PubMedCrossRef 8. Vousden KH, Lane DP: p53 in health and disease. Nat Rev Mol Cell Biol 2007, 8:275–283.PubMedCrossRef

9. Bode AM, Dong Z: Post-translational modification of p53 in tumorigenesis. Nat Rev LEE011 datasheet Cancer 2004, 4:793–805.PubMedCrossRef 10. Brown CJ, Lain S, Verma CS, Fersht AR, Lane DP: Awakening guardian angels: drugging the p53 pathway. Nat Rev Cancer 2009, 9:862–873.PubMedCrossRef 11. Selivanova G: Therapeutic targeting of p53 by small molecules. Semin Cancer Biol 2010, 20:46–56.PubMedCrossRef 12. Puca R, Nardinocchi L, Givol D, D’Orazi G: Regulation of p53 activity by HIPK2: molecular mechanisms and therapeutical implications in human cancer cells. Oncogene 2010, 29:4378–4387.PubMedCrossRef 13. Nardinocchi L, Puca R, D’Orazi G: HIPK2-A therapeutical target to be (re)activated for tumor suppression. Role in p53 activation and HIF-1α inhibition. Cell Cycle 2010, 9:1–6.CrossRef 14. Di Stefano V, Rinaldo C, Sacchi A, Soddu S, D’Orazi G: Homeodomain-interacting protein kinase-2 activity and p53 phosphorylation are critical events for cisplatin-mediated apoptosis. Exp Cell Res 2004,

293:311–320.PubMedCrossRef 15. Dauth I, Kruger J, Hofmann TG: Homeodomain-Interacting Protein kinase 2 is the ionizing radiation-activated p53 serine 46 kinase and is regulated by ATM. Cancer Res 2007, 67:2274–2279.PubMedCrossRef 16. Wesierska-Gadek J, Schmitz ML, Ranftler C: Roscovitine-activated HIPK2 kinase induces phosphorylation of wtp53 at Ser-46 in human MCF-7 breast cancer cells. J Cell Biochem 2007, 100:865–874.PubMedCrossRef 17. Hofmann TG, Moller A, Sirma H, Zentgraf H, Taya Y, Dröge W, Will H, Schmitz ML: Regulation of p53 activity by its interaction find more with homeodomain-interacting protein kinase-2. Nat Cell Biol 2002, 4:1–10.PubMedCrossRef 18. Puca R, Nardinocchi L, Sacchi A, Rechavi G, Givol D, D’Orazi G: HIPK2 modulates p53 activity towards pro-apoptotic transcription.

Mol Cancer 2009, 8:1–14.PubMedCrossRef 19. Gresko E, Roscic A, Ritterhoff S, Vichalkovski A, Del Sal G, Schmitz ML: Autoregulatory control of the p53 Oxymatrine response by caspase-mediated processing of HIPK2. EMBO J 2006, 25:1883–1894.PubMedCrossRef 20. Marchetti A, Cecchinelli B, D’Angelo M, D’Orazi G, Crescenzi M, Sacchi A, Soddu S: p53 can inhibit cell proliferation through caspase-mediated cleavage of ERK-MAPK. Cell Death Differ 2004, 11:596–607.PubMedCrossRef 21. D’Orazi G, Sciulli MG, Di Stefano V, Riccioni S, Frattini M, Falcioni R, Bertario L, Sacchi A, Patrignani P: Homeodomain-interacting protein kinase-2 restrains cytosolic phospholipase A2-dependent prostaglandin E2 generation in human colorectal cancer cells. Clin Cancer Res 2006, 12:735–741.PubMedCrossRef 22. Puca R, Nardinocchi L, Gal H, Rechavi G, Amariglio N, Domany E, Notterman DA, Scarsella M, Leonetti C, Sacchi A, Blandino G, Givol D, D’Orazi G: Reversible dysfunction of wild-type p53 following homeodomain-interacting protein kinase-2 knockdown. Cancer Res 2008, 68:3707–3714.PubMedCrossRef 23.

Normal hospital response to severe trauma begins with trauma team activation following advance notification. This is the ideal in isolated trauma scenarios but is even more imperative in mass casualty

scenarios. Communication has been identified as a key component of disaster preparedness and response. An analysis of the response to three sequential aircraft crashes in Texas, found communication to be one of the major problems encountered in the implementation of the community and hospital disaster Ibrutinib cell line plan [5]. Its total absence meant that we were completely unprepared to receive the first surge of casualties and each subsequent surge was without advance warning. Communication was also needed for mobilizing personnel and other resources from within and outside the hospital, and for information and media management as well as the coordination of response efforts between medical personnel and other agencies of government involved in the disaster response such as the police, military, Red Cross, and other voluntary organizations. The lack of this communication made the overall response efforts disjointed and uncoordinated.

The crisis took place before the introduction of mobile telephony in our city and we do not have pagers or two way radios. The existing hospital intercom system and the fixed lines proved grossly inadequate for the internal and external communication needs respectively. Field triage was crude and did not follow any organized SCH772984 systems. Injured patients were merely conveyed to the hospital if they were fortunate

enough to chance upon a military patrol, aid workers and volunteers, or other good Samaritans who were willing and able to help. The aim of triage is to identify that minority of critically injured patients, out of the large pool of patients with less severe injuries so that trauma care assets can be prioritized in favor of the former. Effective triage is necessary to screen out the majority of non critically FER injured survivors, and results are best when performed by a trained physician in the field [6]. A change in philosophy occurs in the approach to the management of mass casualty: the goal is to do the ‘greatest good for the greatest number’ and not the greatest good for the individual [2, 7]. Most effective triage systems accept an overtriage rate of up to 50%, i.e. patients who have been triaged as having critical injuries when in fact they had less severe injuries. This high rate is necessary to reduce the undertriage rate to below 0.5%, i.e. the proportion of patients who were triaged as having non critical injuries when in fact they had critical injuries [7]. In the absence of systematic field triage, a high proportion of patients brought to our facility had non critical injuries as every injured patient was evacuated to the hospital.

Such analyses might also highlight novel targets for antimicrobials. Moreover, expression profiling is considered as a fingerprint to find common and distinct responses that could aid in the design of combined therapies of unrelated compounds, to which AMP might contribute. However, this type of studies

are still scarce in the case of AMP, with only a few examples in bacteria [26–29] and fungi, mostly yeast [30–33]. Transcriptome LY2606368 molecular weight profiling has been used to characterize the response of the model yeast Saccharomyces cerevisiae to distinct antifungals [34–39], including selected AMP [30, 33]. In this study we aim to compare at a genomic scale the effects onto S. cerevisiae of two AMP with distinctive properties. Melittin is an α-helical membrane active peptide identified from honeybee venom that is recognized as a model pore-forming peptide for the study of peptide interaction with lipid bilayers and cell permeating properties [40]. On the other hand, PAF26 is a short de novo-designed hexapeptide [41], which shares sequence similarity with other AMP from natural [42] or synthetic origin

[43, 44]. It has activity against plant pathogenic fungi as well as several microorganisms of clinical relevance, including the yeast Candida and several dermatophytic fungi [45]. PAF26 at low micromolar (sub-inhibitory) concentrations has been recently shown to have cell penetrating properties in check details the mycelium and conidia of the filamentous plant pathogen Penicillium digitatum [46] and the model fungus Neurospora crassa (A. Muñoz and N. Read, unpublished observations). Contrary to melittin, PAF26 is less active against

bacteria and is not haemolytic under assay conditions in which other peptides including melittin are [45]. We combined global analyses of transcriptomic changes upon exposure of S. cerevisiae to sub-lethal concentrations of either PAF26 or melittin with sensitivity Thymidine kinase tests of strains lacking genes identified by the transcriptomic data. Our results both reinforce and extend similar studies undertaken previously with two unrelated α-helical AMP [33], and reveal that PAF26 and melittin have common but also distinctive effects on yeast. Results Antimicrobial activity of peptides PAF26 and melittin against S. cerevisiae PAF26 and the pore-forming peptide melittin inhibited yeast growth [41], as was confirmed herein with strain FY1679 (Figure 1A and Additional File 1) in experiments that show a slight 2-fold higher potency of melittin. Dose-response experiments with additional strains of yeast with distinct genetic backgrounds and at two temperatures of incubation confirmed the activity of both peptides and also indicated a differential sensitivity of strains (Additional File 1).

The title of his Gordon Conference poster was: “Photosystem II water oxidation: Photothermal beam deflection reveals volume changes associated with proton movements”. Gary F. Moore (2008) Gary F. Moore obtained his B·S. degree from The Evergreen State College (in 2004). He received his PhD (in 2009) under Ana L. Moore, Thomas A. Moore, and Devens Gust from Arizona State University, Tempe, Arizona, USA, where he was a National Science Foundation fellow. Gary is currently working selleck chemicals llc with the Green Energy Consortium at Yale University, New Haven, Connecticut, USA, as The Camille and Henry Dreyfus Foundation Postdoctoral

Fellow with the research groups of Gary W. Brudvig, Robert H. Crabtree, Victor S. Batista, and Charles A. Schmuttenmaer. His research efforts are focused on the design and assembly of bioinspired constructs for solar energy conversion. The intent of this study is to further enhance the understanding of energy flow in biological systems while using these insights to develop hybrid energy transduction schemes to meet human needs. The title of his 2008 Gordon Conference poster was: “Proton Coupled Electron Transfer in a Bioinspired Mediator.” Tim Schulte (2009) Tim Schulte graduated from the Ruhr-University Bochum (RUB), Germany, with a M.S. in Biochemistry in 2006. Tim soon became fascinated with ‘how protein structures are related to their function’. In the laboratory of Eckhard Hofmann, he became involved

with X-ray crystallography to study the molecular structures of proteins. In his Master’s

thesis, PI3K Inhibitor Library order he provided the X-ray structure of a soluble light-harvesting antenna that is unique to dinoflagellates; it was a high-salt variant of Peridinin-Chlorophyll a-Protein (HSPCP). His research, as a part of his current PhD work, is very well expressed by the title of his poster at the 2009 Gordon Conference: “X-ray structures and transient absorption measurements of in vitro refolded Peridinin-Chlorophyll a-Proteins (PCP): Identification of one peridinin-sensing the Chl a excitation—Mapping Photosynthetic Function onto Structure”. Tim is looking forward to finishing his PhD next year in the acetylcholine Institute of Biophysics (Department of Biology and Biotechnology, RUB). Jianzhong Wen (2008) Jianzhong Wen received his B. S. in Physics from Wuhan University in China in 2004. He is currently a doctoral student of Robert E. Blankenship of the Department of Chemistry, Washington University in St. Louis, Missouri, USA. Jianzhong’s goal is to understand how individual protein complexes, in photosynthetic systems, are built into a beautiful architecture to achieve efficient light-harvesting and energy storage processes. He uses chromatography, optical spectroscopy, and mass spectroscopy to achieve his goal. He has contributed to the discovery of the 8th bacteriochlorophyll a molecule in the Fenna–Mathews–Olson (FMO) antenna protein from green sulfur bacteria.

pylori as a class I human carcinogen, it now is well accepted that gastric infection PARP inhibitor by H. pylori is a risk factor for development of gastric cancer [8]. Although the precise pathogenetic role of H. pylori in gastric carcinogenesis remains unclear, it has been clarified that this organism contributes to modifications in epithelial cell proliferation, which may be the initiating event in a cascade culminating in the development of gastric cancer [9], but

it is not known whether the increased risk is due to the presence of mutant p53 generated by chronic gastritis or to a direct action of the bacteria on the p53 oncogene [10, 11]. The p53 gene mutation is associated with approximately 70% of tumors of different orignis [12, 13]. p53 gene serves as a “”gatekeeper of the cell”", for its role in preventing the accumulation of genetic alterations through the regulation of critical checkpoints between the end of G1 and the beginning of S to redirect cells with a mutation in the genome toward apoptosis or programmed cell death. This key oncogene thus prevents the perpetuation of a defective genome selleck inhibitor and the development of a cancer [14]. Several recent studies have been published on the presence of p53 in patients with H. pylori infection, stomach cancer, or both. However, the conclusions are contradictory, and it has

been difficult to develop a single coherent hypothesis that can account for all findings communicated to date [15]. Palli et al [16] found p53 mutants in 33 of for 105 cases of gastric cancer and Domek et al [17] worked with the hypothesis that tumorigenesis involves

deregulation of cell proliferation and apoptosis. These researchers investigated cell proliferation and apoptosis in the gastric epithelium of children infected with H. pylori, and found that the apoptotic index was significantly higher in patients with H. pylori gastritis than in patients with secondary gastritis or healthy control subjects. They also reported that apoptosis decreased when the bacterial infection was eradicated. Wu et al, reported the existence of different pathways of gastric carcinogenesis in different histological subtypes of gastric cancer and its progression, in which H. pylori infection can play an important role [18]. Hibi et al, concluded that persistent H. pylori infection caused gastritis, with degeneration and regeneration of the epithelium that increased cell proliferation and the accumulation of p53 [19]. This in turn increased instability of the gene, as reflected by the development of carcinoma, using immunohistochemical methods to investigate p53 expression, and concluded that expression is associated with histopathological phenotypes, and that genetic alterations may not be affected by H. pylori infection [20]. Chang et al, noted the possibility that H.

79c). Hamathecium of dense, long cellular pseudoparaphyses 1–2 μm broad, septate, branching (Fig. 79b). Asci 125–170(−195) × 15–22 μm (\( \barx = 153.8 \times 19.3\mu m \), n = 10), 8-spored, bitunicate, fissitunicate, cylindrical to cylindro-clavate,

with a short, narrowed, furcate pedicel which is 10–20 μm long, with an ocular chamber best seen in immature asci (to 5 μm broad × 3 μm high) (Fig. 79d and e). Ascospores 22–30 × 11–14 μm check details (\( \barx = 27.1 \times 12.6\mu m \), n = 10) obliquely uniseriate and partially overlapping, ellipsoid, ovoid to fusoid, yellowish to yellowish brown, becoming reddish brown to dark brown, muriform, with 3-(4) transverse septa, constricted at the primary septum, part above central septum wider, vertical septa exist in each cell, ornamentation https://www.selleckchem.com/products/pexidartinib-plx3397.html of foveolae in linear rows (Fig. 79f and g). Anamorph: Camarosporium yuccaesedum Fairm. (Ramaley and Barr 1995). Conidiomata 200–450 μm diam., pycnidial, immersed, scattered, subglobose to conoid, ostiolate. Macroconidiogenous cells determinate or indeterminate, enteroblastic,

hyaline, smooth. Macroconidia holoblastic, 20–36 × 10–15 μm diam., ellipsoid to narrowly ovoid, muriform, yellowish brown, 3–7 transverse septa, constricted at the septa. Microconidiogenous cells produced near or in the ostiole, hyaline, smooth. Microconidia 5–10 × 5–7 μm diam., globose to ovoid, aseptate, hyaline, smooth. Material examined: USA, Colorado, Montezuma County, hillside near entrance to Mesa Verde National Park, on dead leaves of Yucca baccata, 11 Oct. 1992, Ramaley Annette (9237A) (BPI 802381, holotype). Notes Morphology Pleoseptum is a monotypic genus established by Ramaley and Barr (1995) and represented by P. yuccaesedum based on its “immersed ascomata, thick peridium, muriform ascospores, anamorphic stage and the linoeate ornamentation of the ascospores and conidia”. The shape of ascomata of Pleoseptum is comparable with that of Chaetoplea,

but the peridium structure easily distinguishes them. Some species of Curreya, Leptosphaeria and Heptameria are comparable with Pleoseptum, but their anamorphic stages differ. Pleoseptum yuccaesedum and its Camarosporium Protein tyrosine phosphatase yuccaesedum anamorph both formed in the leaves of Yucca baccata and the ascomata and conidiomata were indistinguishable. Camarosporium is the anamorph of diverse teleomorph genera included in Botryosphaeriales and Cucurbitariaceae (Kirk et al. 2008). The genus is in need of revision (Sutton 1980) and is no doubt polyphyletic. Phylogenetic study None. Concluding remarks The placement of Pleoseptum under Phaeosphaeriaceae is still tentative. Pleospora Rabenh. ex Ces. & De Not., Comm. Soc. crittog. Ital. 1: 217 (1863). (Pleosporaceae) Generic description Habitat terrestrial, saprobic or parasitic. Ascomata small- to medium-sized, immersed, erumpent to superficial, papillate, ostiolate. Peridium thin. Hamathecium of dense, cellular pseudoparaphyses.

M. perniciosa strain CEPEC 1108 (designated CP03) of the C biotype of M. perniciosa was also used for morphological studies. Mycelial starter cultures from the culture collection of the Cocoa Research Center (CEPEC, Ilhéus, Bahia, Brazil) were grown on PDA (Potato Dextrose Agar) for three weeks in the dark, at room temperature. Basidiomata were obtained from mycelial mats, as described by Griffith and Hedger [7] with the modifications

introduced by Niella et al. [15]. A solid bran-based medium was prepared (50 g wheat flour; 40 g vermiculite; 6 g CaSO4 × 2H2O, 3 g CaCO3 and 120 mL distilled water; moisture content 65–70%, pH 7.0–7.5). The mixture was placed in Petri dishes, covered with aluminum foil and autoclaved Crizotinib mw twice for 90

min (121°C). The cooled medium was inoculated with two 5-mm disc plugs from 1 to 3-week-old mycelium, grown on 2% PDA medium. Cultures were incubated at 25°C in the dark. After mycelia had completely colonized the surface of the bran medium (usually 3–4 weeks), cultures were covered with a 5-mm thick layer (5–10 g per culture), composed of 200 g coarse peat, 50 g CaCO3, 50 g vermiculite and 125 mL distilled water (moisture content 70–75%, pH 7.0–7.5). These cultures were incubated for 3 to 4 Wnt beta-catenin pathway weeks at 25°C in the dark and then hung vertically in a broom chamber [14], and maintained at 23°C ± 2°C for 75 d. Irrigation consisted of spraying de-ionized water daily for 7 h with a 12 h period of fluorescent warm white light (65–80 W). After 30 d in the chambers, the irrigation was suspended for 7 d, a procedure selleck routinely used to induce fructification. Microscopic analyses

The preparation of mycelial mat samples for light microscopy was conducted according to standard histological methods [66]. For histological studies of basidiomata development at various stages, samples were fixed after collection by dehydration in a gradient of ethanol/tertiary butyl alcohol series (50 to 100%) for 2 h each, and thermally embedded in paraffin (melting point 56.5°C; Paraplast plus; Fisher Sci. Co., Pittsburgh, USA). The embedded tissues were radially cut (5 to 14 μm thick) with a rotary microtome. Serial sections were thermally mounted on microscope slides coated with Haupt’s adhesive and 4% formalin [67]. The sections were immersed/rinsed three times in 100% xylene and passed through a series of xylene and absolute ethyl alcohol (EtOH) 1:1, absolute ETOH, and 70% ETOH. Some sections were stained with Pianeze III-B stain [68, 69]. This procedure specifically stained soluble and insoluble proteins red with acid fuchsin and non-living material, i.e. polysaccharides and phenol, green to dark green [35]. Other sections were stained for 1 h with 1% astra blue and then for 1 h with 1% safranin.

In control bones which received no more than normal functional mechanical loading, NS-398 slightly but significantly decreased trabecular BV/TV of the proximal tibiae. This would be compatible with a small

reduction in bone mass of COX-2 deficient mice [11]. In bones that had been artificially loaded, COX-2 inhibition had no discernible effect on the loading-related lamellar or woven bone response in either trabecular or cortical compartments. As a result, NS-398 showed no influence on the loading-related increase in polar moment of inertia, a parameter of structural bone strength. Although there may be a potential small inhibitory effect of NS-398 on bone’s response to mechanical loading that could Protease Inhibitor Library cell line be detected only by histomorphometry, such an effect would not alter the conclusion of the present study. The present data are consistent with the evidence from female mice lacking COX-2 [11], showing that bone adaptation to two consecutive days of mechanical loading does not require a functional COX-2 gene. The authors [11] suggested a compensatory effect of COX-1 in vivo, though this enzyme does not appear to be important for bone cells’ response to a single period of fluid

flow in vitro [20]. If such compensation exists, it does not seem to be immediately available since in female Ibrutinib datasheet rats a single injection of NS-398 reduces the cortical response to a single period of mechanical Bortezomib loading [9, 10]. The data we present here suggest that compensation for the pharmacological inhibition of COX-2 function does exist and can occur sufficiently swiftly to ensure that adaptive (re)modelling of trabecular and cortical bone to artificial mechanical loading over a 2-week period is not

impaired. The relevance of the present experiment in female mice to the human condition must take into account a number of differences in the two situations. Importantly, however, our experimental data of three-dimensional bone architecture analysed by high-resolution μCT are compatible with clinical evidence that women taking COX-2 selective inhibitors such as celecoxib and rofecoxib do not have lower hip areal BMD [13]. In contrast to women, the use of the COX-2 selective inhibitors is associated with lower hip areal BMD in men [13]. It remains to be elucidated whether there are sex differences in the effects of COX-2 inhibition on bone’s response to mechanical loading. In conclusion, our present data demonstrate that in female mice pharmacological inhibition of COX-2 using daily NS-398 injection does not affect trabecular or cortical bone gain engendered by repeated periods of mechanical loading over a 2-week period.

We report a functional germline mutation (polymorphism) in the galectin-3 gene at position 191 (rs4644) selleck substituting proline with histidine (P64H), which results in susceptibility to matrix metalloproteinase (MMP) cleavage and acquisition of resistance

to drug-induced apoptosis. This substitution correlates with incidence of breast cancer and racial disparity. Of note, Cleavage of galectin-3 by MMPs is related to progression of breast and prostate cancer. We show that galectin-3 regulated functions like chemotaxis, chemoinvasion, heterotypic aggregation, epithelial-endothelial cell interactions and angiogenesis are dependent in part on cleavage of the N terminus of galectin-3 followed by its release in the tumor microenvironment. Breast carcinoma cells harboring cleavable galectin-3 species showed BMS354825 increased chemotaxis towards collagen IV, invasion through Matrigel and heterotypic interactions with endothelial cells resulting in angiogenesis and 3-D morphogenesis in vitro compared to cells harboring non-cleavable galectin-3. Wound healing studies employing a novel cell culture insert showed

increased migration and phosphorylation of focal adhesion kinase in endothelial cells migrating towards H64 cells compared to P64 cells. Using 3- dimensional co-cultures of endothelial cells with breast cells harboring galectin-3 peptides, we show that amino acids 1-62 and 33–250 stimulate migration and interaction of cells with the endothelial cells. Immunohistochemical

analysis of blood vessel density and galectin-3 cleavage in a breast cancer progression tissue array support the in vitro findings. These results indicate that cleavage of galectin-3 in tumor microenvironment leads to breast cancer angiogenesis and progression. In conclusion, Etofibrate we provide novel data implicating a galectin-3 germline nonsynonymous functional polymorphism in breast cancer progression and metastasis. O4 Extracellular Matrix Remodeling Forces Tumor Progression Valerie Marie Weaver 1 1 Department of Surgery, UCSF, San Francisco, CA, USA Tumor progression is accompanied by a desmoplastic response that is characterized by significant extracellular matrix (ECM) remodeling. We have been studying the role of matrix metalloproteinase and lysyl oxidase-mediated collagen cross-linking in ECM remodeling and tissue desmoplasia during breast tumor progression. Thus far we have established a positive association between lysyl oxidase-dependent collagen cross-linking, the accumulation of linear, oriented collagen fibrils, tissue fibrosis and tissue stiffening during breast transformation. We have demonstrated that either pharmacological or antibody-mediated inhibition of lysyl oxidase-induced collagen cross-linking prevents tissue fibrosis, reduces tissue stiffening, enhances tumor latency and decreases tumor incidence in both the MMTV-Neu and PyMT transgenic mouse models of breast cancer.

casei together with dextran, reduces murine and human allergic reaction. FEMS Immunol Med Microbiol 2006, 46:400–409.PubMedCrossRef 40. Schiffer C, Lalanne AI, Cassard L, Mancardi DA, Malbec O, Bruhns P, Dif F, Daëron M: A strain of Lactobacillus casei inhibits the effector phase of immune inflammation. J Immunol 2011, 187:2646–2655.PubMedCrossRef 41. Chow J, Mazmanian

SK: A pathobiont of the microbiota balances host colonization and intestinal inflammation. Cell Host Microbe 2010, 7:265–276.PubMedCrossRef 42. Atarashi K, Tanoue T, Shima T, Imaoka selleck A, Kuwahara T, Momose Y, Cheng G, Yamasaki S, Saito T, Ohba Y, Taniguchi T, Takeda K, Hori S, Ivanov II, Umesaki Y, Itoh K, Honda K: Induction of colonic regulatory T cells by indigenous Clostridium species. Science 2011, 331:337–341.PubMedCrossRef 43. Sokol H, Pigneur B, Watterlot check details L, Lakhdari O, Bermúdez-Humarán LG, Gratadoux JJ, Blugeon S, Bridonneau C, Furet JP, Corthier G,

Grangette C, Vasquez N, Pochart P, Trugnan G, Thomas G, Blottière HM, Doré J, Marteau P, Seksik P, Langella P: Faecalibacterium prausnitzii is an anti-inflammatory commensal bacterium identified by gut microbiota analysis of Crohn disease patients. Proc Natl Acad Sci U S A 2008, 105:16731–16736.PubMedCrossRef 44. Png CW, Lindén SK, Gilshenan KS, Zoetendal EG, McSweeney CS, Sly LI, McGuckin MA, Florin TH: Mucolytic bacteria with increased prevalence in IBD mucosa augment in vitro utilization of mucin by other bacteria. Am J Gastroenterol 2010, 105:2420–2428.PubMedCrossRef 45. Lupp C, Robertson ML, Wickham ME, Sekirov I, Champion OL, Gaynor EC, Finlay BB: Host-mediated inflammation disrupts the intestinal microbiota and promotes the overgrowth of Enterobacteriaceae. Cell Host Microbe 2007, 2:204.PubMedCrossRef 46. Frank DN, St Amand AL, Feldman RA, Boedeker

EC, Harpaz N, Pace NR: Molecular-phylogenetic characterization of microbial community imbalances in human inflammatory bowel Calpain diseases. Proc Natl Acad Sci U S A 2007, 104:13780–13785.PubMedCrossRef 47. Sokol H, Seksik P, Furet JP, Firmesse O, Nion-Larmurier I, Beaugerie L, Cosnes J, Corthier G, Marteau P, Doré J: Low counts of Faecalibacterium prausnitzii in colitis microbiota. Inflamm Bowel Dis 2009, 15:1183–1189.PubMedCrossRef 48. Schwiertz A, Jacobi M, Frick JS, Richter M, Rusch K, Köhler H: Microbiota in pediatric inflammatory bowel disease. J Pediatr 2010, 157:240–244.PubMedCrossRef Authors’ contributions MC conceived and designed the experiments, analyzed the data and wrote the first draft of the paper. SR and ST performed faecal microbial DNA extraction, 16 S rDNA amplification and purification, qPCR bacterial quantifications and PCA analysis. MS, CC, GDB performed all the HTF-Microbi.Array hybridization experiments and data analysis. RM, GR and AP enrolled subjects and performed skin prick test and IgE determination. PB conceived and designed the experiments. All authors read and approved the final manuscript.