This is surprising given that the placenta forms a crucial link between mother and her developing baby. This review will firstly describe our current understanding of how small fetoplacental blood vessels are affected by oxygenation. Secondly, the expression and function of K+ channels GW-572016 in vivo in small fetoplacental blood vessels will be discussed and the possible role of ambient oxygenation highlighted. Measurements of umbilical arterial (16–28 mmHg) and venous (28–35 mmHg; [40, 51]) blood samples suggest that human fetoplacental blood vessels experience oxygenation levels at term similar to those recorded in the IVS (40–45 mmHg; [30,

31, 6, 60]); i.e., a relatively hypoxic environment. Data using the perfused placental cotyledon model suggest that fetoplacental blood vessels can respond to local ambient oxygen [25, 28, 8, 27]; reducing perfusate

oxygenation increased pressure within the vascular circuit suggesting vascular contraction. However, one must question the physiological relevance of this data as oxygenation levels were reduced from “normoxia” of 400–500 mmHg down to 20–50 mmHg “hypoxia” [28, 8, 27, 55]. Data from Hampl et al. demonstrated reproducible HFPV and suggested that oxygen-sensitive K+ channels may be important for the detection and response to the hypoxic stimulus (see below for more detail) [25]. However, oxygen levels in this study were manipulated from ~120 to ~60 mmHg high throughput screening compounds in large diameter placental vessels, conditions more akin to the “pulmonary” physiological range (140–20 mmHg) [41, 75, 57, 56]. Ramasubramanian et al. also noted an HFPV response and additionally suggested this was graded depending on the level of hypoxia [54]; however, these comparisons were made relative to the control oxygenation (140 mmHg) with only a minor differential noted across the likely physiological range (75 ± 3 mmHg peak fetal arterial pressure at 35 mmHg O2 vs. 78 ± 6 mmHg peak fetal arterial pressure at 0 mmHg O2). Data from Pierce et al. have suggested dilatation to hypoxia, not an HFPV effect [52]; perfusion

IKBKE of 25 mmHg O2 in fetal vs. 60 mmHg O2 in maternal perfusate stimulated a significant dilatation of perfused placental cotyledons compared with control data. Most recently, placental perfusion studies to assess hypoxic effects on placental metabolism, such as those of Soydemir et al., have utilized more appropriate conditions. However, significant changes in metabolic markers following the hypoxic challenge were not mirrored by alterations in perfusion pressure [62]. Taken together, it is clear that the existence of a physiologically relevant HFPV response in human placenta still requires definitive proof; i.e., increased vascular tone in response to a hypoxic challenge from a physiologically relevant control oxygenation. Isolated fetoplacental blood vessel studies have also failed to demonstrate consistent effects of oxygenation.

The Ccr7, Slfn1, and Mapk11 genes were weakly induced in mature cell populations from only one of the mutant mice, but remained at background levels across all populations in the samples derived from the second mouse. This observation suggests that some gene-specific variability exists across mutants in their ability to activate genes induced during positive Selleckchem Talazoparib selection, and is in agreement

with the previous results demonstrating impaired expression of genes associated with positive selection in DP cells from Bcl11b-deficient thymocytes 26. Collectively, these analyses indicate that the premature expression of SP-associated genes in Bcl11bdp−/− DP cells reflects gene-specific dysregulation in cells that have not undergone positive selection. To determine if Bcl11b directly controls the expression of some dysregulated genes, we mapped Bcl11b binding Osimertinib cell line to regulatory sequences by performing ChIP-seq experiments on chromatin immunoprecipitated from WT

thymocytes (a full bioinfomatic analysis of these data will be published elsewhere). We found that Bcl11b was present at multiple, specific regions in most of the genes that were dysregulated in our transcriptomic analyses (see Fig. 8 for a representative selection of binding profiles). Of particular interest, Bcl11b bound to several regions within the Zbtb7b locus, including the distal regulatory element, which has been reported to be the target of TCR signal(s) responsible for CD4 lineage commitment Methocarbamol 42. These data indicate that Bcl11b likely acts directly in DP cells to prevent the premature expression of genes encoding critical regulators of the SP differentiation programs. The results presented herein further establish Bcl11b as a key regulator of cellular differentiation in the αβ T-cell lineage. Bcl11b plays a critical role in at least two stages of T-cell development: progression of DN to DP cells, and differentiation of

DP cells into CD4+ and CD8+ SP cells, and NKT cells. Although our results confirm the previous results with respect to the early T-cell block resulting from the germline deletion of Bcl11b 25, and the block of SP T-cell differentiation of CD4-Cre-deleted mice 26, our studies also bring new and important insights. Specifically, we show that Bcl11b is: (i) absolutely and intrinsically required in DP thymocytes for canonical NKT cell development, (ii) required for the correct expression of approximately 1000 genes in DP cells, acting as a bifunctional transcriptional regulatory protein, and (iii) required in CD3lo DP cells to prevent the premature expression of a large number of SP-specific genes, including the key regulators Zbtb7b and Runx3.

Conversely, those studies suggested different mechanisms for the enhancement of innate immunity. Lactobacillus pentosus S-PT84 has been reported to activate

IL-12 production by dendritic cells and to induce IFN-γ production by NK or NKT cells in an IL-12-dependent manner in murine FK228 mouse splenocytes (Koizumi et al., 2008), whereas Shida et al. (2006a) demonstrated that Lactobacillus casei Shirota induced IFN-γ production by T cells through IL-12 secretion by monocytes in human peripheral blood mononuclear cells (PBMCs). It would be important for the clinical application of LAB to understand the mechanisms of the immunomodulating effects by LAB, and thus, further investigation is needed. In the present study, a Lactobacillus paracasei strain, MoLac-1, which strongly induces IL-12, was selected. We investigated the in vitro effects and mechanisms of heat-killed MoLac-1 on IFN-γ production and NK cells and the in vivo effects of oral administration of heat-killed MoLac-1 on NK cells. Further, we evaluated the effectiveness of MoLac-1 in ameliorating

IFV infection using a mouse model. Bacterial strains used in this study are listed in Fig. 1 and were originally isolated from human intestine, intestine of adult, intestine of infant, or dairy. Proteasome inhibition These strains, which were originally isolated mainly from human intestine and dairy source, were obtained from the Morinaga Culture Collection (MCC; Morinaga Milk Industry Co. Ltd, Zama, Japan), the American Type Culture Collection (ATCC; Manassas, VA), and the Japan Collection of Microorganisms (JCM; Riken, Wako, Japan). The MoLac-1 (MCC1375) strain was isolated from the feces of healthy adults and identified as L. paracasei by carbohydrate fermentation patterns using the API 50 CH kit (bioMérieux, Marcy l’Etoile, France), 16S rRNA gene nucleotide sequences, and DNA–DNA hybridization technique. For bacterial Amylase culture, MRS broth (Becton Dickinson, Cockeysville, MD) was used for the strains belonging to Lactobacillus, MRS broth supplemented with 0.05% l-cysteine was used for the strains belonging to Bifidobacterium,

and M-17 broth (OXOID Ltd., Hampshire, UK) supplemented with 1% glucose was used for the strains belonging to Lactococcus, Streptococcus, or Enterococcus. Bacteria were cultured at 37 °C for 16 h, washed twice with phosphate-buffered saline (PBS), and then washed twice with distilled water. The bacteria were heat-killed at 100 °C for 30 min and lyophilized. One microgram of lyophilized MoLac-1 contained approximately 1.9 × 106 microorganisms as enumerated using bacterial counting chamber. Specific pathogen-free BALB/c mice were obtained from Japan SLC (Hamamatsu, Japan). All experiment protocols involving mice were performed according to the guidelines of the Prime Minister’s Office in Japan (no. 6, March 27, 1980). IFV A/PR/8/34 (H1N1) adapted to mice was stored at Japan Biological Science Inc.

037) and mortality (P = 0.001). GM assay is adjunctive to clinical/radiological evidence. A negative GM assay may not reassure the physician against the use of amphotericin in patients with febrile neutropenia, as it does not exclude the diagnosis of clinically relevant other fungal infections, particular mucormycosis. “
“Novel treatment schedules of induction therapy for acute lympoblastic leukaemia (ALL) use combinations of immunosuppressive and cytotoxic

drugs that are associated with neutropenia and acquisition of invasive fungal infections. It has been described that posaconazole, a triazole antifungal drug, is active against a variety of Candida and Aspergillus species in vitro. Moreover, large clinical trials using posaconazole in severely immunosuppressed patients provided data on efficacy against Aspergillus in vivo. As patients with ALL are also affected

by difficult-to-treat Lenvatinib cell line Aspergillus infections, we conducted a pilot study to prove the safety of posaconazole in patients undergoing intensified induction phase treatment. We report on eight patients receiving prophylactic (200 mg t.i.d.) dose of posaconazole and demonstrate good tolerability of the drug. The most obvious side effect was liver toxicity as defined by abnormal serum glutamic pyruvic transaminase, serum glutamic oxaloacetic transaminase and bilirubin levels (Selleck Metformin clear relationship to posaconazole applications. During the study, one patient Carnitine dehydrogenase developed possible aspergillosis of the lung. Therefore,

the observations indicate a favourable toxicity profile of posaconazole in ALL therapy. Efficacy of the drug has to be further validated in prospective clinical trials. “
“Among fungi, Curvularia inaequalis is a rare pathogen. We report the first case of non-invasive fungal rhinosinusitis caused by this species. Endoscopic sinus surgery revealed massive polyposis and the presence of viscous eosinophilic mucus that allowed the growth of the fungus. We diagnosed eosinophilic fungal rhinosinusitis based on the histological findings of fungal hyphae in association with degranulating eosinophils in the sinus mucus. After polypectomy and clearance of the affected sinuses, oral itraconazole was administered to prevent the recurrence. Given the ever-increasing list of opportunistic fungi that cause human infection, the case reported here provides further evidence that proper identification of the infective agents remains crucial for the patient’s management. “
“Onychomycosis is defined as a fungal infection of the nail bed and/or nail plate. The prevalence of onychomycosis has increased dramatically as a worldwide condition in the twentieth century due to occlusive footwear, global wars and natural migration.

The effect of perioperative transfusion of old RBCs on postoperative complications after free muscle sparing transverse rectus abdominis myocutaneous (TRAM) flap surgery was retrospectively

investigated. Two hundred sixty-one patients undergoing breast reconstruction were assigned to two groups: no transfusion and transfusion groups. Transfused patients were further divided according to the RBC storage duration (fresh, ≤14 days; old, >14 days). Postoperative complications such as vascular Proteasome inhibitor thrombosis, hematoma, and flap congestion were noted. Patients who received old blood (n = 34), compared with those received fresh blood (n = 40) or no transfusion (n = 187), had a higher incidence of postoperative complications (44.1% vs. 20.0% or 12.8%, P < 0.05). Perioperative transfusion of old RBCs can be associated with an increase in postoperative complications after free muscle sparing TRAM flap surgery. © 2014 Wiley Periodicals, Inc. Microsurgery 34:434–438, 2014. "
“Lower abdominal, perineal, and AZD1208 groin (LAPG) reconstruction may be performed in a single stage. Anterolateral thigh (ALT) flaps are preferred here and taken as fasciocutaneous (ALT-FC), myocutaneous (ALT-MC), or vastus lateralis myocutaneous (VL-MC) flaps. We aim to present the results of reconstruction from a series of patients and guide flap selection with an algorithmic approach

to LAPG reconstruction that optimizes outcomes and minimizes morbidity. Lower abdomen, groin, perineum, vulva, vagina, scrotum,

and bladder wounds reconstructed in 22 patients using ALT flaps between 2000 and 2013 were retrospectively studied. Five ALT-FC, eight ALT-MC, and nine VL-MC flaps were performed. All flaps survived. Venous congestion occurred in three VL-MC flaps from mechanical cause. Wound infection occurred in six cases. Urinary leak occurred in three cases of bladder reconstruction. One patient died from congestive heart failure. The ALT flap is time tested and dependably addresses most LAPG defects; flap variations are suited for niche defects. We propose a novel algorithm to guide reconstructive decision-making. Chlormezanone © 2014 Wiley Periodicals, Inc. Microsurgery, 2014. “
“Introduction. As peripheral nerve specialists can have a wide variety of training backgrounds, few standards of care exist with respect to necessary incision length, amount of dissection, and operative technique for common nerve decompressions. Methods. Approaches for the following 12 common peripheral nerve surgeries were minimized using shorter incisions and a simple lighted retractor: zygomatico-temporal and auriculotemporal, greater occipital, brachial plexus, ulnar, radial, median, lateral femoral cutaneous nerve of the thigh, peroneal at the groin, fibular neck and lateral calf, and tibial and inner ankle. The new “minimal” incision length was recorded as was that of the “classical” approach as taught to the senior author and frequently represented in atlases.

It could be concluded that all of these changes may be responsible for cellular immune dysregulation observed in these patients especially those with autoimmune manifestation. Common variable immunodeficiency (CVID) is a heterogeneous group of disorders characterized by hypogammaglobulinaemia, defective specific antibody production and an increased susceptibility to recurrent and chronic infections [1-3]. Patients with CVID also have an increased incidence of autoimmune disorders and cancers [4-6]. In addition to reduced Ig production by B cells, several defects in T cell response have been reported in CVID patients including impaired cell proliferation and cytokine production

as well as reduced T cell numbers https://www.selleckchem.com/products/AZD2281(Olaparib).html [7]. The CD4+CD25+FOXP3+ regulatory T lymphocytes (Tregs) constitute about 5–10% of the peripheral blood CD4+ T cells and have an indispensable role in maintaining self-tolerance and immune response to self and non-self antigens [8, 9]. This unique subset of CD4+ T cells Staurosporine purchase have been implicated in regulating

immune response in different conditions like allergic diseases, malignancy, graft vs. host diseases as well as autoimmune disorders [9, 10]. Although cell to cell contact has been considered the major mechanism of Tregs-mediated suppression, the production of regulatory cytokines like Il-10, IL-35 and TGF-β by Tregs should also be noted [8-10]. There are increasing evidences indicating the reduced frequency of Tregs in autoimmune diseases, which has been shown to have inverse correlation with clinical parameters Adenosine triphosphate [11-16]. Recently, few reports have been published

indicating reduced numbers of Tregs in CVID patients and its correlation with chronic inflammation, splenomegaly and autoimmune manifestation in these patients [17-21]. In this study, we proposed to investigate Tregs’ frequency and transcription FOXP3 protein expression in CVID patients. We also evaluated for the first time the mRNA expression of surface markers CTLA-4 and GITR, which are associated with the inhibitory functions of Tregs in CVID patients and compared the results with healthy controls. Thirty-seven patients with CVID who were referred to division of clinical immunology and allergy at Children’s Medical Center of Tehran University of Medical Sciences were enrolled in this study. The diagnosis of CVID disease was based on defined criteria by PAGID (Pan-American Group for Immunodeficiency) and ESID (European Society for Immunodeficiencies) [2]. All patients were receiving monthly regular intravenous immunoglobulin replacement therapy. Medical history and clinical phenotypes of CVID patients were given from the national primary immunodeficiency registry [22, 1, 23]. Eighteen sex- and age-matched healthy volunteers who have no history of autoimmune disease, malignancy and/or any immunodeficiency were chosen as control group.

47–49 The interaction between T cells and macrophages

is known to be critical for prevention of bacterial growth.50–53 However, it is not clear how various M. tuberculosis proteins can trigger the Th1 response. Several factors, such as the affinity between the T-cell receptor (TCR) and peptide–MHC ligand, peptide ligand density and costimulatory signalling during T-cell activation, can play important roles NSC 683864 cell line in the regulation of the Th1/Th2 T-cell response.11,12,54–57 Cytokines induced during innate activation of macrophages have also been shown to be extremely important in controlling the Th1/Th2 balance. For example, induction of IL-12 or TNF-α can trigger a Th1 response;58,59 however, if more IL-10 is produced, the response is likely to be biased towards the Th2 type response.60,61 It has been shown that various M. tuberculosis

secretory proteins bind to a specific receptor on macrophages and influence the downstream signalling cascades and the induction of pro-inflammatory cytokines.62 Although up-regulation of iNOS expression and NO production during infection with M. tuberculosis is well known, very few studies have actually identified the M. tuberculosis proteins directly involved in the up-regulation of the iNOS gene. Our study indicates that rRv2626c affects the macrophage-signalling cascades Ruxolitinib order and up-regulates iNOS induction and NO production mainly by increasing NF-κB activity. Interestingly, flow cytometry data indicate that Rv2626c binds to the macrophage surface with high affinity and specificity. It is possible that the specific binding of Rv2626c on the macrophage surface causes modulation of the downstream signalling pathways triggering NF-κB signalling, which results in increased induction of iNOS23 as well as the cytokines TNF-α63 and IL-12.64 Although the exact beneficial role of iNOS/NO in anti-mycobacterial Rho killing has not been uniformly elucidated,65 studies have confirmed that iNOS/NO is crucial in limiting bacterial growth.66,67 Similarly, the role of TNF-α in TB is paradoxical because, although there is evidence of its protective role,68 it can play a part in the tissue damage that

characterizes human disease.68 A recent study also indicates that M. tuberculosis activates TNF-α production to induce apoptosis of macrophages.62 Our study clearly demonstrates that the secretory M. tuberculosis Rv2626c protein induces pro-inflammatory responses by modulating the expression of iNOS and increasing the secretion of IL-12 and TNF-α, which may play an important role in the initiation of the adaptive immune response in the host. Mycobacterium tuberculosis proteins that induce the Th1 response have been used as targets for subunit vaccines. For example, use of the mycobacterial 30-kDa major secretory protein (antigen 85B, Ag85B) was found to protect animals from M. tuberculosis infection by inducing a Th1-dominant response.

1 mm Na3VO4, 5 μm ZnCl2 to obtain whole cell lysate. Protein was quantified using a bicinchoninic acid protein assay kit (Pierce, Rockford, IL). Gradient sodium dodecyl sulphate –polyacrylamide gel electrophoresis gels (Pierce/Thermo Fisher Scientific, Rockford, IL) were loaded with 10 μg of protein

and transferred to polyvinylidene fluoride membranes (Millipore). Western blots were probed with mouse anti-human Blimp-1 (Novus, Littleton, CO), mouse anti-human AID (Cell Signaling Technology, Beverly, MA), rabbit anti-human Xbp-1 (Novus), rabbit anti-human Pax5 (Millipore, Billerica, MA), mouse anti-human actin control (Calbiochem/EMD Chemicals, Gibbstown, NJ) and anti-GAPDH this website control (Calbiochem). Saracatinib nmr Secondary antibody labelling was performed using horseradish peroxidase-conjugated goat anti-mouse or goat anti-rabbit antibodies (Jackson ImmunoResearch Laboratories, West Grove, PA) after washing. Western blots were visualized by autoradiography after incubation with enhanced chemiluminescence (Perkin Elmer Life Sciences Inc., Boston, MA). Human peripheral blood B cells express Cox-2 upon activation and Cox-2 activity is necessary

for optimal production of IgM and IgG.11,12 To determine if Cox-2 selective inhibitors preferentially influence the production of certain human antibody isotypes, we assessed production of IgM, total IgG, IgG1, IgG2, IgG3 and IgG4 following a 7-day stimulation with CpG plus anti-IgM. Peripheral blood human B cells were treated with either SC-58125 or NS-398, both small molecule Cox-2 selective inhibitors. Production of IgM and total IgG was measured by ELISA (Fig. 1a,b), while IgG1, IgG2, IgG3 and IgG4 (Fig. 1c–f) isotypes were measured

using Luminex Meloxicam technology. We observed a significant decrease in IgM, total IgG, IgG1, IgG2, IgG3 and IgG4 following treatment of B cells with SC-58125. NS-398 also significantly inhibited the production of IgM, total IgG, IgG1, IgG2 and IgG3. Treatment with NS-398 also reduced IgG4 production, although, not in a dose-dependent manner. Based on PGE2 production from isolated PBMC the concentrations of Cox-2 selective inhibitors used to attenuate antibody production are sufficient to significantly inhibit Cox-2 activity (Fig. 1g). These new data demonstrate that both SC-58125 and NS-398 significantly attenuated production of all isotypes, indicating that Cox-2 inhibitors do not selectively inhibit antibody isotype production. The global decrease in antibody production induced by Cox-2 inhibition could be a result of reduced B-cell viability or proliferation. Therefore, we measured the percentage of cells that excluded 7-AAD on days 2, 4 and 6 of culture. Neither SC-58125 (Fig. 2a) nor NS-398 (data not shown) significantly affected the viability of activated human B cells measured on any of these days.

It is well known that SpeB, which is considered

a cysteine protease, degrades M protein on the cell surface and releases the fragments into the supernatant (22, 23). Unexpectedly, a considerable amount of M protein was detected in the culture supernatant proteins of all of the 29 strains tested, in spite of the presence of E-64, which specifically inhibits SpeB protease activity. Herwald et al. have reported a unique pathogenic potential of the emm1 and emm3 strains, a portion of whose M proteins are released into the supernatant where they form complexes with fibrinogen which induce vascular leakage (7). In this study, likewise, M protein was detected in the supernatants of emm6 and 12 strains, raising the possibility that these strains also possess this uncommon pathogenic mechanism. The observations obtained so far imply that csrS gene mutations cause production of large amounts of virulence-associated Inhibitor Library research buy proteins, including M protein, which is essential to the shift from a

pharyngeal to an invasive transcriptome profile (9, 19, 20). The mutations that have been reported to date are of the frameshift variety, causing truncated CsrS forms and a single amino acid substitution in the protein; such mutations are assumed sufficient find more to induce dysfunction or structural instability. In fact, the region proximal to the C-terminal has been reported to be crucial to phosphorylation (19). The fact that two of the M protein-high producers in this study carried two substitutions may underline the importance of the accumulation of point mutations, in addition to those at the mutation site, which

can eventually cause drastic change in the enzymatic activity or configuration of the CsrS protein. However, a significant difference between M protein-high and-low producers in emm gene transcription was not found in the TaqMan analysis. Mirabegron Of the 138 S. pyogenes strains from mild streptococcal infections, most of which were obtained from non-sterile sites, two strains expressed large amounts of M protein; interestingly, these two strains carried two amino acid substitutions in CsrS protein (2/138, 1.4%). Of the S. pyogenes strains clinically isolated from STSS cases, 34.8% carried a csrS mutation; significantly fewer mutations (1.69%) being found in non-STSS S. pyogenes strains (24). Taken together, our results and those of others clearly indicate that the frequency of csrS mutation is largely dependent on the colonization site, for example, whether S. pyogenes occurs on the pharynx or skin versus a subcutaneous site. Interestingly, four emm3 strains, including one of the M protein-high producers, did not have any csrS or csrR mutations. It appears, therefore, that M protein expression is controlled by several different regulatory genes including csrRS, mga and pel (10, 21, 25). Thus, the expression of emm3 may be regulated mainly by genes other than csrRS.

Phagolysosome fusion was determined, as described previously [46]. Briefly, peritoneal macrophages were harvested and plated into eight-well chamber slides (Lab-Tek™, Nunc, Rochester, NY, USA) at 1 × 105 cells/well. After resting in RPMI1640 containing 1% FCS for 6 h, cells were loaded with 50 nM LysoTracker red (Molecular Probes) at 37°C for 30 min and further incubated with FITC-conjugated bacteria (Molecular Probes) of either S. aureus or E. coli (macrophage/bacteria = 1:20) for various time periods.

LysoTracker red was replenished every hour of incubation. After each time point, slides were vigorously washed five times in cold PBS and fixed in 2% paraformaldehyde (Sigma-Aldrich). Cell nuclei were stained with DAPI (Molecular Probes).

Slides were mounted with coverslips and examined under a fluorescent Olympus BX61-TRF microscope Maraviroc (Olympus, Tokyo, Japan). Fluorescent images Staurosporine purchase were acquired using the cell imaging software for life sciences microscopy (Olympus Soft Imaging Solutions, Munster, Germany). Unfused phagosomes containing FITC-bacteria and lysosomes labeled with LysoTracker red were stained in green and red, respectively, whereas phagosomes containing FITC-bacteria after being fused with LysoTracker red-labeled lysosomes were stained in yellow due to the coexistence of the two fluorochromes. All data are expressed as the mean ± SD. Statistical analysis

was performed using the log rank test for survival and the Mann-Whitney U test for all others, with GraphPad software, version 5.01 (Prism, La Jolla, CA, USA). A p-value <0.05 was judged statistically significant. This work was supported by the National Natural before Science Foundation of China (Grant 81272143), the Natural Science Foundation of Jiangsu Province (Grant K200509), Jiangsu Innovation Team (Grant LJ201141), Jiangsu Province Program of Innovative and Entrepreneurial Talents (2011–2014), and in part by the Science Foundation Ireland Research Frontiers Programme (Grant SFI/08/RFP/BIC1734). The authors declare no financial or commercial conflict of interest. “
“Endoscopic stenting is a palliative approach for the treatment of diseases involving biliary obstruction. Its major limitation is represented by stent occlusion, followed by life-threatening cholangitis, often requiring stent removal and replacement. Although it has been suggested that microbial colonization of biliary stents could play a role in the clogging process, the so far available data, particularly on the role of anaerobic bacteria, are not enough for a comprehensive description of this phenomenon.