Introduction: Septic patients undergoing mechanical ventilation (MV) often experience difficulty in weaning. Th aim of this study was to determine whether inflammatory biomarkers of sepsis could be indicative of the failure or success of spontaneous breathing trial (SBT) in these patients. Methods: Sixty-five patients on MV (42 septic and 23 intubated for other reasons) fulfilling the criteria for SBT were included in the study. Blood samples were collected right before, at the end of (30 min) and 24 h after the SBT. Serum inflammatory mediators associated with sepsis (IL-18, IL-18BP, TNF) were determined and correlated with the outcome of SBT. Results: A successful SBT was achieved in 45 patients (69.2%). Septic patients had a higher percentage of SBT failure as compared to non-septic patients (85% vs. 15%, p = 0.026), with an odds ratio for failing 4.5 times (OR = 4.5 95%CI: 1.16–17.68, p 0.022). IL-18 levels and the relative mRNA expression in serum were significantly higher in septic as compared to non-septic patients (p < 0.05). Sepsis was independently associated with higher serum IL-18 and TNF levels in two time-point GEE models (53–723, p = 0.023 and 0.3–64, p = 0.048, respectively). IL-18BP displayed independent negative association with rapid shallow breathing index (RSBI) (95% CI: −17.6 to −4, p = 0.002). Conclusion: Sustained increased levels of IL-18 and IL-18BP, acknowledged markers of sepsis, were found to be indicative of SBT failure in patients recovering from sepsis. Our results show that, although subclinical, remaining septic inflammation that sustaines for a long time complicates the weaning procedure. Biomarkers for the estimation of the septic burden and the right time for weaning are needed.

Adipose tissue has emerged as a pivotal endocrine organ, secreting bioactive proteins termed adipokines that regulate metabolic and immune processes across multiple organ systems. In the context of sepsis and critical illness, conditions defined by a dysregulated host response to infection with life-threatening organ dysfunction, the role of novel adipokines has attracted considerable research interest. This review focuses on three novel adipokines, chemerin, vaspin (SERPINA12), and omentin-1 (intelectin-1). We will discuss current in vitro, in vivo experimental animal models, and clinical evidence, emphasizing their biology, mechanisms of action, and potential as diagnostic and prognostic biomarkers in critically ill patients. All three adipokines are elevated in sepsis compared with healthy controls and correlate with established severity scores, including APACHE II and SOFA. Chemerin and omentin-1 have both been independently associated with 28-day mortality in prospective cohort studies. Vaspin exhibits robust cardioprotective effects in murine sepsis models via inhibition of kallikrein 7 (KLK7) and attenuates lipopolysaccharide (LPS)-induced acute lung injury (ALI) both in vitro and in vivo. Omentin-1 suppresses LPS-induced macrophage activation through TLR4/MyD88/NF-κB inhibition in vitro and protects against LPS-induced ALI in murine models. Despite these promising findings, substantial methodological heterogeneity and limited large-scale clinical data currently preclude clinical implementation. Future research that standardizes assays, expands to multicenter cohorts, and investigates therapeutic modulation of these pathways is urgently needed.

Background/Objectives: Adipokines are candidate biomarkers in critical illness due to their roles in immunity and metabolism, both profoundly altered in sepsis. Omentin-1, vaspin, and chemerin have been studied in selected septic cohorts, but not concurrently in a heterogeneous ICU population including both septic and non-septic patients. Methods: Prospective observational cohort of 200 consecutive ICU patients with 28-day follow-up. Biomarkers were measured by ELISA within 24 h of admission. Analyses included Mann–Whitney U tests, Spearman correlations, ROC curves, and logistic regression with APACHE II and SOFA as comparators. Results: Vaspin was significantly higher in septic versus non-septic patients (406.4 [190.0–799.6] vs. 275.8 [101.8–559.8] pg/mL; p = 0.009). Omentin-1 was elevated in 28-day non-survivors (34.4 [22.5–56.1] vs. 25.1 [15.0–48.4] ng/mL; p = 0.037; AUROC 0.599), but lost significance after APACHE II adjustment (p = 0.295). Chemerin trended lower in non-survivors (p = 0.099); in septic patients, it correlated inversely with SOFA (r = −0.43) and lactate (r = −0.40), both p < 0.001. IL-6 and IL-10 were higher in non-survivors; IL-10 predicted 28-day mortality (AUROC 0.783), comparable to APACHE II (0.785). Conclusions: Vaspin distinguishes sepsis in mixed ICU populations. Omentin-1 shows a severity-driven association with mortality that does not survive APACHE II adjustment (AUROC 0.599, poor standalone discrimination), while chemerin inversely tracks hypoperfusion markers in septic patients, suggesting a potential counter-regulatory role requiring mechanistic confirmation. Individually, these adipokines do not add prognostic value beyond established severity scores, but their biological orthogonality to classical cytokines warrants exploration in multi-marker panel studies.

Adipose tissue has emerged as a pivotal endocrine organ, secreting bioactive proteins termed adipokines that regulate metabolic and immune processes across multiple organ systems. In the context of sepsis and critical illness, conditions defined by a dysregulated host response to infection with life-threatening organ dysfunction, the role of novel adipokines has attracted considerable research interest. This review focuses on three novel adipokines: chemerin, vaspin (SERPINA12), and omentin-1 (intelectin-1). We will discuss current in vitro, in vivo experimental animal models, and clinical evidence, emphasizing their biology, mechanisms of action, and potential as diagnostic and prognostic biomarkers in critically ill patients. All three adipokines are elevated in sepsis compared with healthy controls and correlate with established severity scores, including APACHE II and SOFA. Chemerin and omentin-1 have both been independently associated with 28-day mortality in prospective cohort studies. Vaspin exhibits robust cardioprotective effects in murine sepsis models via inhibition of kallikrein 7 (KLK7) and attenuates lipopolysaccharide (LPS)-induced acute lung injury (ALI) both in vitro and in vivo. Omentin-1 suppresses LPS-induced macrophage activation through TLR4/MyD88/NF-κB inhibition in vitro and protects against LPS-induced ALI in murine models. Despite these promising findings, substantial methodological heterogeneity and limited large-scale clinical data currently preclude clinical implementation. Future research that standardizes assays, expands to multicenter cohorts, and investigates therapeutic modulation of these pathways is urgently needed.