BACKGROUND

Pulmonary infections often lead to poor prognoses in patients with chronic obstructive pulmonary disease (COPD). Activin A and CD64 play crucial pathological roles in the development of COPD.

AIM

To explore the bacterial spectrum analysis of activing A levels, CD64 index, and related mechanisms in COPD patients complicated with pulmonary infection.

METHODS

Between March 2015 and January 2018, a total of 85 patients with COPD, who also suffered from pulmonary infections, were enrolled in this study as the pulmonary infection group. In addition, a total of 96 COPD patients, without pulmonary infection, were selected as the control group. Sputum samples of patients in the pulmonary infection group were cultivated for bacterial identification prior to administration of antibiotics. The neutrophil CD64 index was measured using flow cytometry, serum activin A levels were detected an enzyme-linked immunosorbent assay, and activin A, Smad3, TLR4, MyD88, and NFκB protein expression was analyzed by Western blotting.

RESULTS

Gram-negative bacteria were identified in 57.65% of the sputum samples in the pulmonary infection group. The most prevalent Gram-negative species were and . Conversely, Gram-positive bacteria were identified in 41.18% of the sputum samples in the pulmonary infection group. The most common Gram-positive species was . Fungi were identified in 1.17% of the sputum samples in the pulmonary infection group. The CD64 index was significantly higher in the pulmonary infection group (0.91 ± 0.38) than in the control group (0.23 ± 0.14, < 0.001). The serum activin A levels were significantly higher in the pulmonary infection group (43.50 ± 5.22 ng/mL), compared to the control group (34.82 ± 4.16 ng/mL, < 0.001). The relative expression levels of activin A, Smad3, TLR4, MyD88, and NFκB were all significantly higher in the pulmonary infection group, compared to the control group (all < 0.001).

CONCLUSION

Pulmonary infections in COPD patients are mainly caused by , , and . Pulmonary infections can significantly increase neutrophil CD64 index and serum levels of activin A, thereby activating the activin A/Smad3 signaling pathway, which may positively regulate the TLR4/MyD88/NFκB signaling pathway.