis and sepsis from other causes

Affiliations

The role of SARS-COV-2 infection in promoting abnormal immune response and sepsis: A comparison between SARS-COV-2-related sepsis and sepsis from other causes

Andrea Piccioni et al. Infect Med (Beijing). .

Abstract

Background: COVID-19 caused by SARS-CoV-2 virus is characterized by respiratory compromise and immune system involvement, even leading to serious disorders, such as cytokine storm.

Methods: We then conducted a literature review on the topic of sepsis and covid-19, and in parallel conducted an experimental study on the histological finding of patients who died from SARS-Covid 19 infection and a control group.

Results: Sepsis associated with covid-19 infection has some similarities and differences from that from other causes.

Conclusion: In this paper the complex interplay between the 2 disorders was discussed, focusing on the similarities and on the effect that one could have on the other. A preliminary experimental section that demonstrates the multisystemic involvement in subjects who die from SARS-CoV-2 is also proposed.

Keywords: Cytokine storm; SARS-COV-2; SARS-CoV-2; Sepsis; Septic shock.

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Figures

Image, graphical abstract
Graphical abstract
Fig 1
Fig. 1
Histological findings (H&E, × 40, × 60): congestion, edema fluid focally, and perivascular lymphocytic cuffing (arrow black) and inflammatory cells within the septa.
Fig 2
Fig. 2
Sepsis and SARS-CoV-2 are both complicated diseases in which a variety of organs and systems are involved. In particular, in sepsis, brain dysfunction, and metabolic alterations are predominant, while in SARS-CoV-2 endothelial and lung dysfunction are common. Yet, other organs can be targeted as well and sometimes their characteristics can overlap. Interestingly in both conditions, a cytokine storm can take place and trigger at least in part the different dysfunctions.
Fig 3
Fig. 3
IHC behavior at antiprocalcitonin antibody. A (400×): lung cytoplasmic macrophages positivity; B–F (400×): blood vessels positivity; C (400×): ductal epithelium positivity; C (400×): ductal epithelium positivity; D (400×): glomerular positivity; E (400×): inflammatory cell positivity in lung alveolar septa; G (400×): hepatocyte positivity; H (400×): renal tubules positivity.

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