Therefore, IDO has dual immunoregulatory functions driven by Stem Cell Compound Library high throughput distinct cytokines. Firstly, the IFN-γ–IDO axis is crucial in generating and sustaining the function of regulatory T cells. Secondly, a nonenzymic function of IDO — as a signaling molecule — contributes to TGF-β–driven tolerance. The latter function is part of a regulatory circuit in pDCs whereby — in response to TGF-β — the kinase Fyn mediates tyrosine phosphorylation of IDO-associated immunoreceptor tyrosine-based inhibitory motifs, resulting in downstream effects that regulate gene expression and preside over a proper, homeostatic balance between immunity

and tolerance. All these aspects are covered in this review. Immune regulation is a highly evolved biologic response capable of not only fine-tuning inflammation and innate immunity, but also of modulating adaptive immunity see more and establishing

tolerance to self. Amino acid catabolism is an ancestral survival strategy that can additionally control immune responses in mammals [[1]]. IDO (also referred to as IDO1) catalyzes the rate-limiting step of tryptophan (Trp) catabolism along a degradative pathway that leads to Trp starvation and the production of Trp metabolites collectively known as kynurenines. Regulation of immunity by essential amino acid starvation occurs by two distinct mechanisms. First, some enzymes are upregulated with no need for adaptive immunity, reflecting an innate protective response against inflammatory damage.

Second, there occurs an interplay involving regulatory T (Treg) cells and antigen-presenting cells (APCs), which results in further upregulation of not only IDO, but at least four other essential amino acid-consuming enzymes, capable of restraining selleck chemicals T-cell proliferation and, in addition, promoting Treg-cell expansion via infectious tolerance [[2, 3]]. The first step in the kynurenine pathway of tryptophan catabolism is the cleavage of the 2,3-double bond of the indole ring of tryptophan. In mammals, this reaction is performed independently by IDO, tryptophan 2,3-dioxygenase (TDO; mostly expressed in the liver), and the recently discovered indoleamine 2,3-dioxygenase-2 (IDO2; a paralogue of IDO; from the same ancestor gene but devoid of signaling activity). The initial observation suggesting an immune regulatory role for IDO, previously considered to be a merely “metabolic” enzyme, dates back to the seminal finding that its inhibition by 1-methyl-dl-tryptophan in pregnancy would cause rejection of semiallogeneic, but not syngeneic, fetuses in mice [[4]].

Subsets of T and B lymphocytes were isolated using the MACS magnetic labeling system together with the CD4+ T Cell Isolation Kit II, the CD8+ T Cell Isolation Kit II and the B cell Isolation Kit II (Miltenyi Biotec, Cologne, Germany), as previously described in detail (Bryborn et al., 2008). For all protocols, the isolated cells had a purity of > 95%. Freshly isolated

cells were lysed in RLT buffer (Qiagen) supplemented with 1% 2-mercaptoethanol and stored at −80 °C until use. The pharyngeal epithelial cell line FaDu was obtained from ATCC (Manassas, VA) and cultured at 37 °C in a humidified 5% CO2 air atmosphere in Alvelestat supplier Minimum Essential Medium (MEM) with Earle′s salts and 2 mM l-glutamine (Gibco) supplemented with 10% FBS and 100 U mL−1 penicillin/100 μg mL−1 streptomycin. Epithelial cells were seeded on 24-well culture plates (250 000 cells per well) in 1 mL complete MEM and incubated overnight. Thereafter, cells were cultured for additionally 4, 16 and 24 h in the absence or presence of IL-4, IL-5 and histamine. Cell-free culture supernatants were analyzed for levels of HBD1-3 using ELISA.

RNA was extracted from homogenized tonsils and cells using the RNeasy Mini Kit (Qiagen). The quality and quantity of the RNA was assessed by spectrophotometry based on the A260nm/A280nm ratio (between 1.8 and 2.0 in all preparations). Reverse transcription of total RNA into cDNA was carried ICG-001 cost out using Omniscript™ reverse transcriptase kit (Qiagen) with oligo(dT)16 (DNA Technology, Aarhus, Denmark) in a Mastercycler personal PCR machine (Eppendorf AG, Hamburg, Germany) in a final volume of 20 μL, at 37 °C for many 1 h. Intron over-spanning oligonucleotide primers for detection of HBD1-3 and β-actin were designed to generate PCR products between 100 and 150 bp using Primer Express® 2.0 software (Applied Biosystems, Foster

City, CA) and synthesized by DNA Technology A/S (Aarhus, Denmark) (Table 1). For comparisons of HBD levels in tonsils from allergic patients and control subjects, PCR reactions were performed on a Smart Cycler (Cepheid, Sunnyvale) using the Quantitect SYBR® Green PCR kit (Qiagen) in a volume of 25 μL. For detection of HBD1-3 in isolated lymphocytes and tonsillar pieces cultured with IL-4, IL-5, IL-13 or histamine, PCR reactions were instead performed on a Stratagene Mx3000P (Agilent Technologies, Santa Clara, CA) using the Stratagene Brilliant SYBR® Green QPCR Mastermix in a final volume of 20 μL. Regardless of method, the thermal cycler was set to perform 95 °C for 15 min, followed by 46 cycles of 94 °C for 30 s and 55 °C for 60 s (initially 65 °C, followed by a 2 °C decrease for the six-first cycles). Melting curve analysis was performed to ensure specificity of the amplified PCR products. The mRNA expression was assessed using the comparative cycle threshold (Ct) method where the relative amounts of mRNA for HBD1-3 were determined by subtracting the C t value for these genes with the Ct value for β-actin (ΔC t).

The BCA protein assay (Thermo Fisher) was used to

determine the protein concentration of each of the cleared lysates. A 30 μg sample of each caecum or colon lysate protein was boiled for 5 min in reducing sample buffer containing DTT and resolved by SDS–PAGE, transferred to PVDF membranes and probed with the indicated antibodies. The membranes were exposed to enhanced chemifluorescence substrate (GE Healthcare, Piscataway, NJ), followed by scanning on a Typhoon Trio+ imaging system (GE Healthcare) to obtain a digital image of the probed protein. The bands were then quantified with ImageQuant software PI3K inhibitor (GE Healthcare). Caecum and colon snips obtained from untreated and C. difficile-infected mice were homogenized with a rotor/stator-type homogenizer while immersed in TRIzol RNA reagent (Life Technologies, Grand Island, NY). The TRIzol RNA reagent and the RNeasy Mini kit (Qiagen, Valencia, CA) were used in successive steps to isolate RNA from the caecum and colon samples, each according to its manufacturer’s instructions. An Agilent Bioanalyser (Agilent Technologies, Palo Alto, CA) and a Nanodrop instrument (Thermo Fisher) were used to determine SAHA HDAC concentration the quality and concentration of each RNA isolate, respectively.

Complementary DNA (cDNA) was generated from each RNA sample using the RT2 First Strand kit (Qiagen). Expression levels of the genes under study were determined by using two different sets of mouse RT2 Profiler PCR cards (Qiagen), each custom-made to contain eight replicate sets of

48 primer pairs (Table 1). Each well of the replicate sets was loaded with 5 ng of cDNA reaction product. Each card was run on a LightCycler 480 real-time PCR system (Roche). The relative RNA expression levels were inferred from the Ct values. Xbp1 splicing was assessed as previously described.[39] Briefly, the Superscript III RT-PCR kit (Life Technologies) was used to amplify both unspliced and spliced Xbp1 in RNA samples obtained at the end of the experimental period. The primers used in the assay flanked the Xbp1 intron and had the following sequences: upstream: ttgtggttgagaaccagg; downstream: tccatgggaagatgttctgg. Quantitative RT-PCR, including methods for verifying primer efficiency and specificity, were performed as previously described.[40] The Ct value for each gene Protirelin of each sample was normalized against the geometric mean of the Gapdh and Hprt for that sample.[41] For the following assays, differences between untreated and C. difficile-infected mice were evaluated for significance by using paired t-tests at P ≤ 0.05: diversity of the bacterial community examined by pyrosequencing; cell numbers obtained by analysing the flow cytometric data; mRNA expression for the UPR genes Gadd34 and Wars obtained by single gene quantitative RT-PCR; and protein expression or phosphorylation assessed by immunoblotting.

The major drawback with such techniques is that this process does not guarantee the selection of CD25hi cells compared to the fluorescence activated cell sorter (FACS) sorter, which allows the important see more distinction to be made between the CD4+CD25hi and CD25int cells. In addition,

the process does not allow the selection of Tregs based on multiple parameters and the ∼60% purity of the isolated cells [65] is not comparable with the >95% purity achieved using the FACS sorter [56]. In addition to the automated CliniMACS plus system (Miltenyi Biotec), there are two other commercially available methods for GMP-grade T cell isolation and expansion. Life Technologies Ltd (Paisley, UK) produces the DynaMagTM CTSTM system,

which is a magnetic device used in combination with the Dynabeads® CTS™ and Dynabeads® ClinExVivo™ to positively isolate bead bound cells or deplete unwanted cell types. Dynabeads® CD3/CD28 CTS™ are used to positively isolate T cells; these beads are also able to activate the bound T cells and when cultured in the presence of IL-2 result in a 100–1000-fold expansion of the isolated T cells. The T cells are purified by labelling cells with mouse immunoglobulin check details (Ig)G1 antibodies and using the Dynabeads® IgG1 Binder CTS™ for positive isolation, negative isolation or cell depletion. Stage Cell Therapeutics (Göttingen, Germany) is a cell therapy company that manufactures Streptamer® reagents for isolation of defined lymphocytes. In view of isolating purer Treg populations, their system involves three positive selection steps by magnetically tagged Fab-Streptamers. Following each labelling and positive selection step, the tagged cells are liberated completely from the magnetically tagged Fab-Streptamers by incubation with a competing Streptactin ligand D-biotin that causes disruption

of the Fab-multimer complex, dissociation of the Fab-Streptamer label from the target cell surface and complete removal upon washing. The first positive isolation step involves anti-CD4-Fab-Streptamer labelling, followed by anti-CD25-Fab-Streptamer labelling, and finally anti-CD45RA-Fab-Streptamer labelling is used to isolate a triple-positive Treg cell preparation that is CD4+CD25+CD45RA+. PD184352 (CI-1040) Interestingly, however, the study by Marek et al. [66] showed that regardless of the initial phenotypic markers used for isolation (i.e. CD25hiCD127low, CD45RA+, CD45 RA–) during the expansion process, Tregs were transforming into effector/memory-like cells which produced inflammatory cytokines. They proposed that independent of the phenotypic markers used for Treg isolation, the only variable to help maintain the Treg phenotype and function was limiting the expansion time to 2 weeks. Based on such studies, therefore, it is of particular importance to ensure that the stability of the Tregs is maintained during the expansion process. Basu et al.

Because of the timing of serum EMA and NFR antibodies, circulating ANA were evaluated at three time-points: during EMA-positive results, under EMA disappearance/NFR-positive results and after NFR disappearance. At all time-points, serum ANA were positive in two of 20 CD LY2835219 concentration patients in group 1. In both cases, an ANA-S antibody pattern (subpattern: fine speckled) was visible. None of the 15 subjects in group

3 presented serum EMA-positive results, while two showed an NFR-like pattern on monkey oesophagus sections. The latter two subjects were put on a GFD for 12 months. Serum EMA and NFR antibodies were evaluated each month, showing no changes in the NFR-like pattern. The characterization of this NFR-like pattern showed that it belonged simultaneously to IgA1 and IgA2 subclasses, and that it was localized in the nucleus. The results of the present study demonstrate that serum IgA from CD patients are able to react with two nuclear antigens determining the appearance of a nuclear fluorescence Sirolimus in vivo reactivity (NFR) antibody pattern on monkey oesophagus sections used routinely for EMA detection. Moreover, as NFR antibodies are detectable

in serum as long as the CD patients consume gluten and disappear after gluten withdrawal from the diet, they are gluten-dependent and related strictly to CD. The autoimmune nature of CD is understood clearly [5–7], and the main autoantigen is well known to be tTG [11]. However, tTG is not the only CD-related autoantigen, as other tissue components have been shown to be a target of coeliac autoimmunity [12–15]. In serum of active CD patients, antibodies against thyroid and pancreas structures, cytoskeleton molecules and central nervous

Thalidomide system-related antigens have been found previously [14]. The present study adds a new antigen type to the list, as we found that serum IgA from untreated CD patients react with two NFR-related nuclear antigens of 65 and 49 kDa. The identity of NFR-related autoantigens is as yet unknown, but based on the different distribution of EMA and NFR reaction sites on monkey oesophagus sections it is reasonable to hypothesize that these reactivities are due to distinct antigenic specificity. Indeed, EMA and NFR antibody patterns are never observable simultaneously during total IgA EMA detection but, using secondary mAbs against IgA subclasses (IgA1 and IgA2) coupled with different fluorochromes (FITC and TRITC), the presence of two different and not overlapping fluorescence signals becomes evident. That the main endomysial antigen, known to be tTG [11], has a different molecular weight with respect to the newly identified autoantigens (85 versus 65 and 49 kDa), further confirms the hypothesis that EMA and NFR are two distinct antibodies.

Semi-quantitative analysis of LRRK2 immunohistochemical staining demonstrated regional variation in staining intensity, with weak LRRK2 immunoreactivity consistently recorded in the striatum and substantia nigra. No clear differences were identified in LRRK2 immunoreactivity between control, IPD and G2019S positive PD cases. LRRK2 protein was identified in a small proportion of Lewy bodies. Conclusions: Our data suggest that

widespread dysregulation of LRRK2 mRNA expression may contribute to the pathogenesis of IPD. “
“Epilepsy is a nervous system disorder characterized by recurrent seizures. Among several types of epilepsy, which accounts for a significant portion of the disease worldwide, temporal lobe epilepsy (TLE) is one of the most common types of intractable epilepsy in adulthood. It has been suggested that complex febrile seizures in early life are associated with the development of TLE Ceritinib supplier click here later in life; however, cellular and molecular links between febrile seizures and TLE remain unclear because of the lack of an appropriate in vitro system. Using rat hippocampal slice cultures, in which many features of native organotypic organization are retained, we found that the dentate granule cells exhibit aberrant migration in the dentate hilus via enhanced excitatory GABAA

receptor (GABAA-R) signaling, which results in granule cell ectopia that persists into adulthood. We further found that the granule cell ectopia below is associated with spontaneous limbic seizures in adulthood. Importantly, both of these phenomena were prevented by inhibiting Na+K+2Cl− co-transporter (NKCC1) which mediates the excitatory action of GABA. The hippocampi of individuals with mesial temporal lobe epilepsy (TLE) and corresponding animal models are accompanied by several pathological changes, such as the dispersion of dentate granule cells,[1-3] the emergence of ectopic granule cells,[4-7] the sprouting of hippocampal mossy fibers,[8-10] and hippocampal sclerosis, including selective neuronal loss and reactive gliosis in Ammon’s horn.[11] Each of these features has been suggested to play a role in the initiation and

propagation of epileptic activity in the hippocampus. These pathological changes may be triggered by early-life seizures considering that retrospective studies have suggested a correlation between a history of early-life seizures and hippocampal sclerosis;[12-16] however, direct evidence is lacking. Febrile seizures, which are associated with fevers (typically greater than 38.5°C), are the most common convulsive events in infancy and childhood between 6 months and 5 years of age with a prevalence of 2–14%[17] of the population. Although febrile seizures are benign in most instances, 30–40% of them are “complex”,[18, 19] with a prolonged seizure duration of >15 min, and are subsequently associated with 30–70% of the cases of adult TLE.

Assays with antigen in the absence of sera served as negative controls. Immunoglobulin titres are expressed Forskolin research buy as OD units, with a value obtained for 1 : 100 diluted serum samples. The proteolytic activity of Cwp84 was quantified with azocasein (Sigma); 50 μg of protease was added to 500 μL of a 5 mg mL−1 azocasein solution in 25 mM Tris (pH 7.5). After 16 h of incubation,

intact azocasein was removed by 3% trichloroacetic acid precipitation, and the amount of released dye was measured spectrophotometrically at 336 nm. The neutralizing activity of the specific anti-Cwp84 hamster sera was tested by monitoring Cwp84-mediated degradation of azocasein. Various amounts of sera were added to the protease, resulting in 1 : 50 dilutions, and after 30 min of incubation at 37 °C, an Kinase Inhibitor Library supplier azocasein mixture was added and assays were performed as described above. To assess the specificity of the neutralizing activity of immunized hamster sera, and to exclude the possibility of a steric hindrance effect, negative control experiments were performed with preimmune hamster sera, using the same dilutions. Statistical

analyses were performed to compare the antibody level (OD405 nm values) directed to Cwp84 in the hamster sera sample of the control group to the Cwp84 immunized group. It shows that antibody levels were not normally distributed. Therefore, we used the Mann–Whitney U-test for nonparametric data to test the null hypothesis that there was no difference between the immunized group and the control group. Analyses were performed using the stata 8.0 (Statacorp, College Station, TX). Statistical significance was set at P=0.05. All P-values were two-sided. The survival of animals following infection was analysed using Kaplan–Meier estimates. Survival rates across groups were compared using log-rank tests. P-values of <0.05 were considered to be statistically significant. Statistical analyses were performed using stata 8.0 (Statacorp). Three groups of hamsters were immunized by 100 μg of the protease Cwp84 by several routes of immunization: rectally, intragastrically and subcutaneously. Then clindamycin

was administered either to animals and, 5 days later, hamsters were challenged by C. difficile spores. Each hamster was sampled under anaesthesia directly by heart puncture. Cwp84-specific IgG, IgA and IgM were quantified by ELISA and the capacity of serum antibodies to neutralize Cwp84 activity in vitro was measured. Serum antibodies against Cwp84 were measured before immunization and 15 days after the second boost. The response was variable within groups (Fig. 1). The poorest response was seen with the intragastric route; the mean OD405 nm was 0.5 and there was no significant difference before and after immunization (P=0.13). Hamsters receiving the protease by the subcutaneous route exhibited a relatively strong response, with a mean of OD405 nm of 1.

Overall, existing data in animal models suggest that maintenance in the balance of ROS is critical

to successful microvascular aging. The limited work that has been performed to investigate the role of ROS in human microvascular aging is also discussed, and the need for future investigations of ROS signaling in older humans is considered. Healthy aging, from the microvascular standpoint, is associated with endothelial health and redox balance [23,74]. A decline in the function of the endothelium occurs with advancing age. This decline of function manifests as reduced angiogenic capacity, alteration of expression of adhesion molecules that regulate interaction with circulating factors and cells selleck chemicals of the immune system, and mTOR inhibitor impaired vasodilatory function. The well-documented loss of endothelium-dependent vasodilation that occurs with advancing age is present

in both conduit arteries and resistance arterioles. Animal models have been used to characterize this loss of endothelium-dependent vasodilation and to define the mechanisms that underlie it. The preponderance of data obtained in animal models indicate that age-related endothelial dysfunction of the microcirculation occurs due to decreased availability of NO• [15,60,84,89]. Vasodilatory responses that are inhibited by NOS blockade have been reported to decline with C59 clinical trial age in arterioles from coronary [14,41,42], skeletal muscle [60,84,91,96], cerebral [55], and mesenteric [87] vascular beds. In resistance arteries of skeletal muscle, age-related reduction of NO•-dependent vasodilation is accompanied by reduced expression of eNOS [96]. In contrast, NO•-mediated dilation of soleus muscle resistance arteries declines with

advancing age despite an increase in eNOS protein levels [84]. Thus, the age-related decline in bioavailability of NO• may be dependent upon numerous factors that regulate both its production and degradation. Parallel findings have been reported in studies of the human microcirculation, obtained indirectly through measures of flow-mediated vasodilation or more directly through study of the skin microcirculation [11,34,66]. The eNOS activity is regulated by availability of substrate and cofactors, by protein–protein interactions, and by coordinated phosphorylation and dephosphorylation [22,25,31]. In the absence of sufficient levels of the cofactor, tetrahydrobiopterin, uncoupled eNOS can produce O2•−. Degradation of NO• is heavily dependent upon the presence of cellular O2•−, a by-product of cellular respiration, which reacts readily with NO•, eliminating its vasodilatory action [82]. Increased production of superoxide ions has been reported to reduce NO• availability in coronary, skeletal muscle, and mesenteric arterioles of aged rats [14,20,56,87,92].

Taken together, IC pretreatment can significantly inhibit LPS or CpG ODN-induced maturation of DCs in a FcγRIIb-dependent manner. Mature DC-induced Th1 and Th17 responses are involved in the pathogenesis of some autoimmune Panobinostat price diseases, whereas immature DCs contribute to tolerance induction by downregulation of T-cell response and subsequently attenuate the pathogenesis of some autoimmune diseases. Next we investigated whether IC pretreatment could enhance tolerogenecity of immature DCs. OVA-pulsed immature DCs, which were pretreated with IC/Ig and then stimulated with LPS or CpG ODN, were incubated with OVA323–339-specific CD4+ T cells in vitro. We found that IC pretreatment reduced the

ability of LPS or CpG ODN-stimulated DCs to induce the proliferation and IL-17, IFN-γ secretion of antigen-specific CD4+ T cells (Fig. 1C and D). In contrast, IC/Ig pretreatment could not reduce the ability of FcγRIIb−/− DCs to induce proliferation and IL-17 secretion of antigen-specific CD4+ T cells. Altogether, the data suggest that IC pretreatment could enhance tolerogenecity of immature DCs in FcγRIIb-dependent manner. We previously showed that IC can induce massive amount of PGE2 from macrophages, which is responsible for the inhibition of TLR4-triggered inflammatory response. Similar

to macrophages, immature Daporinad research buy DCs produced large amount of PGE2 once stimulated with IC. LPS or CpG ODN could not further promote IC-induced PGE2 production of immature DCs (Fig. 2A). Also, immature FcγRIIb−/− DCs released some PGE2 in response to IC stimulation, but less than the PGE2 secreted by WT DCs in response to IC stimulation (Fig. 2B). To investigate whether PGE2 was responsible

for the hyporesponsiveness of T cells induced by DCs pretreated with IC, we first observed the direct effect of PGE2 on the proliferation of CD4+ T PKC inhibitor cells by anti-CD3/CD28. As expected, PGE2 inhibited the proliferation of T cells in a dose-dependent manner (Supporting Information Fig. 2). Next, OVA323–339-pulsed DCs were incubated with celecoxib, an inhibitor of COX2, 30 min prior to treatment with IC and TLR ligands. The hyporesponsiveness of OVA323–339-specific T cells disappeared when PGE2 secretion was inhibited, and addition of exogenous PGE2 could restore the inhibitory effect on T-cell proliferation in this system (Fig. 2C). Altogether, these data confirmed that IC-induced PGE2 from DCs was responsible for the downregulation of T-cell response by immature DCs that were pretreated with IC and then stimulated with TLR ligands. The data in the previous sections indicated that IC could downregulate DC-initiated T-cell response by inducing PGE2 production from DCs via FcγRIIb. To investigate whether IC could also inhibit in vivo T-cell response triggered by TLR agonists, we i.v. injected mice with OVA323–339-specific CD4+ T cells 24 h and OVA together with IC before i.p. administration of LPS or CpG ODN.

e., proportion of power increased in) the lower frequencies, as smooth muscle mediated (myogenic) control began to dominate blood flow, an effect most marked with Selleck Saracatinib norepinephrine. Dobutamine and dopexamine had little effect on control of blood flow. Conclusions: Denervation of free flap tissue is demonstrable using spectral analysis of laser Doppler blood flow signals. With norepinephrine the control of blood flow shifts toward low frequency vasomotion where blood flow depends mostly on average blood pressure, making it potentially the most suitable

agent following free tissue transfer. © 2013 Wiley Periodicals, Inc. Microsurgery, 2013. “
“This study reviewed our experience with the gracilis myocutaneous (GMC) flap, potential risk factors for flap necrosis, and long-term morbidity at the donor-site. From 1993 to 2002, 29 GMC flaps were harvested from 27 patients (pedicled n = 21 and free n = 8). The overall incidence of flap necrosis was 13.79% (partial Ibrutinib datasheet (n = 2) and total (n = 2) necrosis). Flap necrosis was correlated with body mass index >25 (P = 0.022), with smoking (P = 0.04 9) and with radiation therapy at the recipient site (P = 0.020). The long-term morbidity

at the donor-site was low, except for scar appearance (17.24%), thigh contour deformity (58.62%), and hypoesthesia (17.24%). Significant age and gender differences were seen for ranking of scar ugliness, with females (P = 0.0061) and younger patients (age ≤55) (P = 0.046) assigned higher values.

Significant age differences were seen for ranking of thigh contour deformity, with younger patients assigned higher values (P = 0.0012). In conclusion, patient overweight, smoking, and previous radiation therapy at the recipient site may be the “potential risk factors” for flap necrosis. The long-term morbidity at the donor-site was low, which was in agreement with previous reported studies. A larger series would be the subject of a future study. © 2011 Wiley-Liss, Inc. Microsurgery, 2011. “
“Reconstruction of extensive abdominal wall defects is a challenge also for reconstructive surgeons. In this report, a case of reconstruction of a large abdominal wall defect using an eccentric perforator-based pedicled anterolateral thigh (ALT) flap is presented. A 30-year-old man presented with recurrent desmoid-type fibromatosis in the abdominal wall. The recurrent tumor was radically excised, and the en bloc excision resulted in a full-thickness, large abdominal wall defect (25 cm × 20 cm). An eccentric perforator-based pedicled ALT flap, including wide fascial extension, was transferred to the abdominal defect; fascial portions were sutured to the remnant abdominal fascia. Plication of the fascia along the sutured portion was performed to relieve the skin tension between the flap and the marginal skin of the abdominal defect. Eight months after surgery, the reconstructed abdomen had an acceptable esthetic appearance without tumor recurrence or hernia.