CX3CR1 might be a promising predictor of systemic lupus erythematosus patients with pulmonary fibrosis.

The inflammatory process in systemic lupus erythematosus (SLE) affects many organs including the lungs. Chemokines are suggested to play important roles in the pathogenesis of SLE with pulmonary fibrosis (PF). In the present study, our objective is to evaluate the correlation between chemokines and PF in SLE patients. Transcriptome sequencing analysis was used to find the different expressed genes between SLE patients with PF and without PF. Enzyme-linked immunosorbent assay (ELISA) was used to detect serum levels of chemokines in SLE patients and healthy controls. Expression of CX3CR1 was measured by real-time polymerase chain reaction (PCR) and flow cytometer. Sixteen differentially chemokine genes were found to be associated to SLE with PF. Meanwhile, the upregulation of C-X3-C motif chemokine receptor 1 (CX3CR1) and its ligand, CX3C chemokine ligand 1 (CX3CL1) were observed in SLE patients with PF than that of SLE patients without PF and healthy control. Phenotypic analysis also showed that the surface expression of CX3CR1 increased in PBMCs from SLE patients with PF. Our observations indicated that CX3CL1/CX3CR1 axis is associated with PF in SLE. CX3CR1 might be a promising predictor of SLE with PF and the interactions between CX3CL1 and CX3CR1 might provide potential candidate target for the treatment of SLE with PF.

Down-regulation of lincRNA-EPS regulates apoptosis and autophagy in BCG-infected RAW264.7 macrophages via JNK/MAPK signaling pathway.

Macrophages play a major role in the control and elimination of invading Mycobacterium tuberculosis (Mtb). Long intergenic noncoding RNA erythroid prosurvival (lincRNA-EPS) plays an important role in regulating various biologic processes in macrophages, including inflammatory responses, cell apoptosis, and autophagy. Whereas the effect of lincRNA-EPS in regulating the immune response of macrophages to Mtb is little studied. This study aimed to explore lincRNA-EPS expression in monocytes from patients with active pulmonary tuberculosis (PTB) and from healthy individuals. We also sought to investigate the effect of lincRNA-EPS on Bacillus Calmette-Guérin (BCG)-infected macrophages apoptosis and autophagy. Our study found that lincRNA-EPS expression was down-regulated in the monocytes from patients with active PTB compared with healthy individuals, accompanied by significant attenuated monocyte apoptosis and enhanced autophagy. In vitro, knockdown of lincRNA-EPS inhibited apoptosis and promoted autophagy in BCG-infected RAW264.7 macrophages. Moreover, we revealed that lincRNA-EPS regulated apoptosis and autophagy of BCG-infected RAW264.7 macrophages via JNK/MAPK signaling pathway. In conclusion, our findings demonstrated that knockdown of lincRNA-EPS inhibits apoptosis and enhances autophagy by activating the JNK/MAPK signaling pathway in BCG-infected RAW264.7 macrophages. Suggesting that lincRNA-EPS could serve as a new potential therapeutic target for PTB.