Published online Mar 16, 2022. doi: 10.12998/wjcc.v10.i8.2382
Peer-review started: October 11, 2021
First decision: November 11, 2021
Revised: November 27, 2021
Accepted: January 29, 2022
Article in press: January 29, 2022
Published online: March 16, 2022
Processing time: 150 Days and 14.3 Hours
A sharp exacerbation of chronic obstructive pulmonary disease (COPD) is often triggered by a lung infection and often has a poor prognosis.
Since COPD induces complex inflammatory events, Activin A and CD64 may collectively contribute to the development and progression of this disorder.
To analyze the bacterial profile of COPD patients with pulmonary infections and to assess activin A levels, CD64 index, and the underlying mechanisms involved in disease development.
The whole data set consisted of 85 COPD patients with pulmonary infection and 96 COPD patients without pulmonary infection. Sputum samples were obtained from patients with pulmonary infections for further bacterial culture. The levels of CD64 index, activin A, Smad3, TLR4, MyD88, and NFκB proteins were assessed and compared between 85 COPD patients with pulmonary infections and 96 COPD patients without pulmonary infections.
In the pulmonary infection group sputum samples, the Gram-negative bacteria, Gram-positive bacteria, and Fungi were 57.65%, 41.18%, and 1.17%, respectively. In addition, the relative CD64 index, and levels of activin A, Smad3, TLR4, MyD88, and NFκB proteins were all significantly higher in the pulmonary infection group, compared to the control group (all P < 0.001).
Pulmonary infections in COPD patients may be caused by a variety of pathogens. In COPD patients, the CD64 index and serum activin A levels were significantly increased in patients with lung infection, compared to those without. This may have a positive regulatory effect on the downstream activin A/Smad3 and TLR4/MyD88/NFκB signaling pathways.
Together, our findings provide a novel mechanism underlying pulmonary infection in COPD patients, and offer a potential therapeutic target for an enhanced and effective therapy against COPD.