Clinical study of rhGM-CSF for the treatment of pulmonary exogenous acute respiratory distress syndrome by modulating alveolar macrophage subtypes: A randomized controlled trial

Background:

By modulating the oxygen partial pressure of alveolar epithelial cells, the granulocyte-macrophage colony-stimulating factor (GM-CSF) can stimulate and enhance the innate immune response in the lungs. This study aimed to investigate the therapeutic efficacy of rhGM-CSF in patients suffering from extrapulmonary-induced acute respiratory distress syndrome (ARDS).

Methods:

A randomized, double-blind, placebo-controlled clinical trial was conducted between February 2018 to July 2019, in which 66 sepsis patients with ARDS were recruited. The study randomly allocated the patients into 2 groups: an experimental group (34 cases receiving rhGM-CSF) and a control group (32 cases receiving placebo). The changes in lung function were assessed using the scores of PaO ₂/FIO ₂ ratio, acute physiology and chronic health evaluation II, sequential organ failure assessment, and lung injury. Additionally, the study analyzed the levels of inflammatory cells, HLA-DR (%), high mobility group protein B1 (HMGB-1) (ng/mL), tumor necrosis factor-alpha (pg/mL), IL-6 (pg/mL), and GM-CSF (pg/mL) in both blood and bronchoalveolar lavage fluid.

Results:

The study results revealed that the experimental group significantly enhanced their pulmonary function compared to the control group. Moreover, the experimental group demonstrated higher levels of inflammatory cells and HLA-DR, whereas levels of HMGB-1 and tumor necrosis factor-alpha were lower in blood ( P < .05, respectively). In addition, the experimental group displayed a higher alternatively activated cell ratio and GM-CSF levels in bronchoalveolar lavage fluid (both P < .05); while HMGB-1 levels were significantly reduced ( P < .05). However, no notable difference observed in mortality between the 2 groups ( P > .05).

Conclusions:

Administering rhGM-CSF to ARDS patients improves lung function and decreases blood inflammation. Nonetheless, while this treatment demonstrates efficacy in reducing these parameters, it does not significantly impact the incidence of ventilator-associated pneumonia or 28-day mortality in ARDS patients.