Interleukin-6 and cachexia inApcMin/+mice

Baltgalvis, Kristen A.; Berger, Franklin G.; Peña, Maria Marjorette O.; Davis, John M.; Muga, Stephanie J.; Carson, James A.

doi:10.1152/ajpregu.00716.2007

Cited by 243 publications

(295 citation statements)

References 42 publications

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“…It has been reported that IL6 −/− APC Min/+ mice have moderately attenuated polyposis (31). To test the notion that MC derived IL6 was contributing to polyposis, we lethally irradiated 6-week-old APC Δ468 mice and reconstituted them with bone marrow (BM) from IL6 −/− mice or from wt control mice.…”

Section: Il6 Focal Mastocytosis and Polyposis Are Independent Of Bonementioning

confidence: 99%

In colorectal cancer mast cells contribute to systemic regulatory T-cell dysfunction

Blatner

Bonertz

Beckhove

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

129

128

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T-regulatory cells (Treg) and mast cells (MC) are abundant in colorectal cancer (CRC) tumors. Interaction between the two is known to promote immune suppression or loss of Treg functions and autoimmunity. Here, we demonstrate that in both human CRC and murine polyposis the outcome of this interaction is the generation of potently immune suppressive but proinflammatory Treg (ΔTreg). These Treg shut down IL10, gain potential to express IL17, and switch from suppressing to promoting MC expansion and degranulation. This change is also brought about by direct coculture of MC and Treg, or culture of Treg in medium containing IL6 and IL2. IL6 deficiency in the bone marrow of mice susceptible to polyposis eliminated IL17 production by the polyp infiltrating Treg, but did not significantly affect the growth of polyps or the generation of proinflammatory Treg. IL6-deficient MC could generate proinflammatory Treg. Thus, MC induce Treg to switch function and escalate inflammation in CRC without losing T-cell–suppressive properties. IL6 and IL17 are not needed in this process.

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Section: Il6 Focal Mastocytosis and Polyposis Are Independent Of Bonementioning

confidence: 99%

In colorectal cancer mast cells contribute to systemic regulatory T-cell dysfunction

Blatner

Bonertz

Beckhove

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

129

128

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“…These expression level changes of COX-2, iNOS, and adipocytokines, especially iNOS, could be associated with intestinal polyp development in Min mice. Indeed, it has been reported that iNOS inhibition, Pai-1 inhibition, COX-2 inhibition, and IL-6 knock out suppressed intestinal polyp development in Min mice (31,38,39,40). It has also been reported that 100-ppm atorvastatin treatment in Min mice slightly, but not significantly, reduced the activity and expression levels of COX-2 in the intestinal polyp (20).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Intestinal Polyp Formation by Pitavastatin, a HMG-CoA Reductase Inhibitor

Teraoka

Mutoh

Takasu

et al. 2011

Cancer Prevention Research

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It has been suggested that hyperlipidemia is positively associated with colon carcinogenesis. Statins, 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitors, reduce serum lipid levels. In this study, we clarified the effects of a novel chemically synthesized statin, pitavastatin, on intestinal polyp formation in Min mice, and further examined serum lipid and adipocytokine levels, and proinflammatory and adipocytokine gene levels in intestinal mucosa of Min mice. Treatment with pitavastatin at doses of 20 and 40 ppm decreased the total number of polyps dose-dependently to 85.2% and 65.8% (P < 0.05) of the untreated value, respectively. Serum levels of total cholesterol and triglyceride were slightly reduced and those of IL-6, leptin, and MCP-1 were decreased by 40-ppm pitavastatin treatment. mRNA expression levels of cyclooxygenase-2, IL-6, inducible nitric oxide (iNOS), MCP-1, and Pai-1 were significantly reduced in intestinal nonpolyp parts by pitavastatin treatment. Among them, iNOS mRNA levels were also reduced in the intestinal polyps. Moreover, oxidative stress represented by 8-nitroguanosine in the small intestinal epithelial cells was reduced by pitavastatin treatment. Related to these proinflammatory genes, PPARg activity was activated in the intestinal nonpolyp parts and in the liver of Min mice with pitavastatin treatment. These results indicated that pitavastatin has potential benefit for the suppression of intestinal polyp development. Cancer Prev Res; 4(3); 445-53. Ó2011 AACR.

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“…Although IL-6 is primarily produced following an immune response, convincing evidence demonstrates that IL-6 is also involved in satellite cell-mediated muscle hypertrophy and regeneration. Chronic systematic elevation of IL-6 leads to muscle atrophy in aging and disease states (29,212; reviewed in Ref. 154).…”

Section: Systemic Milieumentioning

confidence: 99%

Satellite Cells and the Muscle Stem Cell Niche

Yin

Price

Rudnicki

2013

Physiological Reviews

1,759

1,808

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LYin H, Price F, Rudnicki MA. Satellite Cells and the Muscle Stem Cell Niche. Physiol Rev 93: 23-67, 2013; doi:10.1152/physrev.00043.2011.-Adult skeletal muscle in mammals is a stable tissue under normal circumstances but has remarkable ability to repair after injury. Skeletal muscle regeneration is a highly orchestrated process involving the activation of various cellular and molecular responses. As skeletal muscle stem cells, satellite cells play an indispensible role in this process. The self-renewing proliferation of satellite cells not only maintains the stem cell population but also provides numerous myogenic cells, which proliferate, differentiate, fuse, and lead to new myofiber formation and reconstitution of a functional contractile apparatus. The complex behavior of satellite cells during skeletal muscle regeneration is tightly regulated through the dynamic interplay between intrinsic factors within satellite cells and extrinsic factors constituting the muscle stem cell niche/microenvironment. For the last half century, the advance of molecular biology, cell biology, and genetics has greatly improved our understanding of skeletal muscle biology. Here, we review some recent advances, with focuses on functions of satellite cells and their niche during the process of skeletal muscle regeneration.

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Interleukin-6 and cachexia inApc^Min/+mice

Cited by 243 publications

References 42 publications

In colorectal cancer mast cells contribute to systemic regulatory T-cell dysfunction

In colorectal cancer mast cells contribute to systemic regulatory T-cell dysfunction

Inhibition of Intestinal Polyp Formation by Pitavastatin, a HMG-CoA Reductase Inhibitor

Satellite Cells and the Muscle Stem Cell Niche

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