Flap survival was 100%. Pelvic ring defects were reconstructed with A-frame fibula flap struts anastomosed to the distal epigastric vessels of pedicled trans-pelvic VRAM flaps. Complications such as wound healing, infection or hardware failure were not observed. Bony union occurred at an average 2.7 ± 0.6 months. Total sacrectomy reconstruction using a VRAM flow-through flap anastomosed to a two-strut free fibular flap allows initial

assessment of the recipient vessels during the first and ensuing operative stages, satisfies the bone Sirolimus solubility dmso and soft tissue requirements of the defect, and provides a durable, functionally optimized reconstruction. © 2012 Wiley Periodicals, Inc. Microsurgery, 2013. “
“This study aims to compare donor-site morbidity between the traditional fibula osteocutaneous and chimeric fibula flaps for mandibular reconstruction. Twenty-three patients with head and neck cancer were recruited. Fifteen patients underwent the traditional fibula osteocutaneous flap. Eight patients received a chimeric fibula osteocutaneous flap

with a sheet of soleus muscle. Subjective donor-site morbidities were evaluated by questionnaire. Objective isokinetic testing and 6-minute walking test (6MWT) were used to evaluate ankle strength and walking ability. The results revealed no significant C59 wnt datasheet difference was found in total average score of the questionnaire between the traditional (2.57) and the chimeric (2.75) groups

(P > 0.05). There were no significant differences in peak torque/total work of ankle motions and in walking ability at 6MWT between the traditional and chimeric groups (P > 0.05). In Interleukin-2 receptor conclusion, compared with the traditional fibula osteocutaneous flap, the chimeric fibula flap does not increase donor-site morbidity for reconstructive surgery. © 2011 Wiley Periodicals, Inc. Microsurgery, 2012. “
“This study included two parts: 1) cadaver dissection to elucidate the perfusion of toenail flaps by the fibro-osseous hiatus branch (FHB), and 2) clinical application of the toenail flap for reconstruction of a fingernail defect. Four second toes of two fresh Korean cadavers were dissected. The plantar digital artery (PDA) and terminal segment branch (TSB) were ligated, and red latex was injected distally into the ligated PDA. Perfusion of the dye into the toenail bed through the FHB was observed. From Oct 2004 to Sep 2009, eight toenail flaps based on the FHB pedicle with or without the distal phalanx and pulp were applied to seven patients for finger nail reconstruction. The toenail flap was marked at 5 mm distal to the nail fold and 5 mm lateral to the paronychium. The toenail complex based on the FHB was elevated and transferred to the finger. The nail and matrix were elevated with or without including the distal phalanx.

IL-10 levels in infected pregnant B6 mice were statistically significantly reduced relative to infected pregnant A/J mice GSK3235025 on experiment day 9 (median (IQR): 36 (0–46) pg/mL for B6 vs. 550 (431–735) pg/mL

for A/J; P = 0·001), but this pattern was reversed on experiment day 10 (Figure 4a). In both strains, IL-10 levels were enhanced at experiment day 11 in infected pregnant relative to uninfected pregnant mice. Levels of sTNFRII did not differ between infected pregnant A/J and B6 mice at any of the tested time points, although the levels were consistently statistically significantly higher in the infected mice relative to their within strain uninfected counterparts (Figure 4c, d and data not shown). At none of the time points were the differences in IL-10 or sTNFRII observed between infected pregnant and infected non-pregnant mice of either strain nor were across-strain differences between infected non-pregnant mice found (Figure 4). To further evaluate immune changes associated with P. chabaudi AS infection and pregnancy loss in A/J and B6 mice, phenotypes RNA Synthesis inhibitor and levels of splenic leucocyte subsets were analysed flow cytometrically at experiment days 9 and 10, time points at which mice of both strains retain a proportion of viable conceptuses. No statistically significant differences in B-, natural killer (NK) or T-cell counts, including T-cell subsets, were observed between infected pregnant

A/J and B6 mice (Figure 5). However, malarial infection clearly stimulated expansion of all of these cell types in pregnant A/J mice, in whom splenocyte numbers for all subsets (except T cells at experiment day 9) were statistically significantly higher relative to their uninfected pregnant counterparts (Figure 5).

Similar differences in B6 mice were noted only for T, CD8+ T, B and NK cells on experiment day 9, but not on 10 (Figure 5). The total number of lymphocytes and lymphocyte subsets in general did not differ between infected pregnant and infected non-pregnant mice within each strain; only CD4+ T cells on experiment day 9 were significantly expanded in infected pregnant Dapagliflozin relative to infected non-pregnant A/J mice (Figure 5c). Similar to the lymphocyte subsets, numbers of neutrophils, monocytes and monocytes with an inflammatory phenotype (CD11b+/CD115+/Gr1high) were similar in the infected pregnant B6 and A/J mouse spleens on experiment days 9 and 10 (Figure 6). Neutrophil levels were enhanced in infected B6 mice at experiment day 9 relative to uninfected pregnant B6 mice (Figure 6a), a difference that did not reach statistical significance on experiment day 10 (Figure 6b: Kruskal–Wallis, P = 0·0024; Dunn’s pairwise comparisons, all P > 0·05). Monocytes levels were increased in infected pregnant B6 mice compared to their uninfected counterparts on experiment days 9 and 10, and on the former day were also higher than in infected non-pregnant mice (Figure 6c, d).

Information about each patient’s smoking status, including amount used, starting and stopping dates, and changes in use over time were obtained. The dose-response relationships between cigarette smoking and the outcomes were assessed by using multivariate Cox proportional hazards models AP24534 order adjusted for clinically relevant factors. The primary and secondary outcomes were a 50% increase over the baseline serum creatinine level and first complete remission (CR) of proteinuria, respectively. Results: Throughout the observation period (median, 37 months;

interquartile range, 16–71 months), 22 (12.9%) patients developed a 50% increase in the serum creatinine level and 2 (1.2%) progressed to ESRD. CR was achieved by 103 (60.2%) patients. Multivariate Cox proportional hazards models indicated that current smoking was associated with a 50% increase over the baseline serum creatinine level (adjusted hazard ratio [HR], 6.59 [95% confidence interval (CI), 2.13–21.6]) and female sex (adjusted HR, 3.17 [95% CI, find more 1.02–9.80]). The number of cigarettes smoked daily (adjusted HR, 1.62 [95% CI, 1.16–2.27] per 10 cigarettes daily) and cumulative smoking of ≥40 pack-years (adjusted HR, 5.71 [95% CI, 1.80–19.1]) were significant predictors of the primary outcome. However, smoking was not associated with CR. Conclusion: Smoking is a significant and dose-dependent risk factor for IMN progression.

All patients with IMN who smoke should be encouraged to quit. ISMAL KIRANMAI1,4, SAHAY MANISHA2, VALI SHARMAS3, GOWRI SHANKER SWARNALATHA4 1Osmania General Hospital; 2Osmania General Hospital; 3Osmania General Hospital; 4Apollo Hospital Introduction: Malignancy can produce variety of Renal lesions in kidney. Our Aim is to study the prevalence and spectrum Tryptophan synthase of Renal lesions among patients with malignancy who underwent Renal Biopsy. Methods: We

retrospectively analyzed the Data of 100 patients of Malignancy in whom the Renal biopsy was performed.Indications for Biopsy were: Renal failure and Nephrotic syndrome in patients with malignancy. Renal biopsies were processed by standard methods examined under light, fluorescent, Microscopy and EM wherever required. All biopsies are reported by a single histopathologist. Results: There were 100 patients. Ratio of Male and Female was 7:3. 82 were Multiple Myeloma. 14 females/ 68 males. Mean age 59 +/− 11 years. Cases presented as RPRF/ Nephrotic Syndrome with Renal insufficiency and Nephrotic Syndrome. The histological spectrum of Renal lesions were: Cast nephropathy 40% (32), Amyloidosis- 34% (27), LCDD-10% (8), AIN-7.5% (6), ATN-2.5% (2), MCD-1.25% (1), MPGN-5% (4). 9 cases of Lympho Proliferative disease have presented as ATIN(4) 44%, diffuse infiltration of the kidney by lymphoblasts. (3) 33% Amyloidosis (1) 11%, SLE Class IV (1) 11%.

16 They adjusted for differences in case-mix population data between the studies and subgroups used and were able identify some key conclusions: when comparing HD and PD as initial

dialysis therapies, PD is associated with equal or improved survival among younger patients without diabetes In the absence of properly conducted randomized controlled trials, Vonesh et al.16 Wnt inhibition suggests that a clearer picture of survival benefit according to modality is demonstrated when examining the large registry studies with extensive subgroup analyses. Registry data studies such as that of Liem et al.4 analysed nearly 17 000 patients in the Netherlands, stratified for age and diabetic status. The survival advantage with PD was confined to those patients <50 years and without diabetes as the cause of their renal disease and disappeared with time (>15 months). In patients 50 years and older with diabetes, PD was associated with worse survival after 15 months, but there was no particular difference in survival between modalities in the first 14 months. Heaf et al.12 also found that the survival advantage disappeared for those in older cohorts find more and with diabetes. These results are also supported

by Fenton et al.5 and Vonesh and Moran.3 The Fenton et al.5 Canadian group studied nearly 12 000 patients from their national database. A decreased mortality in the PD group was less pronounced among those with diabetes and over 65 years of age. The survival advantage in the PD group was also limited to the first 2 years after initiation. Vonesh and Moran also found PD patients under the age of 50 years to have a significantly lower risk of death than those treated with HD, whether or not they had diabetes.3 When observing patient cohorts with CHF, Stack et al.14 found

that patients treated initially with PD had significantly higher adjusted mortality compared with HD after 6–24 months of follow up (RR 1.47 at 24 months). Similar to the previously mafosfamide mentioned studies, the patient cohort without CHF experienced lower mortality on PD for the first 6–12 months regardless of whether or not they had diabetes. Stack et al.14 did not stratify for age. Ganesh et al.15 also found those cohorts with CAD had worse survival on PD than HD, but an initial survival advantage if they did not have CAD. The patients with diabetes had significantly poorer survival on PD compared with HD, regardless of coronary artery status. The results were not interpreted for age-related differences. The report by Locatelli et al.13 from Italy was the only registry data study of more than 4000 new patients that after stratifying for age, gender, established CVD and diabetes, and did not reveal any significant difference in survival comparing modalities at least until the follow-up period of 20 months post initiation. Of particular interest is a retrospective cohort study performed by Panagoutsos et al.

In addition, LAG-3 is a negative regulator of T cell receptor (TCR)-mediated signal transduction in effector

T cells and functions in the same manner as cytotoxic T lymphocyte antigen-4 (CTLA-4) [9–12]. Finally, LAG-3 controls activated regulatory T cells (Tregs), while it is not expressed by unstimulated natural Tregs[13]. However, LAG-3 is expressed by interleukin Selleck LDK378 (IL)-10-secreting early growth response (Egr)-2+LAG-3+CD4+ Tregs associated with Peyer’s patches [14]. We have shown previously that depleting anti-LAG-3 antibodies prevented the development of alloreactive effector T cells in a heart allotransplant model in rodents and represents an effective treatment for allograft rejection [15]. In this study, we have characterized a cytotoxic anti-LAG-3 chimeric antibody (chimeric A9H12) and evaluated its potential for selective therapeutic depletion in a non-human primate model of delayed-type hypersensitivity (DTH), a low-invasive HIF inhibitor and non-terminal model based on the induction of local T helper type 1 (Th-1)-mediated cellular immune responses [16]. Our investigation demonstrated

that LAG-3+ T lymphocytes could be depleted in vivo in primates and that this resulted in a long-lasting inhibition of immune responses in this preclinical model. C57/B6 mice were immunized three times with Chinese hamster ovary (CHO) cells transfected with human LAG-3 cDNA, followed by an intravenous (i.v.) booster injection of a recombinant hLAG-3Ig protein purified from the supernatant of transfected CHO cells. Three Megestrol Acetate days after the boost, splenocytes were fused with the X63.AG8653 fusion partner [17] to obtain hybridoma cells, using traditional techniques. The A9H12 hybridoma was selected for its antibody-dependent cell cytotoxicity (ADCC) activity towards LAG-3 expressing cells and subcloned to yield a stable cell line. A bicistronic vector coding for the variable heavy (VH) and variable light (VL) domains of A9H12 fused to human CL kappa and CH1-hinge-CH2-CH3 immunlglobulin (Ig)G1 regions was

generated and used to transfect CHO-S cells (Invitrogen, Illkirch, France). After antibiotic selection and limiting dilutions, a stable subclone was selected to produce the chimeric A9H12 in ProCHO5 medium (Lonza, Vervier, Belgium). The product in the supernatant cell was purified by adsorption on a HiTrap recombinant Protein A FF column (GE Healthcare, Velizy, France), eluted by acid pH (Glycin HCl, 0·1 M, pH 2·8) and dialysed against phosphate-buffered saline (PBS; Invitrogen). LAG-3+ CHO cells or human peripheral blood mononuclear cells (PBMCs) stimulated with 1 µg/ml of Staphylococcal enterotoxin B (SEB; Sigma Aldrich, L’Isle D’Abeau Chesnes, France) for 48 h were used as targets. Chimeric A9H12 binding was revealed with a fluorescein isothiocyanate (FITC)-conjugated goat F(ab′)2 anti-human IgG (Southern Biotech, Birmingham, AL, USA).

58 Although kDCs are capable of cytotoxic function, their differentiation into a killer phenotype is largely dependent on the presence of stimulatory factors

such as lipopolysaccharide, IL-15, IFN-α or IFN-γ,59,60 which were not used in any of our cytotoxic functional studies using enriched CD8α− and CD8α+ NK cells (Fig. 5c,e). Given this, we believe that the capacity of CD8α− NK cells to mediate modest (albeit significant) cytotoxic function is in direct correlation Selleck NVP-LDE225 to their activation profile and expression of cytotoxic proteins, and not to the potential acquisition of a killer phenotype by mDCs. Evaluation of PBMCs from SIV-infected macaques for CD8α− NK cells showed that these cells, and their CD16/CD56 subpopulations, are present at frequencies similar to those in naive animals (Fig. 7a,c). On the other hand, we detected a significant decrease in the frequency of CD8α+ CD16+ NK cells, which was accompanied by a significant increase

in the proportion of CD8α+ CD56− CD16− NK cells (Fig. 7b). Interestingly, when comparing CD16/CD56 subpopulations within CD8α− NK cells of naive and SIV-infected macaques, we also observed a decrease in the proportion of CD8α− CD16+ cells MLN0128 supplier and a concomitant rise in the proportion of CD8α− CD56− CD16− NK cells, although these changes did not reach statistical significance (Fig. 7c). This observation suggests that during SIV infection, loss of CD3− CD16+ cells affects both CD8α− and CD8α+ NK cell subsets. Our results are in line with previous descriptions of HIV patients, where CD3− CD8+ CD16+ NK cells are depleted despite an overall increase in CD8+ lymphocytes.61,62 The ability of CD8α− NK cells to mediate ADCC activity during adaptive immune responses when anti-viral antibodies are click here present, could contribute significantly to disease prevention and control.19,21,24 Stratov et al.63 have shown that robust ADCC responses, targeted mainly towards the Env protein, are observed in HIV-infected subjects. Importantly,

the effector cells identified were of the CD3− CD4− CD8− CD14− CD2+ CD56+/− phenotype, which is strikingly similar to the phenotype we describe here for macaque CD8α− NK cells. Despite the significant presence of mDCs in the CD8α− NK cell gate, our results are in line with those reported by Rutjens et al.34 and Reeves et al.,40 and confirm the presence and functional capacity of a CD8α− NK cell population in rhesus macaque PBMCs. Natural killer cells express a wide variety of chemokine receptors and tissue-homing molecules that influence their tissue distribution and migratory potential.29 Chronic SIV infection has been shown to enhance the expression of the gut-homing marker α4/β7 in different subsets of NK cells.47 It will be of interest to analyse the chemokine-receptor and tissue-homing molecule expression profiles of this novel subpopulation of circulatory CD8α− NK cells in naive and SIV-infected macaques.

Following anergy induction in the primary cultures, anergic and control Th1 cells were harvested, washed, counted and restimulated with streptavidin-coated magnetic beads (Dynal) that had been previously incubated Talazoparib datasheet for (1 hr at 4°) with biotinylated anti-CD3 and anti-CD28 antibody at 1 : 1, 1 : 2 or 1 : 4 bead to cell ratio in the presence of anti-IL-2 receptor-α antibody to prevent the attachment of secreted IL-2 to the cells. After 24 hr, cell culture supernatants were collected and analysed for the cytokine content by flow cytometry using a Mouse Th1/Th2 Cytokine Cytometric Bead Array (CBA) kit (BD, San Diego, CA) according to manufacturer’s protocol on FACSCalibur.

Following primary cultures, control or anergic Th1 cells were isolated and restimulated using anti-CD3 and anti-CD28 antibody-coated magnetic beads at 1 : 4 bead to cell ratio for 0–24 hr. Nuclear lysates Tamoxifen in vivo were then prepared using Nuclear Extract kit (Active Motif, Carlsbad, CA). Previously untreated resting Th1 cells were also included as a measure of the baseline level

of transcription factor activity. c-Fos and c-jun activity was measured using TransAM Transcription Factor Activity Assay kits (Active Motif) according to the manufacturer’s protocol. Briefly, duplicate wells of 96-well plates to which the consensus-binding site oligo has been immobilized were incubated with 20 μg lysate/sample. The wells were then washed and the transcription factor of interest that was bound specifically to the coated oligonucleotide was detected by primary antibody specific for an epitope on the bound and active form of the transcription factor. Subsequent incubation with secondary antibody and developing solution provided a colorimetric readout that was acquired at 450 nm. Data are presented as mean ± standard deviation (SD). The statistical analysis of the data was performed using that paired Student’s t-test. A P-value ≤ 0·01 was considered Axenfeld syndrome significant. n-Butyrate effectively blocked

the proliferation of antigen-stimulated cells in primary cultures (Fig. 1a). In accordance with earlier studies,5,8 Th1 cells that were antigen-stimulated in the presence of n-butyrate in primary cultures were largely unresponsive when restimulated with antigen in the absence of n-butyrate in secondary cultures (Fig. 1b). In contrast, the Th1 cells that were stimulated with antigen in the absence of n-butyrate in the primary cultures proliferated in the secondary cultures as well as previously untreated Th1 cells. Although unresponsive to antigen stimulation, anergic Th1 cells proliferated in response to exogenous IL-2, indicating no loss in cell viability. In later experiments, antigen restimulation was preferred when possible because it was more physiological.

Low IgM levels with B cell lymphopenia have been reported

in X-linked dyskeratosis congenita (X-linked DC), with severe combined immunodeficiency (T + B − NK − SCID) reported in the most severe variant of dyskeratosis congenita (Hoyeraal–Hreidarsson syndrome) [36]. Premature ageing is also a feature of this disease [32–34] and TINF2 gene mutation (a component of the telomere protection complex) [35] leading to short telomeres has been described in X-linked DC. It is not clear whether the immune abnormalities are due to the defective tRNA pseudouridylation or the short telomere length. Turner’s syndrome (45,X0) is postulated to have a ribosomal defect due to haploinsufficiency of ribosomal protein RPS4X [48,49]. Variable degrees of antibody deficiency (panhypogammaglobulinaemia [48], selleck chemical low IgM [50,52]) FK228 research buy including decreased T and B cell numbers [50,54] and coeliac disease with IgA deficiency have been recognized in this syndrome [53,55]. Some of these patients with Turner’s syndrome have clinical syndromes of recurrent sinopulmonary infections and other features overlapping with CVID [50,51]. We have looked at the evidence for ribosomal defects being associated with

and possibly causative of immune abnormalities with features of CVID. We describe two such patients with different ribosomal defects who subsequently developed a presentation consistent with CVID. A review of the Anacetrapib literature indicates that patients with ribosomal defects may share abnormalities of T or B cell development with many features of CVID, and which may not be recognized

as such by non-immunologists. Given that the four established genetic defects account for fewer than a fifth of cases of CVID, this hypothesis could be tested in the future by more detailed studies of ribosome genetics and/or function in CVID. This work was supported by the Centre for Immunoglobulin Therapy and Department of Immunology, Hull Royal Infirmary. WACS is Director of Centre for Immunoglobulin Therapy, which has received unrestricted educational grants from Octapharma, Baxter, Grifols, CSL-Behring. The rest of the authors have no financial interests to disclose. “
“Human cytomegalovirus (HCMV) has been reported to reshape the NK-cell receptor (NKR) distribution, promoting an expansion of CD94/NKG2C+ NK and T cells. The role of NK cells in congenital HCMV infection is ill-defined. Here we studied the expression of NKR (i.e., NKG2C, NKG2A, LILRB1, CD161) and the frequency of the NKG2C gene deletion in children with past congenital infection, both symptomatic (n = 15) and asymptomatic (n = 11), including as controls children with postnatal infection (n = 11) and noninfected (n = 20).

Previous study has shown that cross-linking of FcεRI activates PI3K signalling

pathway, leading to intracellular ROS production [25]. To explore whether OVA challenge–induced ROS production and subsequent activation of SOCs are related to PI3K activation, we explored the effect of PI3K inhibitor Wortmannin on ROS production and Ca2+ signalling in OVA-activated mast cells. The results demonstrated that Wortmannin (100 nm, 15 min) pretreatment significantly decreased PD98059 intracellular ROS production by ~30%. Mast cell activation–induced histamine release was similarly reduced (~30%) by inhibiting PI3K pathway. With the reduction of ROS, Ca2+ increase through SOCs in OVA-activated mast cells was diminished by ~30% (Fig. 6A,B). Consistently, the protein expressions of Orai1 and STIM1 were attenuated by ~40% and ~30%, respectively (Fig. 6C,D). We also found that inhibition of PI3K pathway reduced mast cell activation–induced histamine release (~30%) and intracellular ROS Compound Library in vivo production (~30%). The results indicate that PI3K-mediated ROS generation is involved in the regulation of SOCs activity and mast cell activation under food-allergic condition (Fig. 6E,F). Previous studies have demonstrated that mast cells play a critical role in allergic diseases. Using OVA-stimulated food-allergic rat model, we revealed that

mast cells were recruited and activated in the damaged intestinal tissues and peritoneal lavage, and Th2 cytokines and IgE were significantly increased, confirming

the notion that mast cells contribute to the pathogenesis of food allergy. In this study, we demonstrated that the underlying mechanism for mast cell activation Adenosine triphosphate in the food-allergic mouse model is related to increased Ca2+ entry through SOCs. Furthermore, we found that OVA stimulation increased intracellular ROS production in mast cells through activation of phosphoinositide 3-kinase (PI3K) pathway, which results in upregulation of the expression levels of the major subunits of SOC, Orai1 and STIM1, leading to the enhancement of SOC activity and subsequent mast cell activation. Food allergy is one type of adverse reactions to non-toxic food that involves an abnormal immunological response to specific protein(s) in food. Allergens from egg seem to be one of the most frequent causes of food-allergic reaction as reported [26]. In the present study, we use OVA, which comprise 50% of the protein in egg white, to induce food allergy as previously reported [17, 27, 28]. According to our results, the food-allergic model in Brown-Norway rats has been successfully re-established. The OVA-challenged rat showed typical allergic appearances, including puffiness and redness around the eyes and mouth, diarrhoea, pilar erecti, reduced activity and/or decreased activity with increased respiratory rate and cyanosis around the mouth and tail.

These selleck chemicals llc results cannot be extrapolated to other recombinant bacteria, in which the variable is not only the antigen expressed, but also the mouse strain and the model used for the study of the effectiveness of the vaccine. The evaluation of new conserved antigens and innovative strategies for the immunization of the respiratory mucosa continue to pose a challenge to the global scientific community. The induced immune response

is extremely important in the selection of the correct vaccine. Thus, T helper (Th) CD4+ cells play a key role in the adaptive immune response by co-operating with B cells for the production of antibodies through direct contact or through the release of cytokines that regulate the Th type 1 (Th1)/Th2 balance. On the other hand, lactobacilli enhanced the antigen-specific immune response induced by viral or bacterial vaccines [19–21]. However, not all Lactobacillus strains have intrinsic adjuvanticity or can be used as mucosal adjuvants [22,23]. The ability of probiotics to modulate the immune response depends in great part upon the cytokine profile induced,

which varies considerably with RXDX-106 concentration the strain and dose used [24,25]. Previous studies in our laboratory with pneumococcal infection models in immunocompetent [26] and immunocompromised [27] mice showed that oral administration of the probiotic L. casei CRL 431 improved the immune response of the host against respiratory pathogens and that its effect was dose-dependent [26–29]. On the basis of the above, we considered that it would be possible to improve the immunity induced by the recombinant strains by combining their application with a probiotic strain. There are very few comparative studies of the lung mucosal and systemic immune response induced by a live and an inactivated recombinant bacterium, and we think that none of them has dealt with the study of the Epothilone B (EPO906, Patupilone) co-administration of a probiotic strain and a recombinant vaccine. Thus, the aim of this work is to evaluate the adaptive immune response induced by L. lactis-PppA live and inactivated and in association with the oral and nasal administration of a probiotic strain and to analyse the possible mechanism

involved in the protection against a pneumococcal infection. Recombinant Lactococcus lactis-PppA (LL) was obtained in our laboratory and the development of this strain was described in a previous report from our work group [16]. L. lactis-PppA was grown in M17-glu plus erythromycin (5 µg/ml) at 30°C until cells reached an optical density (OD)590 of 0·6 and then induced with 50 ng/ml of nisin for 2 h. Bacteria were harvested by centrifugation at 3000 g for 10 min, then washed three times with sterile 0·01 M phosphate-buffered saline (PBS), pH 7·2, and finally resuspended in PBS at the appropriate concentrations to be administered to mice. For inactivation, bacterial suspensions were pretreated with mitomycin C [30]. The inactivated strain was called dead-L. lactis-PppA: D-LL L.