Using the serum biomarker profile and pulmonary histopathology, researchers sought to investigate the pathomechanism of microscopic polyangiitis (MPA) worsened by interstitial lung disease (ILD).
They looked at the serum biomarkers from 32 MPA-ILD patients, MPA patients without ILD (n=17), and healthy controls (n=10). Principal component analysis (PCA) and cluster analysis were used to divide patients with MPA-ILD into subgroups based on the biomarker profiles. Each subgroup’s clinical traits and prognosis were evaluated. H&E staining and immunostaining were performed on two lung specimens before being evaluated.
In contrast to the MPA without ILD group, the T cell and macrophage polarization in the MPA-ILD group was skewed toward T helper (Th) 2 cells and M2 macrophages. The 19 biomarker profiles could be divided into 3 categories using the PCA: B cell and neutrophil-related cytokines; vascular angiogenesis-related factors; extracellular matrix-producing factors; and Th1-driven cytokines, Th2-driven cytokines, and M1 macrophage-driven cytokines; and M2 macrophage-induced and driven cytokines. The clinically fibrotic-dominant (CFD) and clinically inflammatory-dominant (CID) groups of MPA-ILD patients were identified by the cluster analysis. Notably, the CFD group had considerably more serious infections than the CID group did. Intense CXC motif chemokine ligand 13 stainings were seen by immunohistochemical staining in B cells and Th2 cells in the interstitium of the lungs of MPA-ILD patients.
The pathomechanism of MPA-ILD mostly depends on the activation of M2 macrophages, Th2 cells, and B cells. Therefore, it would be helpful to categorize MPA-ILD based on the serum biomarker profile to be able to anticipate the disease activity and consequences of severe infection.
Reference: jrheum.org/content/49/8/913
