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Wannemacher, R

"Esophageal squamous cell carcinoma at the site of tracheo-esophageal fistula repair in a patient with cystic fibrosis"

qRT-PCR expression patterns (bar charts) were compared with RNA-seq trends (line charts) across CK, LS, MS, and SS ( Fig

Calabrese G, Morgan B

The pivotal role of KCs in ALD has been demonstrated through the use of gadolinium chloride, a compound that selectively depletes KCs.35 Studies have shown that blocking KC activity can alleviate liver injury, underscoring their importance in the progression of ALD.35 Activated KCs contribute to liver fibrosis by secreting profibrogenic factors, such as TGF- and platelet-derived growth factor (PDGF), which promote the activation of HSCs, the main effector cells in liver fibrosis.35 One of the key mechanisms driving macrophage and KC activation in ALD is the upregulation of TLRs, particularly TLR4, in response to ROS.36 Chronic alcohol consumption leads to increased ROS production, which sensitises KCs and macrophages to bacterial endotoxins, such as LPS.37 This sensitisation amplifies the inflammatory response in the liver.37 ROS-mediated activation of the CD14/TLR4 receptor complex on macrophages perpetuates the inflammatory cascade, contributing to ongoing liver injury.31 37 Macrophages, including KCs, exhibit significant plasticity, enabling them to transition between pro-inflammatory (M1) and anti-inflammatory (M2) phenotypes in response to environmental stimuli.32 This dynamic polarisation allows macrophages to adapt to different stages of liver injury and recovery, playing distinct roles in ALD.32 M1 macrophages are typically activated by pathogen-associated molecular patterns (PAMPs) like LPS, primarily via TLRs

The upregulation of HO-1 expression or administration of CO triggers potent anti-inflammatory responses in monocytes and macrophages, reduces tissue damage, and influences their involvement in initiating immune responses (Bell and Maines, 1988)