Serum Histatin Levels in COVID‐19: Association With Disease Severity and Immune Status
Source: PubMed Central Open Access, NCBI / U.S. National Library of Medicine
ABSTRACT Histatins are histidine‐rich antimicrobial peptides with emerging immunomodulatory properties; however, their systemic behavior across the clinical spectrum of COVID‐19 remains unknown. We aimed to characterize serum histatin levels in patients with mild COVID‐19 (without pneumonia) and severe COVID‐19 (with pneumonia) and to explore factors potentially associated with their variation. Ninety individuals were prospectively enrolled: healthy controls (= 30), patients with mild COVID‐19 (without pneumonia (= 30), and patients with severe COVID‐19 (with pneumonia receiving corticosteroid therapy (= 30). Serum histatin‐1, histatin‐3, and histatin‐5 concentrations were quantified by ELISA. Group comparisons were performed using Kruskal–Wallis and Mann–Whitneytests; correlations were assessed using Pearson coefficients. Histatin‐1 did not differ among groups (= 0.161). Both histatin‐3 and histatin‐5 were significantly reduced in mild COVID‐19 compared with controls (= 0.004 and= 0.002, respectively). Unexpectedly, patients with severe COVID‐19, all of whom were receiving corticosteroids, did not exhibit further histatin reductions; their levels were comparable to controls and significantly higher than the mild group (histatin‐3= 0.016; histatin‐5= 0.028). Histatin‐3 correlated significantly with ferritin (= 0.413;= 0.009), D‐dimer (= 0.369;= 0.021), and albumin (= −0.330;= 0.018). SARS‐CoV‐2 infection without pneumonia was associated with significantly lower serum histatin
Abstract
ABSTRACT Histatins are histidine‐rich antimicrobial peptides with emerging immunomodulatory properties; however, their systemic behavior across the clinical spectrum of COVID‐19 remains unknown. We aimed to characterize serum histatin levels in patients with mild COVID‐19 (without pneumonia) and severe COVID‐19 (with pneumonia) and to explore factors potentially associated with their variation. Ninety individuals were prospectively enrolled: healthy controls (= 30), patients with mild COVID‐19 (without pneumonia (= 30), and patients with severe COVID‐19 (with pneumonia receiving corticosteroid therapy (= 30). Serum histatin‐1, histatin‐3, and histatin‐5 concentrations were quantified by ELISA. Group comparisons were performed using Kruskal–Wallis and Mann–Whitneytests; correlations were assessed using Pearson coefficients. Histatin‐1 did not differ among groups (= 0.161). Both histatin‐3 and histatin‐5 were significantly reduced in mild COVID‐19 compared with controls (= 0.004 and= 0.002, respectively). Unexpectedly, patients with severe COVID‐19, all of whom were receiving corticosteroids, did not exhibit further histatin reductions; their levels were comparable to controls and significantly higher than the mild group (histatin‐3= 0.016; histatin‐5= 0.028). Histatin‐3 correlated significantly with ferritin (= 0.413;= 0.009), D‐dimer (= 0.369;= 0.021), and albumin (= −0.330;= 0.018). SARS‐CoV‐2 infection without pneumonia was associated with significantly lower serum histatin‐3 and histatin‐5 levels. In contrast, histatin levels were preserved in patients with severe COVID‐19 and pneumonia who were receiving corticosteroid therapy. Because of the cross‐sectional design, this finding should be interpreted as an association rather than evidence of a treatment effect. The observed correlations between histatin‐3 and ferritin, D‐dimer, and albumin further suggest that histatin‐3 may be linked to acute‐phase and inflammatory responses during COVID‐19.