Innate immunity alterations in idiopathic interstitial pneumonias and rheumatoid arthritis-associated interstitial lung diseases.

摘要: Abstract Background This is a prospective cohort study elucidating innate immunity in idiopathic pulmonary fibrosis (IPF), cryptogenic organizing pneumonia (COP), rheumatoid arthritis-associated usual interstitial (RA-UIP) and RA-associated non specific (RA-NSIP). Methods 23 IPF subjects, 9 COP 5 RA-UIP 8 RA-NSIP subjects were enrolled. 10 excluded. 19 healthy served as controls. Blood bronchoalveolar lavage (BAL) obtained. Natural killer (NK) NKT cells, NK cells apoptosis the expression of triggering receptor expressed on myeloid type 1 (TREM-1) assessed. Tumor necrosis factor-α (TNF-α) production was measured cell cultures after stimulation with lipopolysaccharide endotoxin (LPS) Pam3CysSK3, BAL. Surface Toll-like receptors (TLR) 2 4 peripheral blood monocytes (PBMC's) circulating also Results had low NKs, marginally insignificant ( p  = 0.07). These NKs poorly produced TNF-α LPS stimulation. TLR's similar throughout disease groups PBMC's mainly from patients exhibited but not Pam3CysSK3 stimulation, while TLR4 found normal all groups. TLR2 increased IPF, COP,  = 0.015). TREM-1 significant neutrophils versus Decreased concentration BAL finally observed RA-UIP. Conclusions Innate lungs circulation are more fibrotic than which characterized by depletion dysfunction. likely affect patterns inflammation various lung diseases.