Background/Objectives: Men are more susceptible to sepsis than women, but the underlying pathways have not been fully clarified. Lipopolysaccharide-binding protein (LBP) is an acute-phase protein that is highly elevated in sepsis. Experimental evidence shows that LBP increases to a much greater extent in male than in female mice following exposure to lipopolysaccharide. However, gender-specific studies of circulating LBP levels in sepsis patients are scarce. Methods: In the plasma of 189 patients with systemic inflammatory response syndrome (SIRS), sepsis, and septic shock, LBP levels were measured by enzyme-linked immunosorbent assay. Results: Patients with liver cirrhosis had reduced circulating LBP levels, regardless of gender. Further analysis within the non-cirrhotic patients showed no significant differences in LBP levels between sexes in patients with SIRS, sepsis, and septic shock. Ventilation, dialysis, and vasopressor therapy had no effect on LBP levels in either sex. A positive correlation between LBP and C-reactive protein was observed in the total cohort, males, and females. Infection with Gram-negative or Gram-positive bacteria had no effect on plasma LBP levels in males. However, female patients with Gram-negative infection had increased plasma LBP levels compared to females with negative and Gram-positive blood cultures, and 70 µg/mL LBP discriminates Gram-negative infections in females with a sensitivity of 88% and a specificity of 74%. Infection with SARS-CoV-2 did not change plasma LBP levels in either men or women. Female patients who did not survive had lower plasma LBP levels compared to female survivors and male non-survivors. Conclusions: This investigation highlights the influence of sex on plasma LBP levels in SIRS/sepsis patients, suggesting that LBP could be a sex-specific biomarker in critically ill patients.

Background/Objectives: Interleukin-32 (IL-32) is a pro-inflammatory cytokine primarily produced by immune cells and involved in bacterial and viral infections. This study investigates whether plasma IL-32 is associated with sepsis severity and clinical outcomes. Methods: Plasma IL-32 levels were measured in 186 patients with systemic inflammatory response syndrome (SIRS), sepsis, or septic shock, as well as in 40 controls. The relationship between IL-32 levels and SARS-CoV-2 or bacterial infections, alongside underlying etiological conditions, was assessed. Results: Patients with liver cirrhosis exhibited elevated plasma IL-32 levels. After excluding these patients, IL-32 levels were lower in SIRS/sepsis patients compared to the controls. No significant differences in IL-32 levels were observed among SIRS, sepsis, and septic shock patients. Additionally, underlying conditions such as pancreatitis and cholangitis did not influence IL-32 levels. Patients with bloodstream bacterial infections, SARS-CoV-2 infections, or no documented infection had comparable IL-32 levels. Notably, higher IL-32 levels were associated with increased mortality. Conclusions: These findings suggest that a reduction in plasma IL-32 levels may be protective in SIRS/sepsis patients, as elevated levels are linked to poor survival outcomes.

Infectious diseases are associated with low iron levels and the induction of hepcidin, the primary protein regulating cellular iron export. Bone morphogenetic protein 6 (BMP6), a key regulator of hepcidin expression, has not yet been analyzed in the plasma of patients with systemic inflammatory response syndrome (SIRS) or sepsis. An analysis of 38 SIRS, 39 sepsis, and 78 septic shock patients revealed similar levels of BMP6 in sepsis and septic shock, which were lower compared to patients with SIRS and healthy controls. Plasma BMP6 levels did not correlate with procalcitonin and C-reactive protein levels in patients with SIRS or sepsis/septic shock. Neither bacterial nor SARS-CoV-2 infections affected plasma BMP6 levels. There was no difference in BMP6 levels between ventilated and non-ventilated patients, or between patients with and without dialysis. Vasopressor therapy did not alter BMP6 levels. Survivors had plasma BMP6 levels similar to non-survivors. Due to the high variability of plasma BMP6 levels, these analyses have limited clinical relevance. Iron, ferritin, and transferrin levels were known in at least 50% of patients but did not correlate with plasma BMP6 levels. In conclusion, this study showed normal BMP6 plasma levels in SIRS, which are reduced in patients with sepsis and septic shock. This suggests that the commonly observed increase in hepcidin levels and the decline in iron levels in SIRS, sepsis, and septic shock are not due to higher BMP6.

Background/Objectives: Chemerin is an adipokine involved in inflammatory and metabolic diseases, and its circulating levels have been associated with inflammatory parameters in various patient cohorts. Severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) infection, which causes COVID-19, triggers inflammatory pathways. However, the association between serum chemerin levels and COVID-19 disease severity and outcomes has not been definitively established. Methods: In this study, serum chemerin levels were analyzed in 64 patients with moderate COVID-19 and 60 patients with severe disease. Results: The results showed that serum chemerin levels were comparable between these two groups and slightly higher than in healthy controls. Notably, COVID-19 patients with hypertension exhibited elevated serum chemerin levels, while those with liver cirrhosis had lower levels. When patients with these comorbidities were excluded from the analyses, serum chemerin levels in COVID-19 patients were similar to those in healthy controls. Positive correlations were observed between serum chemerin levels and markers such as alkaline phosphatase, C-reactive protein, eosinophils, and lymphocytes in the entire cohort, as well as in the subgroup excluding patients with hypertension and cirrhosis. Additionally, urinary chemerin levels were comparable between COVID-19 patients and controls, and neither hypertension nor dialysis significantly affected urinary chemerin levels. Both survivors and non-survivors had similar serum and urinary chemerin levels. Conclusions: In conclusion, this study suggests that comorbidities such as arterial hypertension and liver cirrhosis do have a more significant impact on serum chemerin levels than SARS-CoV-2 infection itself.