Abstract:Chemerin is one of the specialized pro-resolving mediators that participate in the early phase of inflammation and contribute to the initiation of the pro-resolving response. There is a paucity of data regarding the time course of chemerin during acute infections. We aimed to evaluate the sequence of inflammatory responses in the acute COVID-19 phase throughout onset and resolution of inflammation. We evaluated changes in selected biomarkers in COVID-19 survivors on the 7-day and 28-day follow up. Chemerin was… Show more
“…Furthermore, higher PTX3 plasma levels were found in 14 patients with subsequent thrombotic complications [ 36 ]. Sulicka-Grodzicka et al, in a manner consistent with previous work, found higher levels of PTX3 in severe COVID-19 patients than in non-severe COVID-19 [ 38 ]. The authors evaluated the sequence of inflammatory responses in acute COVID-19 through a 28-day follow-up, discovering that the resolution of inflammation in the group of moderate/severe SARS-CoV2 infection was associated with decreasing PTX3 serum concentrations [ 38 ].…”
Section: Resultssupporting
confidence: 82%
“…Sulicka-Grodzicka et al, in a manner consistent with previous work, found higher levels of PTX3 in severe COVID-19 patients than in non-severe COVID-19 [ 38 ]. The authors evaluated the sequence of inflammatory responses in acute COVID-19 through a 28-day follow-up, discovering that the resolution of inflammation in the group of moderate/severe SARS-CoV2 infection was associated with decreasing PTX3 serum concentrations [ 38 ]. The authors performed a time course analysis of PTX3 on day 1, day 7, and day 28 after infection [ 38 ].…”
Section: Resultssupporting
confidence: 82%
“…The authors evaluated the sequence of inflammatory responses in acute COVID-19 through a 28-day follow-up, discovering that the resolution of inflammation in the group of moderate/severe SARS-CoV2 infection was associated with decreasing PTX3 serum concentrations [ 38 ]. The authors performed a time course analysis of PTX3 on day 1, day 7, and day 28 after infection [ 38 ]. Their results revealed a constant and progressive decrease in PTX3 from day 1 to day 28 [ 38 ].…”
Section: Resultsmentioning
confidence: 99%
“…The authors performed a time course analysis of PTX3 on day 1, day 7, and day 28 after infection [ 38 ]. Their results revealed a constant and progressive decrease in PTX3 from day 1 to day 28 [ 38 ]. On other hand, analyzing inflammatory markers between non-severe COVID-19 and severe COVID-19, PTX3 was significant only on day 1, unlike TNFα and IL-1β, which were increased also 28 days post-infection [ 38 ].…”
Over the last three years, humanity has been facing one of the most serious health emergencies due to the global spread of Coronavirus disease (COVID-19). In this scenario, the research of reliable biomarkers of mortality from COVID-19 represents a primary objective. Pentraxin 3 (PTX3), a highly conserved protein of innate immunity, seems to be associated with a worse outcome of the disease. Based on the above, this systematic review and meta-analysis evaluated the prognostic potential of PTX3 in COVID-19 disease. We included 12 clinical studies evaluating PTX3 in COVID-19 patients. From our research, we found increased PTX3 levels compared to healthy subjects, and notably, PTX3 was even more augmented in severe COVID-19 rather than non-severe cases. Moreover, we performed a meta-analysis to establish if there were differences between ICU and non-ICU COVID-19 patients in PTX3-related death. We combined 5 studies for a total of 543 ICU vs. 515 non-ICU patients. We found high significative PTX3-related death in ICU COVID-19 hospitalized individuals (184 out of 543) compared to non-ICU (37 out of 515), with an overall effect OR: 11.30 [2.00, 63.73]; p = 0.006. In conclusion, we probed PTX3 as a reliable marker of poor outcomes after COVID-19 infection as well as a predictor of hospitalized patients’ stratification.
“…Furthermore, higher PTX3 plasma levels were found in 14 patients with subsequent thrombotic complications [ 36 ]. Sulicka-Grodzicka et al, in a manner consistent with previous work, found higher levels of PTX3 in severe COVID-19 patients than in non-severe COVID-19 [ 38 ]. The authors evaluated the sequence of inflammatory responses in acute COVID-19 through a 28-day follow-up, discovering that the resolution of inflammation in the group of moderate/severe SARS-CoV2 infection was associated with decreasing PTX3 serum concentrations [ 38 ].…”
Section: Resultssupporting
confidence: 82%
“…Sulicka-Grodzicka et al, in a manner consistent with previous work, found higher levels of PTX3 in severe COVID-19 patients than in non-severe COVID-19 [ 38 ]. The authors evaluated the sequence of inflammatory responses in acute COVID-19 through a 28-day follow-up, discovering that the resolution of inflammation in the group of moderate/severe SARS-CoV2 infection was associated with decreasing PTX3 serum concentrations [ 38 ]. The authors performed a time course analysis of PTX3 on day 1, day 7, and day 28 after infection [ 38 ].…”
Section: Resultssupporting
confidence: 82%
“…The authors evaluated the sequence of inflammatory responses in acute COVID-19 through a 28-day follow-up, discovering that the resolution of inflammation in the group of moderate/severe SARS-CoV2 infection was associated with decreasing PTX3 serum concentrations [ 38 ]. The authors performed a time course analysis of PTX3 on day 1, day 7, and day 28 after infection [ 38 ]. Their results revealed a constant and progressive decrease in PTX3 from day 1 to day 28 [ 38 ].…”
Section: Resultsmentioning
confidence: 99%
“…The authors performed a time course analysis of PTX3 on day 1, day 7, and day 28 after infection [ 38 ]. Their results revealed a constant and progressive decrease in PTX3 from day 1 to day 28 [ 38 ]. On other hand, analyzing inflammatory markers between non-severe COVID-19 and severe COVID-19, PTX3 was significant only on day 1, unlike TNFα and IL-1β, which were increased also 28 days post-infection [ 38 ].…”
Over the last three years, humanity has been facing one of the most serious health emergencies due to the global spread of Coronavirus disease (COVID-19). In this scenario, the research of reliable biomarkers of mortality from COVID-19 represents a primary objective. Pentraxin 3 (PTX3), a highly conserved protein of innate immunity, seems to be associated with a worse outcome of the disease. Based on the above, this systematic review and meta-analysis evaluated the prognostic potential of PTX3 in COVID-19 disease. We included 12 clinical studies evaluating PTX3 in COVID-19 patients. From our research, we found increased PTX3 levels compared to healthy subjects, and notably, PTX3 was even more augmented in severe COVID-19 rather than non-severe cases. Moreover, we performed a meta-analysis to establish if there were differences between ICU and non-ICU COVID-19 patients in PTX3-related death. We combined 5 studies for a total of 543 ICU vs. 515 non-ICU patients. We found high significative PTX3-related death in ICU COVID-19 hospitalized individuals (184 out of 543) compared to non-ICU (37 out of 515), with an overall effect OR: 11.30 [2.00, 63.73]; p = 0.006. In conclusion, we probed PTX3 as a reliable marker of poor outcomes after COVID-19 infection as well as a predictor of hospitalized patients’ stratification.
“…In patients with moderate or severe acute infection, serum chemerin levels first decreased on Day 7 in comparison to the day of hospital admission and subsequently increased at the 28-day follow-up. As this profile of plasma chemerin levels was not observed in COVID-19 patients with mild disease over this 28-day period, it was suggested that serum chemerin levels are considered as a marker for the resolution of inflammation [63]. However, while randomized clinical trials proved that anti-inflammatory and pro-resolving corticosteroids can improve survival in severe COVID-19 [64], dexamethasone therapy did not affect plasma chemerin levels [62].…”
Accumulating evidence implicates obesity as a risk factor for increased severity of disease outcomes in patients infected with severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2). Obesity is associated with adipose tissue dysfunction, which not only predisposes individuals to metabolic complications, but also substantially contributes to low-grade systemic inflammation, altered immune cell composition, and compromised immune function. This seems to impact the susceptibility and outcome of diseases caused by viruses, as obese people appear more vulnerable to developing infections and they recover later from infectious diseases than normal-weight individuals. Based on these findings, increased efforts to identify suitable diagnostic and prognostic markers in obese Coronavirus disease 2019 (COVID-19) patients to predict disease outcomes have been made. This includes the analysis of cytokines secreted from adipose tissues (adipokines), which have multiple regulatory functions in the body; for instance, modulating insulin sensitivity, blood pressure, lipid metabolism, appetite, and fertility. Most relevant in the context of viral infections, adipokines also influence the immune cell number, with consequences for overall immune cell activity and function. Hence, the analysis of the circulating levels of diverse adipokines in patients infected with SARS-CoV-2 have been considered to reveal diagnostic and prognostic COVID-19 markers. This review article summarizes the findings aimed to correlate the circulating levels of adipokines with progression and disease outcomes of COVID-19. Several studies provided insights on chemerin, adiponectin, leptin, resistin, and galectin-3 levels in SARS-CoV-2-infected patients, while limited information is yet available on the adipokines apelin and visfatin in COVID-19. Altogether, current evidence points at circulating galectin-3 and resistin levels being of diagnostic and prognostic value in COVID-19 disease.
The review summarizes and analyzes the results of major foreign studies on the role of adipokine imbalance in the development of a severe course and complications of novel coronavirus infection (COVID-19). Adipokines are biologically active compounds produced by adipose tissue cells and involved in the regulation of metabolism and the functioning of the immune system. Obesity is a proven risk factor for severe COVID-19 due to high hormonal and metabolic activity of visceral adipose tissue. A deep understanding of COVID-19 pathogenesis from the point of view of the role of adipokine imbalance in it can provide the grounds for the development of effective pathogenetic approaches to the prevention of a severe course and complications of novel coronavirus infection.
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