Cardiovascular disease |
atherosclerosis |
Intracellular components TLR-mediated NF-κB signaling via necrotic cells |
[40] |
Pancreas |
Type 2 diabetes |
High levels of IL-1β, IL-6, TNF-α, CRP, fibrinogen, serum amyloid A, plasminogen activator inhibitor, and haptoglobin, sialic acid, IL-1 receptor antagonist (IL-1RA), activation of NF-κB, MAPK, and JAK-STAT pathways |
[42] |
Pancreas |
Pancreatitis |
Activation of macrophages, neutrophils, and granulocytes, inflammatory cytokines mediated pancreatic stellate cells (PSCs) activation |
[43] |
Kidney |
glomerulonephritis, end-stage renal disease, or acute or chronic kidney disease (CKD |
Activation of transcription factors (NF-κB or MAPK), DAMPs, and PAMPs, and Nod-like receptors (NLRs). |
[49–50] |
Liver |
alcoholic or nonalcoholic steatohepatitis, drug-induced liver injury, and ischemia/reperfusion |
DAMPs (during SI) and PAMPs activation and formation of inflammasome, high levels of of IL-1β and other pro-inflammatory cytokines, activation of Kupffer cell leading to hepatocyte damage, and/or cholestasis. |
[45–47] |
Lung |
COPD, asthama |
Asthama :Activation and uncontrolled infiltration of macrophage, neutrophil, and T lymphocyte into airways COPD: production of cytokines (TNF-α, IL-6 and IL-8) chemokines, oxygen radicals, proteases. |
[41] |
Intestine |
Ulcerative colitis (UC) and Crohn disease (CD) |
CD: IFN-γ/IL-17 and IL-12/IL-23 UC: IL-13 |
[44] |