Interleukin 2 modulates ion secretion and cell proliferation in cultured human small intestinal enterocytes

O’Loughlin, Edward; Pang, Guangchang; Noltorp, Rhiannon S.; Koina, Craig; Batey, Robert T.; Clancy, R. L.

doi:10.1136/gut.49.5.636

Cited by 26 publications

(17 citation statements)

References 38 publications

(34 reference statements)

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“…1). Previous studies (6,34) showed that supplementing IL-2 in FBS-containing growth media promoted proliferation even at a lower concentration in BN cells, while a biphasic effect was observed in a similar concentration range in IEC 6 cells. This raises the question as to the physiologic levels of IL-2 that might occur in the intestines.…”

Section: Discussionmentioning

confidence: 99%

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Molecular mechanism of interleukin-2-induced mucosal homeostasis

Mishra

Waters

Kumar

2012

American Journal of Physiology-Cell Physiology

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Section: Discussionmentioning

confidence: 99%

“…The specific role of IL-2 in intestinal epithelial homeostasis is not known. In vitro studies using different IEC lines from human and rat show that IL-2 promotes IEC proliferation and ion secretion (2,34). However, IL-2 has also been shown to enhance susceptibility to apoptosis in colonic epithelial cells (44).…”

mentioning

confidence: 99%

Molecular mechanism of interleukin-2-induced mucosal homeostasis

Mishra

Waters

Kumar

2012

American Journal of Physiology-Cell Physiology

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“…These early studies found that leukotrienes C4, D4 and E4 stimulated chloride secretion and inhibit sodium and chloride absorption in rat and rabbit ileum mounted in Ussing chambers [136,137]. Ex vivo studies in small intestinal preparations revealed antagonistic effects of cytokines on chloride secretion with IL-2 and IL-15 enhancing cyclic adenosine monophosphate (cAMP)-mediated chloride secretion [120] while IL-4 and IL-10 diminished chloride secretion by reduction of intracellular cAMP [33,100].…”

Section: Ion Channels Regulating Fluid Distributionmentioning

confidence: 98%

Ion channels in inflammation

Eisenhut

Wallace

2011

Pflugers Arch - Eur J Physiol

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Most physical illness in vertebrates involves inflammation. Inflammation causes disease by fluid shifts across cell membranes and cell layers, changes in muscle function and generation of pain. These disease processes can be explained by changes in numbers or function of ion channels. Changes in ion channels have been detected in diarrhoeal illnesses, pyelonephritis, allergy, acute lung injury and systemic inflammatory response syndromes involving septic shock. The key role played by changes in ion transport is directly evident in inflammation-induced pain. Expression or function of all major categories of ion channels like sodium, chloride, calcium, potassium, transient receptor potential, purinergic receptor and acid-sensing ion channels can be influenced by cyto- and chemokines, prostaglandins, leukotrienes, histamine, ATP, reactive oxygen species and protons released in inflammation. Key pathways in this interaction are cyclic nucleotide, phosphoinositide and mitogen-activated protein kinase-mediated signalling, direct modification by reactive oxygen species like nitric oxide, ATP or protons and disruption of the cytoskeleton. Therapeutic interventions to modulate the adverse and overlapping effects of the numerous different inflammatory mediators on each ion transport system need to target adversely affected ion transport systems directly and locally.

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“…IL-2 is able to augment endothelial cell proliferation and hence vascularization [156]. Other studies have shown that IL-2 affects enterocyte ion secretion and proliferation [157], and it has also been demonstrated to be an important neuroregulatory molecule implicated in neurite survival and extension, oligodendrocyte proliferation, hypothalamic-pituitary function and analgesia [158].…”

Section: The Il-2/il-2r Pathway In Other Immune Cell Typesmentioning

confidence: 99%