Effects of Interleukin-8 on the Developing Human Intestine

Maheshwari, Akhil; Lu, Wenzhe; Lacson, Atilano; Barleycorn, Aaron A.; Nolan, Sheila M.; Christensen, Robert D.; Calhoun, Darlene A

doi:10.1006/cyto.2002.1996

Cited by 64 publications

(64 citation statements)

References 62 publications

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“…IL-8 at doses similar to those obtained by LPS and TGF-␤2 costimulation (1-10 ng/ml) induced cell proliferation and migration following injury, indicating positive functions of IL-8 in intestinal repair. These findings are in agreement with earlier observations reporting IL-8 in fetal intestinal tissues, with effects on cell proliferation, differentiation, and prevention of cell death (20,22). In addition, in line with previous results (24), similar doses of IL-8 did not further activate inflammatory signaling cascades such as NF-B and COX-2, which was in contrast with a high IL-8 dose of 100 ng/ml.…”

Section: G695 Tgf-␤2 and Lps Regulate Intestinal Il-8 Levelssupporting

confidence: 93%

“…However, in the fetal intestine, IL-8 exerts other effects, stimulating maturation, but without associated inflammation (23). IL-8 also stimulates intestinal cell proliferation, differentiation, migration, protection from injury, and prevention from cell death (20,22). The role of IL-8 in intestinal homeostasis and inflammation may be age-and dose-dependent, but the threshold levels remain to be elucidated.…”

mentioning

confidence: 99%

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Transforming growth factor-β2 and endotoxin interact to regulate homeostasis via interleukin-8 levels in the immature intestine

Nguyen

Sangild

Østergaard

et al. 2014

American Journal of Physiology-Gastrointestinal and Liver Physi

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Section: G695 Tgf-␤2 and Lps Regulate Intestinal Il-8 Levelssupporting

confidence: 93%

mentioning

confidence: 99%

Transforming growth factor-β2 and endotoxin interact to regulate homeostasis via interleukin-8 levels in the immature intestine

Nguyen

Sangild

Østergaard

et al. 2014

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…In addition, gastric digestion of proteins is reduced during the first 3 months of life because of the limited secretion of pepsin and H+ ions and the general immaturity of the newborn's digestive abilities. These factors favour the survival and the intestinal absorption of intact polypeptides, thereby allowing them to exert their biological activities (Maheshwari et al, 2002).…”

Section: Breast Milkmentioning

confidence: 99%

Breastfeeding and its Relationship with Reduction of Breast Cancer: A Review

França-Botelho¹,

Ferreira²,

França³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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In this review, we describe the patterns of known immunological components in breast milk and examine the relationship between breastfeeding and reduced risk of breast cancer. The top risk factors for breast cancer are a woman's age and family history, specifically having a first-degree relative with breast cancer. Women that have a history of breastfeeding have been shown to have reduced rates of breast cancer. Although the specific cause has not been elucidated, previous studies have suggested that breastfeeding reduces the risk of breast cancer primarily through two mechanisms: the differentiation of breast tissue and reduction in the lifetime number of ovulatory cycles. In this context, one of the primary components of human milk that is postulated to affect cancer risk is alpha-lactalbumin. Tumour cell death can be induced by HAMLET (a human milk complex of alpha-lactalbumin and oleic acid). HAMLET induces apoptosis only in tumour cells, while normal differentiated cells are resistant to its effects. Therefore, HAMLET may provide safe and effective protection against the development of breast cancer. Mothers should be encouraged to breastfeed their babies because the complex components of human milk secretion make it an ideal food source for babies and clinical evidence has shown that there is a lower risk of breast cancer in women who breastfed their babies.

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“…Besides their "classical" function of providing migrational signals for leukocytes in adults, ELR ϩ -CXC chemokines promote angiogenesis, cell proliferation, and survival during development. 8 -10 CXCL8 stimulated cell migration, proliferation, and differentiation in the developing intestine and central nervous system 11,12 and enhanced endothelial cell survival and proliferation and the production of matrix metalloproteinases for matrix reconstruction and angiogenesis. 10 Because they are expressed by UB cells, we hypothesized that ELR ϩ -CXC chemokines may also function in metanephric differentiation, cell proliferation, survival, angiogenesis, or migration.…”

mentioning

confidence: 99%

ELR+-CXC Chemokines and Their Receptors in Early Metanephric Development

Levashova

Sharma

Timofeeva

et al. 2007

Journal of the American Society of Nephrology

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Although originally identified as mediators of inflammation, it is now apparent that chemokines play a fundamental role in tissue development. In this study, ELR ϩ -CXC chemokine family members CXCL2 and CXCL7, along with their preferred receptor CXCR2, were expressed at the earliest stages of metanephric development in the rat, and signaling through this receptor was required for the survival and maintenance of the undifferentiated metanephric mesenchyme (MM). A specific antagonist of the CXCR2 receptor SB225002 induced apoptosis in this population but did not affect more mature structures or cells in the ureteric bud. CXCL7 treatment of isolated MM elicited an angiogenic response by upregulation of matrix metalloprotease 9 and endothelial and mesangial markers (platelet-endothelial cell adhesion molecule, Megsin, Thy-1, PDGF receptor ␣, and vascular ␣-actin) and induced SB225002-sensitive cell invasion through a matrix. Because Wilms' tumor cells may similarly depend on CXCR2 signaling for survival, primary tumor samples were analyzed, and 15 of 16 Wilms' tumors were found to be CXCR2 positive, whereas grossly normal kidney tissues from tumor patients or renal cell carcinomas were CXCR2 negative. Furthermore, cell lines derived from Wilms' tumors but not those from renal cell carcinomas were sensitive to SB225002-induced apoptosis. These data provide evidence for a prosurvival and proangiogenic role of ELR ϩ -CXC chemokines and their receptor CXCR2 during metanephric development and suggest a novel mechanism for chemotherapeutic intervention in Wilms' tumor.

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Effects of Interleukin-8 on the Developing Human Intestine

Cited by 64 publications

References 62 publications

Transforming growth factor-β2 and endotoxin interact to regulate homeostasis via interleukin-8 levels in the immature intestine

Transforming growth factor-β2 and endotoxin interact to regulate homeostasis via interleukin-8 levels in the immature intestine

Breastfeeding and its Relationship with Reduction of Breast Cancer: A Review

ELR+-CXC Chemokines and Their Receptors in Early Metanephric Development

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