Giamila Fantuzzi

Cytokines: Pulling the Body Together as a Whole

We recently reported that after LPS stimulation, IL-37 translocates to the nucleus and reduces the expression of proinflammatory cytokines. The aim of this study was to investigate whether transiently expressed IL-37 in mice reduces inflammation in concanavalin A (ConA)-induced hepatitis and LPS-induced sepsis. Transgene IL-37 expression was detected in the liver lysate of mice injected with IL-37 plasmid-DNA after hydrodynamic tail vein injection. All mice developed severe acute hepatitis after ConA injection. No difference in the histological score and serum ALT was observed between the two groups that might be explained by patchy expression of IL-37 protein in the liver. However, 2 hrs after ConA injection, serum levels for IL-1<i>α</i>, IL-6, IL-5, and IL-9 were significantly reduced in IL-37-expressing mice as seen for the LPS model. In conclusion, in vivo expression of human IL-37 in mice reduces local and systemic inflammation in ConA-induced hepatitis and LPS challenge.

Ana-Maria Bulau

Michaela Fink

Christof Maucksch

Roland Kappler

Doris Mayr

Kai Wagner

Philip Bufler

In Vivo Expression of Interleukin-37 Reduces Local and Systemic Inflammation in Concanavalin A-Induced Hepatitis

Hepcidin is the main regulator of systemic iron homeostasis and is primarily produced by the liver but is also expressed, at the mRNA-level, in periphery tissues including the subcutaneous and visceral adipose tissue. Obesity is associated with elevated hepcidin concentrations and iron depletion suggesting that the exaggerated fat mass in obesity could contribute significantly to circulating hepcidin levels consequently altering iron homeostasis. The objective of this study was to determine if abdominal subcutaneous adipose tissue (AbScAT) releases hepcidin <i  >in vivo</i> and if release is modified by obesity. Arterio-venous differences in concentrations of hepcidin were measured across AbScAT in 9 obese and 9 lean adults. Overall (<svg style="vertical-align:-0.17555pt;width:42.912498px;" id="M1" height="10.9125" version="1.1" viewBox="0 0 42.912498 10.9125" width="42.912498"  xmlns="http://www.w3.org/2000/svg">
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</svg>), mean plasma hepcidin concentrations were significantly higher in arterialized compared to AbScAT venous samples [mean difference (arterialized-AbScAT venous plasma hepcidin) = <svg style="vertical-align:-1.09097pt;width:56.849998px;" id="M2" height="12.175" version="1.1" viewBox="0 0 56.849998 12.175" width="56.849998"  xmlns="http://www.w3.org/2000/svg">
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</svg>&#x2009;ng/mL, <svg style="vertical-align:-0.17555pt;width:56.150002px;" id="M3" height="10.9125" version="1.1" viewBox="0 0 56.150002 10.9125" width="56.150002"  xmlns="http://www.w3.org/2000/svg">
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</svg>]. Net regional release was not calculated because mean venous plasma hepcidin concentrations were lower than mean arterialized concentrations indicating no net release. Significant correlations between AbScAT venous and arterialized plasma hepcidin concentrations with anthropometric variables were not observed. Findings from this vein drainage study suggest there is no net release of hepcidin from the AbScAT depot and thereby no ability to signal systemically, even in obesity. 

Lisa Tussing-Humphreys

Keith N. Frayn

Steven R. Smith

Mark Westerman

A. Louise Dennis

Elizabeta Nemeth

Jessica Thomson

Cenk Pusatcioglu

Subcutaneous Adipose Tissue from Obese and Lean Adults Does Not Release Hepcidin <i>In Vivo</i>

The cloning of leptin in 1994 by Zhang et al. introduced a novel concept about white adipose tissue (WAT) as a very dynamic organ that releases a plethora of immune and inflammatory mediators, such as adipokines and cytokines, which are involved in multiple diseases. Actually, adipokines exert potent modulatory actions on target tissues involved in rheumatic diseases including cartilage, synovial, bone and immune cells. The goal of this paper is to elucidate the recent findings concerning the involvement of adipokines in rheumatic diseases, such as rheumatoid arthritis (RA), osteoarthritis (OA), and systemic lupus erythematosus (SLE).

Morena Scotece

Javier Conde

Rodolfo Gómez

Veronica López

Francisca Lago

Juan Jesus Gómez-Reino

Oreste Gualillo

Beyond Fat Mass: Exploring the Role of Adipokines in Rheumatic Diseases

The inflammasome is an important innate immune pathway that regulates at least two host responses protective against infections: (1) secretion of the proinflammatory cytokines IL-1<i>&#x3b2;</i> and IL-18 and (2) induction of pyroptosis, a form of cell death. Inflammasomes, of which different types have been identified, are multiprotein complexes containing pattern recognition receptors belonging to the Nod-like receptor family or the PYHIN family and the protease caspase-1. The molecular aspects involved in the activation of different inflammasomes by various pathogens are being rapidly elucidated, and their role during infections is being characterized. Production of IL-1<i>&#x3b2;</i> and IL-18 and induction of pyroptosis of the infected cell have been shown to be protective against many infectious agents. Here, we review the recent literature concerning inflammasome activation in the context of bacterial infections and identify important questions to be answered in the future.

Manoranjan Sahoo

Ivonne Ceballos-Olvera

Laura del Barrio

Fabio Re

Role of the Inflammasome, IL-1
                        <svg style="vertical-align:-3.56265pt" height="16.6625" version="1.1" viewBox="0 0 10 16.6625" width="10" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
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			<path id="x1D6FD" d="M558 587q0 -32 -14 -61t-40 -53.5t-48.5 -41t-54.5 -36.5q144 -51 144 -174q0 -55 -43.5 -108t-104.5 -87q-77 -42 -131 -42q-31 0 -54 20t-31 47l11 18q48 -29 108 -29q79 0 119.5 43t40.5 109t-44.5 107.5t-119.5 50.5l22 47q34 1 65 21q96 61 96 157q0 42 -24 67.5 t-62 25.5q-24 0 -43.5 -9t-35 -29.5t-27 -44t-22.5 -63t-19.5 -75.5t-18.5 -91q-57 -294 -68 -380q-26 -190 -35 -200q-26 -31 -97 -37l-4 26q19 9 48 170l77 413q23 121 52.5 187.5t83.5 114.5q70 62 148 62q51 0 88.5 -34t37.5 -91z"/>
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	</svg>, and IL-18 in Bacterial Infections

In obesity and type 2 diabetes, efficient skeletal muscle repair following injury may be required, not only for restoring muscle structure and function, but also for maintaining exercise capacity and insulin sensitivity. The hypothesis of this study was that muscle regeneration would be impaired in ob/ob and db/db mice, which are common mouse models of obesity and type 2 diabetes. Muscle injury was produced by cardiotoxin injection, and regeneration was assessed by morphological and immunostaining techniques. Muscle regeneration was delayed in ob/ob and db/db mice, but not in a less severe model of insulin resistance &#8211; feeding a high-fat diet to wild-type mice. Angiogenesis, cell proliferation, and myoblast accumulation were also impaired in ob/ob and db/db mice, but not the high-fat diet mice. The impairments in muscle regeneration were associated with impaired macrophage accumulation; macrophages have been shown previously to be required for efficient muscle regeneration. Impaired regeneration in ob/ob and db/db mice could be due partly to the lack of leptin signaling, since leptin is expressed both in damaged muscle and in cultured muscle cells. In summary, impaired muscle regeneration in ob/ob and db/db mice was associated with reduced macrophage accumulation, angiogenesis, and myoblast activity, and could have implications for insulin sensitivity in the skeletal muscle of obese and type 2 diabetic patients.

Mai-Huong Nguyen

Ming Cheng

Timothy J. Koh

Impaired Muscle Regeneration in Ob/ob and Db/db Mice

Inflammasomes are intracellular multiprotein complexes that coordinate the maturation of interleukin (IL)-1&#x3b2; and IL-18 in response to pathogens and metabolic danger. Both cytokines have been linked to intestinal inflammation. However, recently evolving concepts ascribe a major role to the inflammasome in maintaining intestinal homeostasis. This review recapitulates its position in the development of inflammatory bowel disease, thereby outlining a model in which hypo- as well as hyperfunctionality can lead to an imbalance of the system, depending on the specific cell population affected. In the epithelium, the inflammasome is essential for regulation of permeability and epithelial regeneration through sensing of commensal microbes, while excessive inflammasome activation within the lamina propria contributes to severe intestinal inflammation.

Donata Lissner

Britta Siegmund

The Multifaceted Role of the Inflammasome in Inflammatory Bowel Diseases

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Cytokines & Chemokines

Cytokines & Chemokines

Articles

Cytokines: Pulling the Body Together as a Whole

In Vivo Expression of Interleukin-37 Reduces Local and Systemic Inflammation in Concanavalin A-Induced Hepatitis

Subcutaneous Adipose Tissue from Obese and Lean Adults Does Not Release Hepcidin In Vivo

Beyond Fat Mass: Exploring the Role of Adipokines in Rheumatic Diseases

Role of the Inflammasome, IL-1 , and IL-18 in Bacterial Infections

Impaired Muscle Regeneration in Ob/ob and Db/db Mice

The Multifaceted Role of the Inflammasome in Inflammatory Bowel Diseases