Serum autophagy protein 5 is positively related to T helper 2/T helper 1 ratio, inflammation, and exacerbation in adult asthma patients

BACKGROUND: Autophagy protein 5 (ATG5) regulates airway epithelial cell autophagy, immune response, and inflammation, which is involved in asthma progression.

This study aimed to evaluate ATG5 levels and its clinical roles in adult asthma patients.

METHODS: Totally, 200 adult asthma patients and 100 healthy controls (HCs) were enrolled in this case-control study.

Subsequently, serum ATG5 was measured by enzyme-linked immunosorbent assay.

RESULTS: ATG5 was increased in asthma patients compared with HCs [median (interquartile range): 44.2 (31.7–77.8) vs. 23.2 (16.7–39.2) ng/mL] (P < 0.001).

In asthma patients, ATG5 was positively related to male gender (P = 0.022), a family history of asthma (P = 0.035), eosinophil count (P < 0.001), and immune globulin E (P < 0.001), while it was negatively correlated with forced expiratory volume in 1 s (FEV(1))/forced vital capacity (P < 0.001) and FEV(1) (Predicted) (P < 0.001).

Meanwhile, ATG5 was inversely associated with T helper (Th) 1 cells (P = 0.008), while it was positively linked with Th2 cells (P < 0.001), Th2/Th1 ratio (P < 0.001), interleukin (IL)-4 (P = 0.002), and IL-4/interferon-γ ratio (P = 0.015).

Additionally, ATG5 was positively correlated with tumor necrosis factor-α (P < 0.001), IL-1β (P = 0.001), IL-6 (P = 0.003), and IL-17 (P = 0.029).

Notably, ATG5 was elevated in asthma patients at exacerbation compared to those at remission [median (interquartile range): 53.6 (37.6–90.0) vs. 35.6 (28.2–51.5) ng/mL] (P < 0.001).

It was also noteworthy that ATG5 was positively linked with exacerbation severity in asthma patients (P = 0.005).

CONCLUSION: Serum ATG5 is related to increased Th2/Th1 ratio, inflammation, exacerbation risk and severity in adult asthma patients, which serves as a candidate marker for the management of asthma.

However, further validation is still needed.

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13223-023-00821-3.