Differential Expression of Proinflammatory Cytokines IFN-γ and TNF-α in CKD Patients from South India.

Abstract

Objective: To explore the proinflammatory cytokine expression from chronic kidney disease patients (CKD) with its secondary complications.Methods: A total of 133 CKD patients and 149 healthy controls were evaluated for TNF-α and IFN-γ cytokine mRNA expression by qRT- PCR methods.Results: We found upregulated expression for TNF-α (FC: 2.5) and IFN-γ (FC:1.76) in pooled CKD patients when compared to controls. The expression profile for TNF-α and IFN-γ was 2.6 and 1.71 fold respectively for dialysis patients. However, in Non-Dialysis patients, a down regulated expression for TNF-α (FC: 0.19) and upregulated expression for IFN-γ (FC:1.6) were noticed. The IFN-γ and TNF-α expression level was 2.02 and 1.79 fold respectively for CKD patients with diabetes. Whereas in non-diabetic CKD patients, the IFN-γ and TNF-α expressions were 1.79 and 1.87 fold respectively. When we grouped the data based on with and without complications, we found a significant upregulated expression for IFN-γ (FC:1.64) and down regulated expression for TNF- α (FC:0.65) were observed in without complications. A significant upregulated expression were observed for IFN-γ (FC:1.82) and TNF- α (FC:2.27) in with complications. We have observed a significant positive correlation between TNF-α and IFN-γ (R=0.620; p< 0.0001). Analysis of data showed negative correlation between eGFR and Creatinine in Dialysis and Non-Dialysis group of patients. The disease severity progression showed that, 84.2% (n=112) of individuals fall under <15 eGFR.Conclusion: Increased TNF-α and IFN-γ expression suggests that Th1 cells are involved in CKD inflammation and its disease pathogenesis.

Therapeutic Potential of Photobiomodulation for Chronic Kidney Disease

“…TNF-α is secreted by invading immunologic cells, specifically by monocytes/macrophages [ 41 ]. A clinical study with 133 CKD patients found that TNF-α and INF-γ, Th1 (T helper cell type 1) cytokines significantly increased in CKD patients, suggesting that Th1 cells were activated in the inflammatory response induced by CKD [ 42 ]. It is well known that TGF-β1 is a key mediator of kidney fibrosis, with the TGF-β1 pathway shown to be modified by photobiomodulation [ 18 ].…”