4(a)) The reason for this is that if very old adults cannot be b

4(a)). The reason for this is that if very old adults cannot be boosted then reduction in varicella incidence (reduced exposure to VZV) will have little effect on their risk of developing zoster. Thirdly, more effective vaccines (or effective programs) against varicella will produce the greatest increases in zoster cases (Fig. Autophagy Compound Library mw 4(b)). However, in the long-term the worst vaccines will produce a higher zoster incidence as more people will be infected with varicella

and therefore will have the possibility of reactivation (Fig. 4(b)). Finally, age-specific effective mixing can largely influence the impact of varicella on zoster. If older adults have very little contact with varicella cases (e.g. low contact rates with infected children) then reduction in varicella incidence following vaccination will only have a small impact on zoster (see England and Wales mixing scenario ( Fig. 4(c)). The expected increase in zoster predicted by the model is directly related to estimates of the force of infection in adults; the force

of infection in 25–44 years olds for the base case, Lonafarnib mouse England and Wales, Finland and Germany are 0.06, 0.03, 0.04 and 0.04 per person-year, respectively. Fig. 5 shows the impact of 2-dose varicella vaccination programs on varicella and zoster. The base model predicts that a 2-dose varicella vaccination program will significantly reduce varicella incidence under the three strategies investigated (Infant, Pre-school and Grade 4 ( Fig. 5)). Of note, our results suggest that giving the second second dose in Grade 4 could help avoid the predicted epidemic of varicella 10 years into the 1-dose program by acting as: (1) catch-up vaccination in those yet to be immunised with a first dose and (2) a booster dose in vaccinees whose protection

will have waned. The main benefit of the second dose is its effectiveness at reducing breakthrough varicella (Fig. 5(b)). However, the short to medium term increase in zoster incidence (Fig. 5(c)) is predicted to be slightly higher under a 2-dose program (compared to 1-dose) because of its greater effectiveness at preventing varicella. Fig. 6 illustrates the incremental benefits of adding a second dose for different vaccine efficacy, mixing matrix and boosting assumptions. The base case model (range: min; max) predicts that adding a second dose will reduce varicella and zoster cases by an additional 22% (0%; 82%) and 6% (0%; 14%) over 80-years, respectively. Importantly, although the incremental benefit of adding the second dose is highly sensitive to assumptions regarding vaccine efficacy and mixing, the overall effectiveness of a 2-dose strategy at preventing varicella is not (Fig. 6). A 2-dose infant strategy (90% coverage) is predicted to reduce varicella cases by 72%–97%.

Flow cytometric analysis of the interaction of the generated anti

Flow cytometric analysis of the interaction of the generated antibodies with diverse pneumococci showed that antibodies to PspA 245/00 and 94/01 were able to increase complement deposition on the widest range of pneumococci tested. The complement deposition on the different pneumococci appeared to be also influenced by the serotype. We observed that some serotypes exhibited an increased complement deposition in the absence of anti-PspA antibodies, as demonstrated previously with serotype 6B strains [31]. We tested the ability of these antisera to induce the complement deposition in pneumococcal

strains bearing family 2 PspAs (data not shown), and no increase in complement deposition was observed. This result is in accordance with our previous

findings see more [21], and suggests that, although some family 1 molecules can broaden cross-reactivity within this family, this effect is not extended to family 2. Our results demonstrated a significant variability in the cross-reactivity this website of antisera generated against PspAs of the same clade, which correlates with differences in antibody mediated complement deposition on pneumococci. In order to correlate the results of cross-reactivity with protection, we evaluated the ability of the two most cross-reacting sera to promote the opsonophagocytosis of different pneumococcal strains by peritoneal phagocytes. Since it has been difficult to show killing using the classical OPA by anti-PspA antisera (unpublished data), we have optimized this assay in order to overcome the protective effect of the capsule. Using peritoneal cells Resminostat recovered from mice stimulated with a polyclonal T-cell activator, we were able to demonstrate the ability of anti-PspA antibodies to induce complement mediated phagocytosis of pneumococci of different serotypes.

The results demonstrate that both sera were able to induce complement-mediated phagocytosis leading to a minimum reduction of 30% on the number of pneumococci. This effect was observed for pneumococci of diverse capsular types, including serotypes 1, 3 and 6B, demonstrating the viability of this adapted opsonophagocytic assay for measuring the protective role of anti-PspA antibodies, which can overcome the inhibitory effects of different capsule types. Although these two sera were generated against PspAs of different clades, both were equally efficient against all family 1 strains. These results are in accordance with the complement deposition assay, in which both sera were able to increase complement deposition onto pneumococci containing PspA clades 1 and 2. This cross-reactive effect within strains bearing family 1 PspA has been previously reported using anti-PspA1 antibodies [21] and [22]. Moreno et al.

Moreover, antimicrobial susceptibility can inform guidelines for

Moreover, antimicrobial susceptibility can inform guidelines for selection of appropriate drugs for treatment of pneumococcal infections. This work was funded by Wyeth-Ayerst (Thailand) Ltd. and in GSK1349572 in vivo part by the Faculty of Medicine Siriraj Hospital, Mahidol University. We thank the following hospitals for supplying pneumococcal isolates: Bangkok Hospital, Bhummipol Hospital, Bumrungrad International Hospital, Chaophya Hospital, King Chulalongkorn Memorial Hospital, Mongkutwattana General Hospital, Phayathai Hospital, Queen Sirikit National Institute of Child Heath, Nakorn Pratom Hospital, Rajavithi Hospital,

Ramkhamhaeng Hospital, Somdejprapinklao Hospital and Taksin Hospital. We thank Dr. Michelle McConnell for her critical inputs and helps to this manuscript. “
“Streptococcus pneumoniae remains one of the most important

human pathogens in our era, together with malaria, TB and HIV [1]. The primary ecological reservoir of S. pneumoniae Apoptosis antagonist is the nasopharynx of young children who are colonized asymptomatically early in life [2]. When the balance between host and pathogen is disturbed, the nasopharynx can become a launching pad for pneumococcal disease. Colonizing pneumococci may spread to adjacent mucosal tissues to cause infections such as acute otitis media and pneumonia, or enter the bloodstream causing invasive infections such as sepsis and meningitis [3] and [4]. The first 2 years of life are the period of greatest risk for pneumococcal disease [5], and methods that could suppress nasopharyngeal colonization by disease-causing pneumococci are believed to represent means of preventing or decreasing the frequency of pneumococcal infections. The majority of pneumococci causing life-threatening disease in children in the USA, and to a certain extent also in Europe, express on their surface seven chemically different capsular types (vaccine types—VT), which are included

in the 7-valent pneumococcal conjugate vaccine (PCV7) [6]. Several surveillance and randomized controlled studies have shown that routine vaccination with PCV7 is efficacious about against VT pneumococcal invasive disease in children younger than 2 years old [6], [7], [8] and [9]. Concerning pneumococcal colonization, the foremost conclusion of several studies is that PCV7 reduces nasopharyngeal carriage of VT pneumococci but, in parallel, there is an increase in non-vaccine type (NVT) carriage, a phenomenon termed serotype replacement carriage [10], [11], [12] and [13]. Traditionally, the most common method used to study the pneumococcal colonizing flora has been the serotyping of a single isolate recovered from the nasopharynx of each individual carrier. However, studies have shown that most individuals carry simultaneously more than one pneumococcal isolate (co-colonization), which can differ in properties such as serotype and genotype [2] and [14].

5 Clinical education is a prerequisite for program accreditation;

5 Clinical education is a prerequisite for program accreditation;6 however, the rising student numbers is challenging the capacity of health service organisations to deliver this fundamental component of physiotherapy education.4 Assigning multiple students to one educator in physiotherapy clinical placements is one strategy being adopted to cope with this increase selleck screening library in demand, and the popularity

of the 2:1 or ‘paired’ model — where two students are supervised by one clinical educator — is growing. In theory, the paired model offers an immediate increase in capacity, compared to the 1:1 model traditionally used in physiotherapy placements. However, a search of four databases BGJ398 supplier (Medline, CINAHL, SCOPUS and ERIC) up to June 2011, using key search terms synonymous with peer-assisted learning and physiotherapy, yielded no randomised trials and little evidence of the actual effects of paired student models on student, educator or patient outcomes.7, 8, 9, 10 and 11 Physiotherapy clinical educators consider peer-assisted learning models to be feasible8, 9 and 12 and some prefer this to the 1:1 model.12 Those authors recommend implementation of the paired student model in physiotherapy and reference the need for clinical educators to be prepared to facilitate peer engagement. Despite the recommendation for the

paired model, no studies have provided a reproducible framework, set of activities or specific tools to assist educators and learners in applying the model. Topping and Ehly13 defined peer-assisted learning as ‘the acquisition of knowledge and skill through active helping and supporting among status equals or matched companions’. Implementation of paired student placements might vary for several reasons, such as student and clinical educator preparation, placement environment and the cohesion of the student-peer relationship.8, 9, 12, 14, 15 and 16 Peer interactions

may take place in a number of ways – from purely social support to formalised Bay 11-7085 peer-assisted learning tasks. There is little knowledge of how particular aspects of the peer interaction contribute to learning and how to maximise the impact on learning outcomes. Qualitative investigations into physiotherapy education models have reported that the company of another student on placement reduces student anxiety and aids learning.12, 15, 16 and 17 No study provided a description or evaluation of the amount or type of peer interaction occurring within the paired placements. A model of paired student clinical education that specifically aims to facilitate peer-assisted learning may present immediate benefits within the placement and help to develop more sustainable and productive learner behaviours.18 The ability to collaborate with peers is highly valued by workplaces19 and is particularly important in the provision of effective healthcare.

The location of antibody binding sites (epitopes) or escape from

The location of antibody binding sites (epitopes) or escape from binding can also be inferred from correlating the antibody cross-reactivity of viruses to their capsid sequence similarities [11]. Epitopes can also be predicted, in the absence of antibody recognition data, using different epitope

prediction programmes using viral crystal structure [12]. However, there are no reports for analysis of epitopes or vaccine strain selection studies using serotype A isolates originating from East Africa. Temsirolimus Most FMD outbreaks in East Africa have been caused by serotype O, followed by serotype A and SAT-2 [13], [14] and [15]. The serotype A viruses are present in all areas of the world where FMD has been reported and are diverse both antigenically and genetically. More than 32 subtypes [16] and 26 genotypes of serotype A FMDV have been reported [17]. Control of FMD mainly depends on the availability ABT-888 price of matching vaccines that can be selected based on three criteria: epidemiological information, phylogeny of the gene sequence for evolutionary

analysis and serological cross-reactivity of bovine post-vaccinal serum (bvs) with circulating viruses [18] and [19]. Mono-, bi- and quadri-valent vaccines are currently in use in East African countries for FMD control [20], [21] and [22]. These vaccines are mainly produced in vaccine production plants located in Ethiopia and Kenya using relatively historic viruses

and regular vaccine matching tests to select the best vaccine for use in the region are rarely carried out. Hence, the existing vaccines may not provide optimal protection against recently circulating FMD viruses. This study was, therefore, designed to characterise recently circulating FMD viruses in the region both antigenically and genetically and recommend matching vaccine strains to for use in FMD control program in East African countries. Fifty-six serotype A viruses from Africa submitted to the World Reference Laboratory for FMD (WRLFMD) at Pirbright were used in this study. These viruses were from five East African countries, Ethiopia (n = 8), Eritrea (n = 9), Sudan (n = 6), Kenya (n = 6), Tanzania (n = 7) and from three neighbouring countries: Democratic Republic of Congo (COD, n = 5), Egypt (n = 10) and Libya (n = 5). These samples are known to have been derived from cattle epithelial tissues except eight viruses from Egypt and one virus from Kenya where the host species is not known (Supplementary Table 1). All the samples were initially grown in primary bovine thyroid cells (BTY) with subsequent passage in either BHK-21 or IB-RS2 cells. The virus stocks were prepared by infecting cell monolayers and stored at −70 °C until use. Viruses are named according to a three letter code for the country of origin followed by the isolate number and the year of isolation, e.g. A-COD-02-2011.

The positive and negative effects of TNF must be taken into accou

The positive and negative effects of TNF must be taken into account when its production is induced by candidates for protective vaccines. Although in vitro assays cannot entirely be used as substitutes for in vivo methods, the effective and specific blockage of bacterial attachment to HEp-2 cells strongly indicates that the antibodies induced by the recombinant Smeg and BCG generated to express BfpA and/or intimin may be active in vivo. In a previous study, we demonstrated that an IgY antibody raised against recombinant BfpA identifies E. coli OSI-744 order that express

BfpA, blocks colonization of HeLa cells by EPEC-EAF(+) in vitro and inhibits the in vitro growth of EPEC-EAF(+) but not of EPEC-EAF(−) (the BfpA-cured counterpart bacteria) [24]. More recently, we also showed that EPEC-EAF(+)-expressing BfpA, but not EPEC-EAF(−), induced apoptosis in HeLa cells. This effect was blocked by prior neutralization of BfpA with an IgY anti-BFP antibody [25]. These data agree with previous observations indicating that induction of epithelial cell death by E. coli depends on the expression of bundle-forming pili by the bacterium

[26]. Therefore, BfpA is an important virulence factor expressed by EPEC and is significantly involved in bacterial cell adhesion and induction of host cell death, either by necrosis or apoptosis. Intimin is a 94–97 kDa outer membrane protein [4] that mediates intimate contact between the bacteria and the target cell selleck products upon interaction with its translocated intimin receptor (Tir) [27]. Recent observations indicate that Lactobacillus casei expressing intimin-β fragments and containing the immunodominant epitopes of Int280 induced both humoral and cellular immune responses in mice. The antibodies were able to bind to EPEC and inhibit no bacterial adhesion to the epithelial cell surface in vitro. C57BL/6 mice immunized with this recombinant

strain became partially protected against intestinal colonization by Citrobacter rodention, a mouse intestinal pathogen that also expresses intimin-β [28]. BfpA and intimin are therefore significant immunogens to be used in vaccines. We would like to thank the following individuals: Dr. Luciana C.C. Leite, Butantan Institute, São Paulo, Brazil, for her assistance and permission to use the Laboratory of Biotechnology IV; Dr. Brigitte Gicquel, Institute Pasteur, Paris, France, for providing the pMIP12 vector; Dr. Albert Schriefer, Fiocruz Institute, Salvador, Brazil, for providing the original enteropathogenic E. coli (EPEC)-EAF(+) and -EAF(−) strains; and Dr. Dunia Rodriguez for expert laboratory help and assistance in our results. “SBA-15 silica” was kindly provided by Osvaldo Augusto Sant́Anna, Butantan Institute, Brazil.


“En France, comme dans d’autres pays, la bronchopneumopath


“En France, comme dans d’autres pays, la bronchopneumopathie chronique obstructive (BPCO) fait l’objet d’un nombre croissant d’initiatives institutionnelles visant à en améliorer la prise en charge. À titre d’exemple, les recommandations de la Société de pneumologie de langue française (SPLF) ont été mises à jour en 2009 [1] et vont bientôt

faire l’objet de nouvelles prises de position de la Société, notamment sur la détection précoce, les traitements au long cours, les exacerbations ; de son côté, la Haute Autorité de santé vient de publier des fiches « Points clés et solutions » sur la réhabilitation et les exacerbations, après avoir proposé un parcours de soins en 2012, tout récemment mis à jour [2], [3] and [4] ; elle met aussi à disposition depuis peu un questionnaire de click here screening [5] ; enfin, la CNAM est sur le point de finaliser son Programme de retour à domicile (PRADO), destiné aux patients hospitalisés pour exacerbations de BPCO. Comment se justifie cette

dynamique, qui pourrait paraître étonnante compte-tenu de l’intérêt limité dont la BPCO a longtemps fait l’objet ? La principale raison est la prise de conscience de son impact épidémiologique, Selleck Cobimetinib clinique et économique sur la population. Les dernières données épidémiologiques collectées dans notre pays remontent à une dizaine d’années. Elles faisaient état

d’une prévalence de 7,5 % de la population adulte de plus de 40 ans [6]. Ce chiffre se situe dans la fourchette des autres pays industrialisés, notamment en Europe occidentale [7]. La BPCO est impliquée dans près de 17 000 décès chaque année en France [8]. À l’échelle mondiale, elle se situait en 2010 au 3e rang des causes de mortalité, alors qu’elle était au 4e rang 20 ans auparavant [9]. Plus peut-être que la mortalité, la perte d’années Tryptophan synthase de vie en bonne santé (disability-adjusted life years ou DALYs) est un outil utile pour traduire l’impact de la BPCO sur la population : elle figure actuellement au 9e rang des causes de perte de DALYs [10]. Il est difficile de prédire précisément comment l’impact de la BPCO évoluera dans le monde au cours des années à venir : en effet, cette évolution dépendra étroitement de celles des caractéristiques démographiques de la population (vieillissement) et des facteurs de risque auxquels elle est exposée (tabagisme bien sûr mais aussi, dans certains pays, pollution domestique par les fumées de combustion de biomasse, facteurs professionnels…). Quoiqu’il en soit, en l’état actuel, rien ne laisse présager d’une atténuation significative du fardeau qu’elle représente dans un futur proche.

The age JAK inhibit

The age MK-1775 ic50 at which the children was administered the first dose might play an important role in determining seroconversion rates. In this study and

the study with Rotarix™ in Vietnam the average age of first dose administration was 8 weeks. In comparison, the average age for the first dose in the US is 9–11 weeks and 11–17 weeks in Singapore [23] and [24]. In Finland and Italy, vaccine has been used at even older age (3 months) [17]. It is generally believed that vaccination at older age induces better immune responses possibly due to a more mature immune system of the child and declining maternal antibody titers in breast milk or from placental transmission. This notion is also supported by a study of Rotarix™ in the Philippines in which children were 5.5 weeks of age at the first dose and the seroconversion rate was lower compared to that in Vietnamese children. As vaccines, Rotavin-M1 is very similar to Rotarix™ in that both are derived from common G1P [8] strains attenuated

by serial passage and prepared in Vero cells. Like Rotarix™, the majority of children buy INCB024360 shed after the 1st dose of Rotavin-M1, whereas this proportion declined considerably after 2nd dose, similar to other studies [24]. Shedding of Rotarix™ in different studies worldwide is 35–80%, corresponding to the shedding rate of this vaccine found in our study [27]. One interesting difference between the behavior of the two vaccines is the increased shedding observed for Rotarix™ (65%) compared to Rotavin-M1 (44–48%) after the 1st dose although this was not accompanied by an increased immune response. Another difference between the two vaccines is that Rotavin-M1 vaccine, at the dosage of 106.0 FFU or 106.3 FFU caused delayed in virus shedding compared to Rotarix™ at doses of 106 CCID50 (corresponding to 105.5 FFU/dose). These differences between the two vaccines suggest that further research on vaccine formulation, improving the yield of virus so that higher titer candidates could be available which helps advance the development

of this locally manufactured vaccine through efficacy trials. In this study, the Rotavin-M1 was administered separately from Suplatast tosilate the oral polio virus vaccine (OPV) (10–20 days from the EPI schedule), thus the study was not designed to investigate the effect of other vaccines, in particular OPV on Rotavin-M1. While the coadministration of Rotarix or RotaTeq with OPV seemed to reduce seroconversion rates, antibody titers and vaccine take compared to rotavirus vaccines without OPV, the reductions were not statistically significant [28] and [29]. Thus further study should be designed to investigate whether there is any interference to Rotavin immunogenicity due to concomitant usage of OPV and Rotavin-M1. This study has several limitations which will need to be addressed as development of this vaccine progresses.

The collected samples were stored at 4 °C Starch degrading micro

The collected samples were stored at 4 °C. Starch degrading microbes were isolated using Strach Agar Medium (SAM). The isolates showing maximum clear halo zone were sub-cultured.7 Selective isolates with maximum starch degrading activities were identified up to species level.8 and 9 The most potent isolates were finally chosen for further studies. The inoculum for further enzyme modulation and other studies was prepared using Luria

Broth (LB) medium. The fresh overnight culture was used as an inoculum for the production of amylase.10 The inoculated medium was incubated at 37 °C for 48 h by shake flask fermentation method at 200 rpm. The culture broth was then centrifuge at 8000 × g 10 min at 4 °C. The free cell supernatant Pexidartinib supplier was used as an extracellular crude enzyme. 11 Total protein concentrations were determined by Bradford’s method using Bovine Serum Albumin (BSA) as the protein standard.12 α-Amylase activity was determined by measuring the formation of reducing sugars released during starch hydrolysis. The amount of liberated reducing sugar was determined by Dinitrosalicylic acid (DNS) method. Glucose was used to construct selleck kinase inhibitor the standard curve.4 Five percent bacterial inoculum was added aseptically to 500 ml of sterile growth

medium and incubated at 37 °C at 150 rpm. Twenty ml of culture was taken periodically for 48 h at every 6 h intervals. The amylase activity was determined in the culture filtrate. The effect of pH on amylase activity was determined at different pH (6.5, 7, 7.5, 8, 8.5 and 9) and the effect of temperature on enzyme activity was determined using different temperature (26 °C, 29 °C, 32 °C, 35 °C, 38 °C and 41 °C).11

Different carbon and nitrogen sources (both at concentration of 10 g/L) were used in minimal medium, pH 7 and incubated at 32 °C for 24 h. Similarly different amino acids like glycine, alanine, aspartic acid and cysteine were used in the medium for optimization.13 The culture filtrates were assayed for total protein content before and amylase activity. The culture filtrate was precipitated using 80% w/v Ammonium sulfate precipitation method.14 Then the precipitate was separated by centrifugation at around 6700 × g for 10 min. The pretreatment of the dialysis membrane was done Ashwini et al, 2011. Genomic DNA was extracted using phenol–chloroform extraction method. The PCR parameters for the amplification of 16S ribosomal DNA were optimized. 50 μl of PCR master mix contained universal primer set 27 F- (5′-AG AGT TTG ATC MTG GCT CAG-3′)/1492 R- (5′-G GYT ACC TTG TTA CGA CTT-3′), 10 mM dNTPS, 10× PCR Buffer, 1 U Taq DNA polymerase, 2 mM Mg+ and (100–200 ng) template DNA. PCR steps included initial denaturation at 95 °C for 5 min, 35 cycles of denaturation at 95 °C for 1 min, annealing at 56 °C for 2 min, elongation at 72 °C for 1 min and final extension at 72 °C for 10 min. Approximately 1.5 kb amplicons were generated.

In contrast, the number of eosinophils and neutrophils was dramat

In contrast, the number of eosinophils and neutrophils was dramatically reduced in infant PCV7 immunized group mice compared with the OVA group (2.15 ± 0.29 × 104 cells/mlvs 14.75 ± 1.77 × 104 cells/ml, 20.13 ± 3.7 × 104 LY2835219 datasheet cells/ml vs 63.39 ± 9.28 × 104 cells/ml, respectively, P < 0.001) ( Fig. These data demonstrated that infant PCV7 immunization can suppress OVA-induced airway eosinophilic and neutrophilic inflammation in young adulthood BALB/c mice asthma model. In control group mice, there was little tissue inflammation. Pulmonary alveolar, peribronchiolar and perivascular inflammatory infiltrate of inflammatory cells in OVA group mice was denser than that in control group mice. In infant PCV7 immunized group mice, pulmonary alveolar,peribronchiolar and perivascular cellular infiltration significantly lower than DNA Synthesis inhibitor that in OVA group (Fig. 2). As shown in Fig. 3, the inflammation scores of pulmonary alveolitis, pulmonary perivasculitis and pulmonary peribronchiolitis in infant PCV7 immunized mice were significantly lower than that in OVA group (3.00 ± 0.26 vs 1.17 ± 0.17, P < 0.001, 3.67 ± 0.21 vs 2.17 ± 0.31, P < 0.001, 3.33 ± 0.21 vs 1.83 ± 0.31, respectively, P < 0.01). Thus, infant PCV7 immunization suppressed airway inflammation in young adulthood asthmatic mice. AHR was evaluated by the calculation

of Penh values (enhanced pauses) 24 h ADAMTS5 after

the final challenge. OVA sensitization and challenge resulted in increased AHR. The Penh value for OVA group was significantly higher than that in the control group at methacholine concentrations 6.25 mg/ml (P < 0.01), 12.5 mg/ml (P < 0.001), 25 mg/ml (P < 0.001), and 50.0 mg/ml (P < 0.001). However, PCV7 + OVA group mice had significantly lower Penh values compared to values obtained from mice in the OVA group from 25 to 50.0 mg/ml (P < 0.001, respectively) ( Fig. 4). To investigate the effects of infant PCV7 immunization on CD4+T cell subsets production during AAD, CD4+T cell cytokines in BALF were analyzed. As expected, OVA sensitized and challenged mice exhibited dramatically increased IL-13, IL-17A production (87.14 ± 7.12 pg/ml vs 40.62 ± 3.59 pg/ml, P < 0.001, 247.70 ± 35.81 pg/ml vs 158.90 ± 16.40 pg/ml, P < 0.05) and significantly decreased IFN-γ, IL-10 production (18.07 ± 1.13 pg/ml vs 33.16 ± 1.87 pg/ml, P < 0.001, 122.30 ± 18.53 pg/ml vs 223.10 ± 35.92 pg/ml, P < 0.05) compared with the control group mice. However, the production of IL-13, IL-17A in the infant PCV7 immunized group mice were significantly lower than that in the OVA group mice(31.93 ± 4.36 pg/ml vs 87.14 ± 7.12 pg/ml, P < 0.001, 120.90 ± 9.56 pg/ml vs 247.70 ± 35.81 pg/ml, P < 0.01). IFN-γ, IL-10 was significantly higher in the infant PCV7 immunized group mice than that in the OVA group mice. (27.89 ± 1.83 pg/ml vs 18.07 ± 1.13 pg/ml, P < 0.001, 228.50 ± 27.47 pg/ml vs 122.30 ± 18.53 pg/ml, P < 0.05).