Ulcerative Colitis

Inflammatory Pathways


The pathway to inflammation

In UC, the activity of pro- and anti-inflammatory mediators is dysregulated, provoking an exaggerated immune response and initiating a chronic inflammatory cycle.1-3

Proinflammatory mediators, such as TNF-a and IL-13, recruit immune cells to sites of inflammation through intracellular signalling pathways. These pathways include the JAK-STAT, MAPK, and NF-kB pathways.4,5

Dysregulation of JAK-STAT, MAPK, or NF-kB activity is associated with inflammatory cytokine secretion through transcription factors. Excessive inflammatory cytokine production can lead to tissue damage, haemodynamic changes, and ultimately organ failure.4

An understanding of inflammatory pathways reveals multiple proinflammatory cytokines and signalling complexes that are of therapeutic interest.4


Cytokines and the JAK-STAT pathway 

Discover JAK-STAT and inflammatory cytokines in UC.

JAK-STAT Pathway

Find out more about the JAK-STAT pathway in UC.

IL, interleukin; JAK, Janus kinase; MAPK, mitogen-activated protein kinase; NF-kB, nuclear factor kappa-light-chain-enhancer of activated B cells; STAT, signal transducer and activator of transcription; TNF, tumour necrosis factor; UC, ulcerative colitis.

REFERENCES: 1. Coskun M, Salem M, Pedersen J, Nielsen OH. Pharmacol Res. 2013;76:1-8. 2. Fernández-Clotet A, Castro-Poceiro J, Panés J. Curr Pharm Des. 2019;25(1):32-40. 3. Neurath MF. Nat Rev Immunol. 2014;14(5):329-342. 4. Chen L, Deng H, Cui H, et al. Oncotarget. 2017;9(6):7204-7218. 5. Pedersen J, Coskun M, Soendergaard C, Salem M, Nielsen OH. World J Gastroenterol. 2014;20(1):64-77.