It is one of the leading causes of maternal, as well as perinatal morbidity and Osimertinib supplier mortality, even in developed countries. Despite intensive research efforts, the aetiology and pathogenesis of pre-eclampsia are not understood completely.

Increasing evidence suggests that an excessive maternal systemic inflammatory response to pregnancy with activation of both the innate and adaptive arms of the immune system is involved in the pathogenesis of the disease [1,2]. We have demonstrated previously that the complement system is activated with increased terminal complex formation in the third trimester of normal human pregnancy, and further in pre-eclampsia, as shown by the elevated amounts of activation markers in the systemic circulation [3]. However, in our recent study, the role of the mannose-binding lectin (MBL)-mediated

lectin pathway has been ruled out in the pathological complement activation observed in pre-eclampsia [4]. Ficolins are pattern recognition molecules of the innate immune system that bind to carbohydrate moieties present on the surface of microbial pathogens, apoptotic and necrotic cells. They act through two distinct routes: by initiating the lectin pathway of complement activation in concert with attached MBL-associated serine proteases (MASPs) and by a primitive opsonophagocytosis [5]. Ficolins are oligomeric proteins consisting of an N-terminal Small molecule library cysteine-rich region, a collagen-like domain and a C-terminal globular fibrinogen-like domain. The latter is responsible Clostridium perfringens alpha toxin for carbohydrate binding [6]. Three types of ficolins have been identified in humans: ficolin-2 (L-ficolin), ficolin-3 (H-ficolin) and ficolin-1 (M-ficolin). The mRNA of ficolin-2 is expressed primarily

in the liver and its protein product is secreted into the blood circulation. Ficolin-2 exhibits lectin activity toward N-acetyl-glucosamine (GlcNAc) and 1, 3-β-D-glucan. Ficolin-3 mRNA is expressed in the liver and lung. In the liver, ficolin-3 is produced by bile duct epithelial cells and hepatocytes, and is secreted into the bile and circulation. In the lung, ficolin-3 is produced by ciliated bronchial epithelial cells and type II alveolar epithelial cells, and is secreted into the bronchus and alveolus. Ficolin-3 binds to GlcNAc, N-acetyl-galactosamine (GalNAc) and fucose. Ficolin-1 mRNA is expressed in monocytes, the lung and spleen. Its protein product has been identified in secretory granules of neutrophils and monocytes, as well as in type II alveolar epithelial cells. Nevertheless, it is present in the circulation at very low levels compared to ficolin-2 and ficolin-3. Ficolin-1 exhibits binding activity towards GlcNAc, GalNAc and sialic acid [7].

VIN may be human papillomavirus (HPV)-related classic VIN or -unrelated VIN. The former is by far the most frequent vulvar cancer precursor. It occurs in adult women and tends to be multi-focal. It is caused by high-risk HPV (HR-HPV) types, essentially type 16, and histologically is made of poorly Opaganib solubility dmso to undifferentiated basal cells and/or highly atypical squamous epithelial cells [1]. The involvement

of the entire thickness of the epithelium defines grade 3 of the disease. The disease progresses towards invasion in about 3% of treated patients and 9% of untreated patients, according to a review of more than 3000 cases [2]. Classic VIN can also regress spontaneously [3] in young women presenting with multi-focal pigmented papular lesions. Previously, we studied a patient who presented with multi-focal classic VIN and showed complete clearance of viral lesions 8 months after disease onset and 2 months after electrocoagulation of less than 50% of the classic VIN lesions [4]. Immunohistochemical

study of her initial vulvar biopsy revealed a marked dermal infiltrate containing a majority of CD4+ T lymphocytes and an epidermal infiltrate made up of both CD4+ and CD8+ T cells. She also showed a proliferating response against one peptide from E6 protein and a high-frequency anti-E6 and anti-E7 effector blood T cells by ex vivo enzyme-linked immunospot–interferon-γ (ELISPOT–IFN-γ) assay GSK-3 inhibitor just before clinical regression. Such a study of blood cellular immune responses, together with the analysis of vulvar biopsies obtained simultaneously

and correlated with clinical outcome, has not been reported previously. In an anti-HPV vaccine trial conducted by Davidson et al.[5], classic VIN lesions regressed completely in a patient following vaccination. Interestingly, immunostaining of vulvar biopsy prior to the vaccine showed a marked CD4+ and CD8+ T lymphocyte infiltrate of both epithelial and subepithelial sheets. It may be speculated whether the regression of these patient lesions could be related to a spontaneous regression. Therefore, the observation of a CD4+ and CD8+ infiltrate within subepithelial and epithelial sheets in the biopsy and the visualization of very strong blood anti-HPV T cell responses in patients with classic VIN could be predictive of spontaneous clinical outcome. Quisqualic acid It may also be thought that high numbers of blood CD4+ and CD8+ lymphocytes after therapeutic vaccination could allow clearance of HPV-16 lesions in classic VIN, assuming that anti-HPV vaccine-induced T effector cells could home into the HPV cutaneous and mucosal lesions. In the present study, we assessed cellular responses against HPV-16 E6 and E7 peptides in 16 patients presenting with classic VIN with the aim of mapping and characterizing the highest immunogenic regions from these proteins as potential candidates for a peptidic therapeutic vaccination.

T lymphocytes and B lymphocytes specific for other antigens are not activated in the current model. CD4+ regulatory T lymphocytes.  Innate (or natural) regulatory T lymphocytes (iTregs), representing

CD4+CD25+ T lymphocytes, anti-PD-1 antibody inhibitor are modelled as a distinct population of thymic-derived cells, distinguished from the aforementioned aTregs by not requiring further differentiation to express regulatory activity [52]. Once activated via presentation of autoantigen on MHC class II molecules (MHCII antigen), regulatory T lymphocytes exhibit both cell contact-mediated and cytokine-mediated immunosuppressive activity [46,53,54]. CD8+ T lymphocytes.  CD8+ T lymphocytes in the model are initially activated by MHCI-antigen in the PLN, with help provided buy Palbociclib by activated CD4+ T lymphocytes [55–58]. Acquired cytotoxic effector activity includes both cell contact- and cytokine-mediated mechanisms [59,60]. B lymphocytes.  B lymphocytes in the model interact with DCs, natural killer (NK) cells and T lymphocytes. They differentiate (in the PLN), present antigen to CD4+ and CD8+ T lymphocytes and produce cytokines and autoantibodies [61–63]. Autoantibodies form immune complexes, influencing antigen uptake

[26,64]. NK cells.  On the recommendation of the scientific advisory board, NK cells were included in the model based on a high degree of scientific interest and investigation [65–68]. Because the data characterizing NK cells in type 1 diabetes and their relative role in disease are sparse relative to other cell types, the use of the NK cell module is optional (i.e. it can be omitted from the virtual mouse simulations). Inclusion of the NK cell module may be used to explore specific hypotheses on the role of NK cells in disease. PAK5 Activation of NK cells in the model is mediated by DCs and B lymphocytes and is regulated further by cytokines and co-stimulatory molecules [69–74]. Effector activities include cytokine synthesis and killing of immature

DCs and β cells [75,76]. Blood glucose.  The level of blood glucose in the model is regulated by insulin-dependent and insulin-independent mechanisms, based on deviations of insulin and glucose from their basal levels [77,78]. Dietary glucose intake is assumed to be constant and implicitly accounted for in the basal glucose level. Gut and gut-associated lymphoid tissue.  The gut and gut-associated lymphoid tissue (GALT) were built to investigate the role of local immune activity on the efficacy of oral insulin therapy. The gut tissue in the model is simplified to include only DCs. The GALT includes all the biological components present in the modelled PLN. Following the design phase, the components of the model were represented mathematically. As illustrated in Fig.

The trend has therefore emerged to start ART at higher CD4 counts for all patients. Alternatively, an early start of ART could be recommended primarily to those patients see more who have a higher risk of complications or more rapid disease progression [8–10]. However, this approach probably requires better clinical predictors than CD4+ T cell counts and HIV-RNA concentrations [11,12]. Currently, predictors reflecting HIV-related chronic

immune activation have proved promising, particularly the expression of CD38 on CD8+ T cells [12–14]. Progression markers should reflect the development of HIV-related pathogenetic events. For example, chronic immune activation is associated with enhanced mucosal translocation of endotoxin into the circulation [15,16], whereas slow

disease progression has been related to high frequencies of HIV-specific T cell responses with polyfunctional [17] and proliferative capacity [18]. Unfortunately, assessment of these parameters may require cautious standardization which may complicate clinical evaluation. In this exploratory study of new putative prognostic markers in untreated, asymptomatic patients we used CD4+ loss rates and CD38 as measures for actual progression and progression risk. Furthermore, progression was related to T cell response distributions to three major selleck inhibitor HIV antigenic regions (Gag, Env and Nef) and the expression of inhibitor programmed death receptor-1 (PD-1; CD279) on these specific T cells for the following reasons: first, T cell responses to certain HIV epitope sequence regions, Fossariinae such as Gag and Env, may be more or less important for clinical progression [19–22]. The individual frequencies and their distributions between CD8+ and CD4+ T cell responses to three different optimized peptide panels [23] representing Gag, Env and Nef were tested on freshly isolated peripheral blood mononuclear cells (PBMC). Antigen specificity was ensured by a robust one-step detection of the activation-specific transient expression of CD107a on CD8+[24]

and CD154 on CD4+[25] T cell subsets, respectively, although mobilization of CD154 (CD40 ligand) on CD4+ cells may be hampered in chronic HIV infection [26]. Secondly, PD-1, a reversible inhibitor of T cell-specific activation [27–29], may be elevated particularly on HIV-specific CD8+ T cells [28,30–32]. This explorative study showed that both the magnitude and relations between Env and Gag responses and their PD-1 expression were better predictors for CD4+ T cell loss rates than the conventional indicators for ART in asymptomatic patients, and probably even better than expression of CD38. Thirty-one asymptomatic, HIV-1 seropositive, adult patients without ART were included from our out-patient clinic (Table 1).

3 and 1.9 mm. The most common perforator was medial (present in 85.6% of thighs); found near the adductor magnus at 3.8 cm from midline and 5.0 cm below the gluteal fold. The second most common perforator was lateral (present in 65.4% of thighs); found near the biceps femoris and

vastus lateralis at 12.0 cm from midline Selleckchem GS 1101 and 5.0 cm below the gluteal fold. Nearly 48.3% were purely septocutaneous. And 51.7% had an intramuscular course (average length 5.7 cm). Preoperative imaging corresponded to suitable perforators at the time of dissection of all PAP flaps. Thirty five PAP flaps (18 patients) were performed with 100% flap survival. Conclusion: Analysis of preoperative posterior thigh imaging confirms our intraoperative findings that a considerable number of suitable posterior thigh profunda perforators

are present, emerge from the fascia in a common pattern, and are of sufficient caliber to provide adequate flap perfusion and recipient vessel size match. © 2012 Wiley Periodicals, Inc. Selleck 3-deazaneplanocin A Microsurgery, 2012. “
“Injury of peripheral nerve is associated with the development of post-traumatic neuroma at the end of the proximal stump, often being the origin of neuropathic pain. This type of pain is therapy-resistant and therefore extremely nagging for patients. We examined the influence of the microcrystallic chitosan gel applied to the proximal stump of totally transected sciatic nerve on the neuroma formation and neuropathic pain development in rats. In 14 rats, right sciatic nerve was transected and the distal stump was removed to avoid spontaneous rejoining. In the chitosan (experimental) group (n = 7), the proximal stump was covered with a thin layer of the microcrystallic chitosan gel. In

control animals (n = 7), the cut nerve was left unsecured. Autotomy, an animal model of neuropathic pain, was monitored daily for 20 weeks following surgery. Then, the animals were perfused transcardially and the proximal stumps of sciatic nerves were dissected and subjected to histologic evaluation. The presence, size, and characteristics of neuromas as well as extraneural fibrosis were examined. In chitosan group, the incidence and the size of the neuroma were markedly reduced, Avelestat (AZD9668) as compared with the control group; however, there was no difference in autotomy behavior between groups. In addition, extraneural fibrosis was significantly reduced in chitosan group when compared to the control group. The results demonstrate beneficial influence of microcrystallic chitosan applied to the site of nerve transection on the development of post-traumatic neuroma and reduction of extraneural fibrosis, however without reduction of neuropathic pain. © 2011 Wiley Periodicals, Inc. Microsurgery, 2011. “
“Skin flap necrosis, as well as positive resection margins in the context of skin-sparing mastectomy and immediate breast reconstruction, may require reoperation, potentially associated with tissue loss, and thereby impair the aesthetic result.

Monocyte infection was performed over coverslips,

using a total volume of 0·5 ml of RPMI-1640 supplemented with 1% antibiotic/anti-mycotic, 1% 1 mm l-glutamine and 10% FCS. The monocytes were incubated with either medium alone or medium + 50 µm of captopril. Parasites were added immediately at a ratio of 5:1 TCT/monocytes and incubated for 3, 48 or 96 h at 37°C, 5% CO2. The monolayers were washed three times with PBS to remove free parasites. Infection was evaluated PLX3397 nmr by two methods: light and confocal microscopy. For the light microscopy, preparations were incubated with Giemsa dye for 15 min, washed and analysed using a Nikon light microscope (Melville, NY, USA). We analysed 15 field/samples using a power magnification of ×600, and the frequencies of adherent cells infected were expressed as percentage of positive cells in relation to the total cell count. For confocal microscopy analysis, immunofluorescence was carried out by staining with 4′,6′-diamidino-2-phenylindole (DAPI),

as follows. Coverslips were incubated DAPI diluted 1:300 in PBS supplemented with 2% bovine serum albumin (BSA) for 10 min and mounting using anti-fade medium. Slides were kept at 4°C and protected from light until acquisition. Confocal analyses were performed using a Meta-510 Zeiss laser scanning confocal system running LSMix software (Oberkochen, Germany) coupled to a Zeiss microscope using an oil immersion Plan-Apochromat objective (63X, 1·2 numerical aperture, Oberkochen, Germany). We performed six independent anti-CTLA-4 antibody experiments and analysed 15 fields per sample. Infection of monocytes in suspension was assessed O-methylated flavonoid by flow cytometry using 5 and 6-carboxyfluorescein diacetate succinimidyl ester (CFSE)-labelled TCT, as performed previously by us [18]. Parasites

were incubated with 5 µm CFSE for 10 min at 37°C, 5% CO2. Labelled parasites were washed three times with PBS by centrifugation and used for infection of adherent cells treated or not with captopril, as described above. Cells were then stained with anti-CD14-phycoerythrin (PE) monoclonal antibodies by incubation for 15 min at 4°C. Samples were washed and fixed for 20 min with a 4% formaldehyde solution. Stained cells were acquired in a Becton Dickinson fluorescence activated cell sorter (FACScan, Franklin Lakes, NJ, USA). Intensity of infection was evaluated by CFSE fluorescence intensity in gated CD14+CFSE+ cells. Infection with unlabelled parasites and incubation of infected cells with mouse immunoglobulin G1 (IgG1)-PE-labelled isotype control were used as parameters to set markers. A minimum of 30 000 gated events from each sample were collected and analysed using FlowJo software (Ashland, OR, USA). Two independent experiments were performed, with three individuals in each experiment.

In conclusion, in this study, an altered peptide ligand p321-1Y9L (YLIGETIKL) was identified with enhanced binding stability and immunogenicity derived from the native peptide in COX-2. Our results showed that p321-1Y9L could induce more potent CTL response in vitro and in vivo, which could lyse tumour cells in COX-2-specific and HLA-A2-restricted manners. This CTL epitope could serve as an attractive component of peptide-based vaccines to the immunotherapy of cancer patients. This work was supported by grants from the National Natural Science Foundation of China (No. 81172893, 30901362, 81000673), and the National Science and Technology Major Projects

of New Drugs PLX3397 purchase (2012ZX09103301-023). There are no conflicts of interest. “
“Blood levels of regulators of the complement system in preterm babies were reported in few studies only. The aim of this study was to set up a complement profile in premature and term babies focusing on the development of blood

levels of MBL, key regulatory proteins click here and on classical pathway activity, which may allow an estimation of potential susceptibility to infection. Complement activity (CH50), levels of mannan-binding lectin (MBL), complement regulators (factors H and I, C1 inhibitor, properdin) and C3a as marker of complement activation were assessed in three groups of healthy newborns: (1) prematures (≤34 weeks); (2) late prematures (>34–<37 weeks) and (3) term neonates (≥37 weeks). CH50 increased

with gestational age with lower Olopatadine titres in cord blood than in day 5 post-delivery venous blood. MBL concentrations were not significantly different among groups. Quantitative and functional C1 inhibitor were below adult normal range in prematures <34 weeks and lower in cord blood as compared to day 5. Factor I, factor H and properdin remained below adult values in all groups. Low C3a levels excluded that low complement titres were due to activation-induced consumption. These results demonstrate the relative immaturity of the complement system and its regulation, especially in premature infants. "
“We assessed the mucosal response of previously infected hamsters to low-dose challenge with the hookworm, Ancylostoma ceylanicum. Hamsters were assigned to five treatment groups (Groups 1–5, respectively): naïve, controls; uninterrupted primary infection from day 0; infected, but treated with anthelmintic on day 35 p.i.; challenge control group given only the second infection on day 63; infected initially, cleared of worms and then challenged. Animals were culled on days 73 and 94 (10 and 31 days after challenge), but additional animals were culled from Group 5 on days 80 and 87. The results showed that villus height declined markedly and progressively over time after challenge in Group 5, whilst depth of the Crypts of Lieberkühn and number of mitotic figures in the crypts increased.

For this study, Tregs from healthy individuals were chosen in order to examine the effect of MSCs from OA patients on functional T lymphocytes. However, as

stated above, it is necessary to conduct further research on how MSCs and Tregs taken from the same patients interact. In our experiments, blood volumes up to 150 ml were necessary to isolate a sufficient number of Tregs to conduct the co-culture experiments. While this is unproblematic for healthy individuals, in the context of a perioperative setting of a total hip arthroplasty with its high blood loss these volumes were considered too important to be taken from the OA patients. We are currently working on optimizing the isolation procedures as well as on methods that can provide Tregs from find more OA patients without taking

important blood samples, such as collecting cells during the intraoperative autotransfusion procedure. This study addressed only changes in phenotypical Treg properties and its important activation marker FoxP3. Our experiments cannot provide information on functional changes in Treg suppression potency. These experiments will need to be carried out in future to determine whether MSC immunomodulation has an effect on the functional properties of Tregs. Joint inflammation may have differed among the patients recruited in this study; whether this has an effect on MSC Selleck AZD1152 HQPA immunomodulatory processes in vitro will need to be determined in future experiments. Therefore, it may be necessary to correlate inflammation in the synovium with the in-vitro immunomodulatory properties of MSCs. We were able to detect IL-6 as an important factor in MSC–Treg interaction; however, future studies should focus upon other possible cytokines involved. We would like to acknowledge Patrick Göthlich, Marc Hoffmann and Elena Tripel for their support. The study was carried out with internal funding by the Forschungsfond Orthopädische Universitätsklinik (F.200086). None of the authors received external funding in connection with the study presented in this publication.

The authors declare that they have no competing interests. “
“Modified vaccinia Ankara-expressing Ag85A (MVA85A) is a new tuberculosis (TB) vaccine aimed at enhancing immunity induced by BCG. We investigated the safety and immunogenicity of MVA85A Calpain in healthy adolescents and children from a TB endemic region, who received BCG at birth. Twelve adolescents and 24 children were vaccinated and followed up for 12 or 6 months, respectively. Adverse events were documented and vaccine-induced immune responses assessed by IFN-γ ELISpot and intracellular cytokine staining. The vaccine was well tolerated and there were no vaccine-related serious adverse events. MVA85A induced potent and durable T-cell responses. Multiple CD4+ T-cell subsets, based on expression of IFN-γ, TNF-α, IL-2, IL-17 and GM-CSF, were induced.

The facts that the pain observed in patients with CRPS can result from multiple mechanisms and that patients with CRPS do not respond equally to the same medications may be due in

part to its evolution in time, but it also suggests that CRPS may result from multiple aetiologies. The results of this study demonstrating that a subset of CRPS patients show elevated numbers of the CD14+CD16+ monocyte subgroup may aid in elucidating some of the different mechanisms involved in its pathophysiology. A better understanding of these mechanisms may lead to novel treatments for this very severe, life-altering condition. This study has demonstrated an increase in the percentage of the CD14+CD16+ monocyte subgroup in individuals afflicted

with CRPS. In addition, other investigators have reported mast cell involvement [47], Raf inhibitor leucocyte accumulation in the affected selleck compound extremity [48] and impaired neutrophil function [49] in patients with CRPS. Thus, further evaluation of the role the immune system plays in the pathogenesis of CRPS is warranted, and may aid in elucidating disease mechanisms as well as the development of novel therapies for its treatment. We wish to graciously thank Eric B. Wong MS and Jeffrey J. Gerbino for their technical assistance. This study was supported by grants from the Commonwealth of Pennsylvania Department of Health, Drexel University College of Medicine Pain Initiative and gifts from the Tilly Family Foundation and the Sunstein family. The authors certify that they have no commercial associations that might pose a conflict of interest in connection with this article. All funding sources for this study are listed in the Acknowledgements section. PatID Gender/ Age Initiating Event/Duration Signs/Symptoms/Overall

Non-specific serine/threonine protein kinase Pain Score NRS(0-10) Pain Medications Other Conditions CRPS01 F/68 Kyphoscoliosis; disc disease at L5-S1/22 years L5-S1 sensory loss; spontaneous burning pain in both legs; weakness; inability to move toes; severe dystrophic changes. Pain (NRS) 8 NSAIDs; anti-epileptic drugs (AED), antidepressants; intermittent narcotics; spasmolytics. L4-L5 bilateral radiculopathy; arthrosclerosis; GERD; osteoporosis; osteoarthritis; IBS; headaches CRPS02 F/44 Fall; brachial plexus traction injury (BPTI)/4·5 years Paresthesias; deep ache; deep muscle joint pain; dynamic and static allodynia; generalized from BPTI; weakness; poor initiation of movement. Pain (NRS) 8 Intravenous ketamine; intravenous lidocaine; narcotics; AED; antidepressants, lenalidomide. C5-C6 disk herniation; L4-L5-S1 radiculopathy; mitral valve prolapse; Asthma; headaches. CRPS03 F/46 Fall; repetitive strain of right brachial plexus/9 years Dynamic and static mechano allodynia; cold allodynia right upper quadrant; autonomic dysregulation; neurogenic oedema; dystonia of trunk; weakness.

After 3 days, HSCs were isolated from the bone marrow. After 10 days in culture, 1×105 cells of two different HSC populations were injected into Rag-2/γC−/− mice expressing either H-2Kd or H-2Kb. Mice were analyzed 4–5 wk after HSC transfer. Animal experiments were done in compliance with the guidelines of German law and the Max-Planck-Institute of BMS-354825 mouse Immunobiology and Epigenetics. HSCs were grown in Iscove’s medium (Biochrom) supplemented

with 2% of heat inactivated FCS (PAN Biotech), 10 mM L-glutamine, 100 U/mL penicillin, 100 U/mL streptomycin (GIBCO), 50 mM 2-mercaptoethanol, 0.03% primatone (Sigma-Aldrich), 4.2 mg/mL insulin (Sigma-Aldrich), IL-6, IL-3 and c-kit-ligand. The expression of H-2d and H-2b was determined by flow cytometry using the specific monoclonal antibodies H-2Dd-PE and H-2Kb-FITC

(BD). Cells were stained with anti-B220/CD45R-PerCP (RA3-6B2, BD), anti-CD43-PE (S7, BD), anti-CD19-PE/-PerCP (1D3, BD), anti-CD21-APC (7G6, BD), anti-CD23-PE/biotin (B3B4, BD/PharMingen), anti-IgM-Cy5 (Jackson Immunoresearch) and anti-idiotype 54.1 (kindly provided find more by D. Nemazee). Flow cytometric analysis was performed with FACS-Calibur (BD). Statistical analysis was performed with the GraphPad Prism 4 software using Student’s t-test as the statistical hypothesis test. The authors thank U. Stauffer, N. Joswig and C. Johner for mouse work and further assistance. They thank E. Hobeika for the mb1-lox-GFP mice, P. Nielsen, D. Nemazee and M. Reth for critical reading of the manuscript. This work was supported by the Deutsche Forschungsgemeinschaft (SFB620 and SFB746). Conflict of interest: The authors declare no financial or commercial conflict of interest. Detailed facts of importance to specialist readers are published as ”Supporting Information”.

Such documents are peer-reviewed, but not copy-edited or typeset. They are made available as submitted by the authors. “
“Two outbreaks of Streptococcus suis ST7 occurred in humans in 1998 and 2005 in China. PFGE of Rebamipide chromosome restriction fragments found all ST7 isolates to be indistinguishable. Due to the genetic homogeneity of ST7 isolates, development of a rapid sub-typing method with high discriminatory power for ST7 isolates is required. In this study, a novel method, MLVA, was developed to type S. suis serotype 2 strains. Further, this method was used to analyze outbreak-associated ST7 strains in China. A total of 144 ST7 S. suis isolates were sub-typed into 34 MLVA types. Among these, eight isolates from the 1998 outbreak were sub-typed into five MLVA types, of which four MLVA types were also detected in Sichuan in 2005. These data indicate that the pathogens responsible for the two outbreaks had the same origin. In addition, some observations also provided molecular evidence for the transmission route, possibly indicating that the MLVA method has usefulness in epidemiology. The developed MLVA scheme for S.