Comparison of interleukin-11 and epidermal growth factor on residual small intestine after massive small bowel resection

Fiore, N.F.; Ledniczky, George; Liu, Qi; Orazi, Attilio; Du, Xunxiang; Williams, David A.; Grosfeld, Jay L.

doi:10.1016/s0022-3468(98)90354-2

Cited by 52 publications

(29 citation statements)

References 17 publications

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“…61 In a murine model of short bowel syndrome, treatment with IL-11 ameliorated the nutritional deficits of decreased absorptive capacity by stimulating intestinal epithelial growth and function. 62,63 These data suggest that IL-11 has a trophic effect on small intestinal enterocytes, causing cell proliferation and increased mucosal thickness. Epidermal growth factor, which was used for comparison, has a more generalized effect on intestine causing proliferation of both enterocytes and myocytes.…”

Section: In Vivo Models Of Epithelial Damagementioning

confidence: 89%

“…61 Following 90% resection of the small bowel, rhIL-11 had a trophic effect as measured by villus height and crypt cell mitosis. 62,63 Studies in transgenic animals over-expressing IL-11 in the lung demonstrated that IL-11 markedly diminishes hyperoxic lung injury. The observed protection was associated with small changes in lung antioxidants, diminished hyperoxiainduced IL-1␣ and TNF␣ production, and markedly suppressed hyperoxia-induced DNA fragmentation.…”

Section: Models Of Inflammationmentioning

confidence: 99%

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1999

Leukemia

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Interleukin 11 (IL-11) is a pleiotropic cytokine with biological activities on many different cell types. Recombinant human IL-11 (rhIL-11) is produced by recombinant DNA technology in Escherichia coli. Both in vitro and in vivo, rhIL-11 has shown effects on multiple hematopoietic cell types. Its predominant in vivo hematopoietic activity is the stimulation of peripheral platelet counts in both normal and myelosuppressed animals. This activity is mediated through effects on both early and late progenitor cells to stimulate megakaryocyte differentiation and maturation. rhIL-11 has been approved for the treatment of chemotherapy-induced thrombocytopenia. The hematopoietic effects of rhIL-11 are most likely direct effects on progenitor cells and megakaryocytes in combination with other cytokines or growth factors. rhIL-11 also induces secretion of acute phase proteins (ferritin, haptoglobin, C-reactive protein, and fibrinogen) from the liver. The induction of heme oxidase and inhibition of several P450 oxidases have been reported from in vitro studies. In vivo, rhIL-11 treatment decreases sodium excretion by the kidney by an unknown mechanism and induces hemodilution. rhIL-11 also exhibits anti-inflammatory effects in a variety of animal models of acute and chronic inflammation, including inflammatory bowel disease, inflammatory skin disease, autoimmune joint disease, and various infection-endotoxemia syndromes. rhIL-11 has trophic effects on non-transformed intestinal epithelium under conditions of mucosal damage. The mechanism of the anti-inflammatory activity of rhIL-11 has been extensively studied. rhIL-11 directly affects macrophage and T cell effector function. rhIL-11 inhibits tumor necrosis factor-alpha (TNF␣), interleukin 1␤ (IL-1␤), interleukin 12 (IL-12), interleukin 6 (IL-6), and nitric oxide (NO) production from activated macrophages in vitro. The inhibition of cytokine production was associated with inhibition of nuclear translocation of the transcription factor, nuclear factor kappa B (NF-B). The block to NF-B nuclear translocation correlates with the ability of rhIL-11 to maintain or enhance production of the inhibitors of NF-B, IB-␣ and IB-␤. In addition to effects on macrophages, rhIL-11 also reduces CD4 ؉ T cell production of Th1 cytokines, such as IFN␥ induced by IL-12, while enhancing Th2 cytokine production. rhIL-11 also blocks IFN␥ production in vivo. The molecular effects of rhIL-11 have also been studied in a clinical trial. Molecular analysis of skin biopsies of patients with psoriasis before and during rhIL-11 treatment demonstrates a decrease in mRNA levels of TNF␣, IFN␥ and iNOS. These activities suggest that in addition to its thrombopoietic clinical use, rhIL-11 may also be valuable in the treatment of inflammatory diseases. The clinical utility of the anti-inflammatory properties of rhIL-11 is being investigated in patients with Crohn's disease, psoriasis and rheumatoid arthritis. These diseases are believed to be initiated and maintained by activated CD4 ؉ Th1 cells in conjunction w...

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Section: In Vivo Models Of Epithelial Damagementioning

confidence: 89%

Section: Models Of Inflammationmentioning

confidence: 99%

True

1999

Leukemia

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“…Possible mechanisms of action include a reduction in apoptosis of intestinal cells, increased expression of the anti-apoptotic gene bcl-w, and decreased expression of the pro-apoptotic gene bax [75]. Several authors have investigated the synergistic role of EGF in experimental studies along with other factors such as interleukin-11, bombesin and neurotensin, and found that they further enhance the adaptive action of EGF [76][77][78]. Promising results with the use of EGF were reported in a pilot study by Sigalet et al [79] who investigated the effect of enterally administered recombined EGF on nutrient absorption and tolerance feeding in infants with severe PSBS (<25% bowel length for predicting age).…”

Section: Epidermal Growth Factor (Egf)mentioning

confidence: 99%

Short-Bowel Syndrome in Children — An Update in Management Strategies

Zavras¹,

Misiakos²,

Velaoras³

et al. 2015

Pediatric Nursing, Psychiatric and Surgical Issues

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“…IL-11 also improves survival rate and decreases bacterial translocation in burned mice [55]. Recent studies suggest that IL-11 enhances a small intestine mucosal mass after massive small bowel resection [56,57]. However, these studies did not determine if there were changes in the function at the remnant small intestine.…”

Section: Interleukin-11 (Il-11)mentioning

confidence: 99%

Factors Enhancing Intestinal Adaptation after Bowel Compensation

Botsios

Vasiliadis²

2003

Dig Dis

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Intestinal failure (IF) refers to the condition in which certain causes lead to derangements in nutrient absorption capacity. Gut adaptation occurs in response to IF and it is both morphologic and physiologic in nature and can be mediated by growth factors and nutrients. Our paper reviews certain trophic growth factors that have important interactions relevant for intestinal growth, function and adaptation. Data Source: The literature was reviewed (data from both animal and human studies) and certain trophic factors that modulate intestinal adaptation are summarized. The factors reviewed are: epidermal growth factor, insulin-like growth factor I and II, transforming growth factor α and β, neurotensin, interleukin-11, glucagon-like peptide-2, keratinocyte growth factor, human growth hormone, short-chain fatty acids, and glutamine. Conclusions: Growth factors augment intestinal proliferation, diminish programmed apoptosis, and modulate the adaptive process. They also have the potential to improve nutrient absorption in some bowel disease. The enhancement of gut adaptation may allow patients to transition of parenteral/enteral to normal nutrition, in a shorter period of time, which reduce the rate of adverse effects caused by artificial nutrition and improve quality of life.

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Comparison of interleukin-11 and epidermal growth factor on residual small intestine after massive small bowel resection

Cited by 52 publications

References 17 publications

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Short-Bowel Syndrome in Children — An Update in Management Strategies

Factors Enhancing Intestinal Adaptation after Bowel Compensation

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