scholarly journals The Drosophila Chitinase-Like Protein IDGF3 Is Involved in Protection against Nematodes and in Wound Healing

2015 ◽  
Vol 8 (2) ◽  
pp. 199-210 ◽  
Author(s):  
Lucie Kucerova ◽  
Vaclav Broz ◽  
Badrul Arefin ◽  
Houda Ouns Maaroufi ◽  
Jana Hurychova ◽  
...  
Keyword(s):  
Wound Healing ◽  
Entomopathogenic Nematode ◽  
Glycosyl Hydrolase ◽  
Structural Similarity ◽  
Protective Role ◽  
Transcriptional Analysis ◽  
Inflammatory Reactions ◽  
Human Disorders ◽  
Molecular Context ◽  
Inflammatory Processes

Chitinase-like proteins (CLPs) of the 18 glycosyl hydrolase family retain structural similarity to chitinases but lack enzymatic activity. Although CLPs are upregulated in several human disorders that affect regenerative and inflammatory processes, very little is known about their normal physiological function. We show that an insect CLP (Drosophila imaginal disc growth factor 3, IDGF3) plays an immune-protective role during entomopathogenic nematode (EPN) infections. During these infections, nematodes force their entry into the host via border tissues, thus creating wounds. Whole-genome transcriptional analysis of nematode-infected wild-type and Idgf3 mutant larvae have shown that, in addition to the regulation of genes related to immunity and wound closure, IDGF3 represses Jak/STAT and Wingless signaling. Further experiments have confirmed that IDGF3 has multiple roles in innate immunity. It serves as an essential component required for the formation of hemolymph clots that seal wounds, and Idgf3 mutants display an extended developmental delay during wound healing. Altogether, our findings indicate that vertebrate and invertebrate CLP proteins function in analogous settings and have a broad impact on inflammatory reactions and infections. This opens the way to further genetic analysis of Drosophila IDGF3 and will help to elucidate the exact molecular context of CLP function.

scholarly journals Apoptosis and inflammation

1995 ◽  
Vol 4 (1) ◽  
pp. 5-15 ◽  
Author(s):  
C. Haanen ◽  
I. Vermes
Keyword(s):  
Cell Death ◽  
Inflammatory Reaction ◽  
Inflammatory Diseases ◽  
Apoptotic Cell ◽  
Cell Damage ◽  
Target Cells ◽  
Apoptotic Bodies ◽  
Accidental Injury ◽  
Inflammatory Reactions ◽  
Inflammatory Processes

During the last few decades it has been recognized that cell death is not the consequence of accidental injury, but is the expression of a cell suicide programme. Kerr et al. (1972) introduced the term apoptosis. This form of cell death is under the influence of hormones, growth factors and cytokines, which depending upon the receptors present on the target cells, may activate a genetically controlled cell elimination process. During apoptosis the cell membrane remains intact and the cell breaks into apoptotic bodies, which are phagocytosed. Apoptosis, in contrast to necrosis, is not harmful to the host and does not induce any inflammatory reaction. The principal event that leads to inflammatory disease is cell damage, induced by chemical/physical injury, anoxia or starvation. Cell damage means leakage of cell contents into the adjacent tissues, resulting in the capillary transmigration of granulocytes to the injured tissue. The accumulation of neutrophils and release of enzymes and oxygen radicals enhances the inflammatory reaction. Until now there has been little research into the factors controlling the accumulation and the tissue load of granulocytes and their histotoxic products in inflammatory processes. Neutrophil apoptosis may represent an important event in the control of intlamtnation. It has been assumed that granulocytes disintegrate to apoptotic bodies before their fragments are removed by local macrophages. Removal of neutrophils from the inflammatory site without release of granule contents is of paramount importance for cessation of inflammation. In conclusion, apoptotic cell death plays an important role in inflammatory processes and in the resolution of inflammatory reactions. The facts known at present should stimulate further research into the role of neutrophil, eosinophil and macrophage apoptosis in inflammatory diseases.

scholarly journals PPARs in Irradiation-Induced Gastrointestinal Toxicity

PPAR Research ◽  
2010 ◽  
Vol 2010 ◽  
pp. 1-12 ◽  
Author(s):  
Christine Linard ◽  
Maâmar Souidi
Keyword(s):  
Normal Tissue ◽  
Treatment Time ◽  
Therapeutic Benefit ◽  
Gastrointestinal Toxicity ◽  
Overall Treatment Time ◽  
Inflammatory Reactions ◽  
Normal Tissues ◽  
Inflammatory Processes ◽  
Patients Experience ◽  
Abdominal Irradiation

The use of radiation therapy to treat cancer inevitably involves exposure of normal tissues. Although the benefits of this treatment are well established, many patients experience distressing complications due to injury to normal tissue. These side effects are related to inflammatory processes, and they decrease therapeutic benefit by increasing the overall treatment time. Emerging evidence indicates that PPARs and their ligands are important in the modulation of immune and inflammatory reactions. This paper discusses the effects of abdominal irradiation on PPARs, their role and functions in irradiation toxicity, and the possibility of using their ligands for radioprotection.

scholarly journals Xylanase Gene Transcription in Trichoderma reesei Is Triggered by Different Inducers Representing Different Hemicellulosic Pentose Polymers

2013 ◽  
Vol 12 (3) ◽  
pp. 390-398 ◽  
Author(s):  
Silvia Herold ◽  
Robert Bischof ◽  
Benjamin Metz ◽  
Bernhard Seiboth ◽  
Christian P. Kubicek
Keyword(s):  
Trichoderma Reesei ◽  
Plant Cell Wall ◽  
Glycosyl Hydrolase ◽  
Xylose Reductase ◽  
Genome Mining ◽  
Transcriptional Analysis ◽  
Cell Wall Degrading Enzymes ◽  
Content Type ◽  
Knockout Mutants ◽  
Catabolite Repressor

ABSTRACTThe ascomyceteTrichoderma reeseiis a paradigm for the regulation and production of plant cell wall-degrading enzymes, including xylanases. Four xylanases, including XYN1 and XYN2 of glycosyl hydrolase family 11 (GH11), the GH10 XYN3, and the GH30 XYN4, were already described. By genome mining, we identified a fifth xylanase, XYN5, belonging to GH11. Transcriptional analysis reveals that the expression of all xylanases butxyn3is induced byd-xylose, dependent on the cellulase and xylanase regulator XYR1 and negatively regulated by the carbon catabolite repressor CRE1. Impairment ofd-xylose catabolism at thed-xylose reductase and xylitol dehydrogenase step strongly enhanced induction byd-xylose. Knockout of thel-xylulose reductase-encoding genelxr3, which connects thed-xylose andl-arabinose catabolic pathways, had no effect on xylanase induction. Besides the induction byd-xylose, theT. reeseixylanases were also induced byl-arabinose, and this induction was also enhanced in knockout mutants inl-arabinose reductase (xyl1),l-arabitol dehydrogenase (lad1), andl-xylulose reductase (lxr3). Induction byl-arabinose was also XYR1 dependent. Analysis of intracellular polyols revealed accumulation of xylitol in all strains only during incubation withd-xylose and accumulation ofl-arabitol only during incubation withl-arabinose. Induction byl-arabinose could be further stimulated by addition ofd-xylose. We conclude that the expression of theT. reeseixylanases can be induced by bothd-xylose andl-arabinose, but independently of each other and by using different inducing metabolites.

scholarly journals Impact of Diabetes on the Protective Role of FOXO1 in Wound Healing

2015 ◽  
Vol 94 (8) ◽  
pp. 1025-1026 ◽  
Author(s):  
E. Xiao ◽  
D.T. Graves
Keyword(s):  
Wound Healing ◽  
Protective Role

KdPT: Novel protective role against impaired wound healing in diabetes?

2013 ◽  
Vol 29 ◽  
pp. S3
Author(s):  
ParaskeviGkogkolou ◽  
Michal Sarna ◽  
Thomas A. Luger ◽  
Markus Böhm
Keyword(s):  
Wound Healing ◽  
Protective Role ◽  
Impaired Wound Healing

Anti-inflammatory properties of probiotic bacteria on Salmonella-induced IL-8 synthesis in enterocyte-like Caco-2 cells

2010 ◽  
Vol 1 (2) ◽  
pp. 121-130 ◽  
Author(s):  
J. Malago ◽  
P. Tooten ◽  
J.F. Koninkx
Keyword(s):  
Tissue Damage ◽  
Protective Role ◽  
Bifidobacterium Bifidum ◽  
Probiotic Bacterium ◽  
Hsp70 Expression ◽  
Bacterial Cells ◽  
Salmonella Enterica Serovar Enteritidis ◽  
Inflammatory Reactions ◽  
Mediated Reduction

Invasion of the gut by pathogenic Salmonella leads to production of IL-8 that initiates inflammatory reactions to combat the bacterium. However, its persistent production causes tissue damage and interventions that suppress IL-8 production prevent tissue damage. We hypothesised that probiotics could mediate their benefits via inhibition of IL-8 synthesis. Caco-2 cells were infected with probiotic Bifidobacterium infantis W52, Lactobacillus casei W56, Lactococcus lactis W58, Lactobacillus acidophilus W70, Bifidobacterium bifidum W23, or Lactobacillus salivarius W24 or pathogenic Salmonella enterica serovar Enteritidis 857 at 0, 0.2, 1, 2, 10, 20, 100 or 200 bacterial cells/Caco-2 cell for 1 hour. Cells were also exposed to a combination of one probiotic bacterium (200 bacterial cells/Caco-2 cell) and the graded numbers of Salmonella as either co-incubation (1 hour) or pre-incubation of the probiotic bacterium (1 hour) followed by Salmonella (1 hour). The cells recovered for 2 or 24 hours. IL-8 and Hsp70 were determined by ELISA and Western blot respectively. Both probiotics and Salmonella induced a dose- and time-dependent synthesis of IL-8 but probiotics induced far lower IL-8 levels than Salmonella. The Salmonella-induced IL-8 was significantly suppressed by B. infantis W52, L. casei W56 and L. lactis W58 at low numbers of Salmonella (0.2 to 20 bacterial cells/Caco-2 cell) and within 2 hours of recovery. The observed probiotic-mediated reduction in IL-8 secretion was transient, and lost after a few hours. In addition, these three probiotics induced a significant increase in Hsp70 expression while L. acidophilus W70, B. bifidum W23 and L. salivarius W24 induced a weak Hsp70 expression and could not suppress the Salmonella-induced IL-8 synthesis. We conclude that suppression of Salmonella-induced IL-8 synthesis by Caco-2 cells is exhibited by probiotics that induce expression of Hsp70, suggesting that the protective role of probiotics could be mediated, at least in part, via Hsp70 expression. This suppression is limited to a low number of infecting pathogenic Salmonella.

scholarly journals Testosterone-Induced Effects on Lipids and Inflammation

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Stella Vodo ◽  
Nicoletta Bechi ◽  
Anna Petroni ◽  
Carolina Muscoli ◽  
Anna Maria Aloisi
Keyword(s):  
Chronic Pain ◽  
Adult Population ◽  
Protective Role ◽  
Gonadal Hormones ◽  
The Body ◽  
Pain Mechanisms ◽  
Proinflammatory Mediators ◽  
General Terms ◽  
Inflammatory Processes ◽  
Report Data

Chronic pain has to be considered in all respects a debilitating disease and 10–20% of the world's adult population is affected by this disease. In the most general terms, pain is symptomatic of some form of dysfunction and (often) the resulting inflammatory processes in the body. In the study of pain, great attention has been paid to the possible involvement of gonadal hormones, especially in recent years. In particular, testosterone, the main androgen, is thought to play a beneficial, protective role in the body. Other important elements to be related to pain, inflammation, and hormones are lipids, heterogenic molecules whose altered metabolism is often accompanied by the release of interleukins, and lipid-derived proinflammatory mediators. Here we report data on interactions often not considered in chronic pain mechanisms.

Atrial fibrillation and physical activity

2013 ◽  
Vol 154 (13) ◽  
pp. 503-509
Author(s):  
Péter Apor
Keyword(s):  
Oxidative Stress ◽  
Physical Activity ◽  
Atrial Fibrillation ◽  
Vagal Tone ◽  
Protective Role ◽  
Mental Illnesses ◽  
Endurance Sports ◽  
Inflammatory Processes ◽  
Regular Medium ◽  
Underlying Pathology

Atrial fibrillation is the most frequent arrhythmia. Its „lone” form (when underlying pathology is not discovered) can be detected in a few percent of endurance sports participants, and in growing occurrence among the veterans, probably on the basis of some cardiac or other irregularities. Enhanced vagal tone and sudden sympathetic impulse, repetitive oxidative stress, inflammatory processes, enlarged atria, electric instabilization can explain the higher occurrence. Treatment of atrial fibrillation enables the affected persons to participate in regular medium-intensity exercise, 3–5 hours a week, which offers a protective role against cardiovascular, metabolic and mental illnesses. Orv. Hetil., 2013, 154, 503–509.

Novel stabilin-1 interacting chitinase-like protein (SI-CLP) is up-regulated in alternatively activated macrophages and secreted via lysosomal pathway

Blood ◽  
2006 ◽  
Vol 107 (8) ◽  
pp. 3221-3228 ◽  
Author(s):  
Julia Kzhyshkowska ◽  
Srinivas Mamidi ◽  
Alexei Gratchev ◽  
Elisabeth Kremmer ◽  
Christina Schmuttermaier ◽  
...  
Keyword(s):  
Direct Interaction ◽  
Activated Macrophages ◽  
Blood Leukocytes ◽  
Alternatively Activated Macrophages ◽  
Inflammatory Reactions ◽  
Chitin Binding Domain ◽  
Endocytic Sorting ◽  
Catalytically Active ◽  
Human Disorders ◽  
Alternatively Activated

Abstract Mammalian Glyco_18-domain–containing proteins include catalytically active chitinases and chitinase-like proteins with cytokine activity involved in host defense and Th2-type inflammatory reactions. Here, we describe a novel human Glyco_18-domain–containing protein, SI-CLP, as an interacting partner of the endocytic/sorting receptor stabilin-1. Similarly to the chitinase-like cytokines YKL-39, YKL-40, and YM1/2, SI-CLP lacks a chitin-binding domain and catalytic amino acids. Using a novel mAb 1C11, we demonstrated that SI-CLP is sorted into late endosomes and secretory lysosomes in human alternatively activated macrophages. The direct interaction of SI-CLP with stabilin-1, their colocalization in the trans-Golgi network, and the reduced sorting of SI-CLP into lysosomes in macrophages treated with stabilin-1 siRNA suggest that stabilin-1 is involved in intracellular sorting of SI-CLP. Expression of SI-CLP in macrophages was strongly up-regulated by the Th2 cytokine IL-4 and by dexamethasone. This effect was suppressed by IFNγ but not affected by IL-10. In contrast, expression of YKL-40 was induced by IFNγ and suppressed by dexamethasone. Macrophages treated with IL-4 secreted SI-CLP, while costimulation with dexamethasone blocked secretion and resulted in intracellular accumulation of SI-CLP. The 1C11 mAb detected SI-CLP in human bronchoalveolar lavage and peripheral-blood leukocytes (PBLs), and can be used to analyze the role of SI-CLP in human disorders.

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