LTBP1 inhibits severe pneumonia caused by Staphylococcus aureus following cytomegalovirus reactivation via regulation of TGF-β1/Smad signaling pathway.

INTRODUCTION

Severe viral and bacterial pneumonia are among the most common causes of death worldwide. This study investigated the effects and mechanisms of latent transforming growth factor beta binding protein 1 (LTBP1)'s on methicillin-sensitive Staphylococcus aureus (MSSA)-induced severe pneumonia following cytomegalovirus (CMV) reactivation.

METHODOLOGY: A young mouse model of severe pneumonia was established using Staphylococcus aureus and CMV. LTBP1 overexpression was induced, and pathological changes in lung tissue were assessed through H&E staining. Serum levels of inflammatory factors, including tumor necrosis factor (TNF)-α, interleukin (IL)-6, and interleukin (IL)-1β, were measured using ELISA. Bacterial load in the lungs was quantified, and protein expression levels of LTBP1, TGF-β1, Smad2, p-Smad2, Smad3, and p-Smad3 in lung tissue were analyzed using Western blot.

RESULTS

The LTBP1 expression was reduced in the young mouse model of severe pneumonia induced by Staphylococcus aureus after cytomegalovirus reactivation. Overexpression of LTBP1 inhibited lung damage, reduced serum levels of inflammatory factors (IL-6, IL-1β, and TNF-α), and decreased bacterial load in the lungs. Additionally, overexpression of LTBP1 inhibited the activation of the TGF-β1/Smad signaling pathway.

CONCLUSIONS

LTBP1 efficiently reduces severe pneumonia by activating the TGF-β1/Smad signaling pathway, highlighting its potential as a therapeutic target for treating this condition.