An increasing number of studies have implicated Stat protein acti

An increasing number of studies have implicated Stat protein activation, particularly Stat3, in transformation and tumor progression[4]. Activated Stat3 has been shown to promote cell proliferation, metastasis, and angiogenesis, as well as protect tumor cells from apoptosis by regulating associated genes, such as Bcl-xL, Mcl-1, Bcl-2, Fas, cyclin D1, survivin, c-Myc, VEGF, MMP-2, and MMP-9[5–7]. Recently, accumulating evidence has

indicated that abnormalities in the Stat3 pathway are involved in the oncogenesis of several cancers. For example, Scholz [8] and coworkers reported that activation of the Stat3 signaling pathway plays an selleck kinase inhibitor important role in the progression of pancreatic cancer, and constitutive activation of Stat3 correlates with cell proliferation in stomach adenocarcinoma[9], prostate cancer[10], breast carcinoma[11], and non-small cell lung cancer[12] and also inhibits apoptosis[13, selleck compound 14]. Conversely, inhibition of the Stat pathway suppresses cancer cell growth and invasion and induces this website apoptosis in various cancers[8, 11, 15, 16]. Jak is responsible for the tyrosine phosphorylation of Stat3 in response to extracellular signals and oncogenes. The newly described Jak inhibitor AG490 blocks the constitutive activation of Stat3[17]. AG490 was used to selectively

block the Jak/Stat3 signaling pathway and inhibit activation of Stat3 in colorectal cancer cells[18]. The pleiotropic cytokine interleukin-6 (IL-6) is a major activator of Stat3; IL-6 stimulates the formation of tyrosine-phosphorylated Stat3 (p-Stat3) in cancer cells[19, 20]. Through the Jak/Stat3 signaling pathway, IL-6 plays an important role in cell proliferation, apoptosis, metastasis, and other biological activities [21]. In the present study, we used AG490 to deplete Stat3 protein in the human pancreatic cancer cell line SW1990 and IL-6 to activate Stat3 protein in the human pancreatic cancer cell line Capan-2; we then investigated the changes in cell proliferation and invasion.

We also examined the expression Farnesyltransferase of Stat3 and its active phosphorylated form in human pancreatic cancer cell lines. In addition, we evaluated the changes in matrix metalloproteinase 2 (MMP-2) and vascular endothelial growth factor (VEGF) mRNA and protein expression. Our aim was to demonstrate that the Stat3 signaling pathway may be critical for the invasive behavior of pancreatic tumors. Inhibition of this pathway may offer a novel strategy for pancreatic cancer treatment. Methods Cells and reagents The human pancreatic cancer cell lines SW1990 and Capan-2 were obtained from the American Type Culture Collection. Tumor cells were maintained in Dulbecco’s modified Eagle’s medium (DMEM), supplemented with 10% fetal calf serum, 100 units/ml penicillin and 100 μg/mL streptomycin, in a humidified incubator with an atmosphere of 5% CO2 and 95% air at 37°C.

Results are the average of the motility zones of sixteen Petri di

Results are the average of the motility zones of sixteen Petri dishes per strain. Data was statistically analyzed using one-way ANOVA (p < 0.05). Acknowledgements We thank Rodrigo Vena for assistance with the confocal microscopy AR-13324 facility, Microquin for the culture media, Catalina Anderson (INTA Concordia, Argentina), Gastón Alanis and Rubén Díaz Vélez (Proyecto El Alambrado) for the citrus plants, Sebastián Graziati and Diego Aguirre for plant technical

assistance and the Proteomics eFT-508 cost laboratory from the Biosciences core laboratory, King Abdullah University of Science and Technology, for providing the facility and equipment for gel electrophoresis and mass spectrometry analyses. This work was supported by grants from the Argentine Federal Government: ANPCyT (PICT2010-1507 to NG and PICT2010-0300 to JO) and CONICET (PIP2010-2012 to JO and NG), the Fundación Josefina Prats to CGG and FAF. JO and NG are staff members and TZ, GGS, CGG and FAF are fellows of the Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET, Argentina). Electronic supplementary material Additional file 1: Figure

S1: Characterization of the hrpB − complemented strain on HR and pathogenicity. (A) Schematic organization of the hrp cluster of X. citri that was constructed based on the X. citri subsp. citri strain 306 genome sequence [1]. Boxes correspond to ORFs, arrows this website indicate orientation of the hrp operons. The hrp, hpa and hrc genes are indicated. Dotted boxes indicated the genomic regions replaced by mutagenesis. Bellow of the scheme, the black box represents the genomic fragment cloned in pBBR1MCS-5 to complement the hrpB − mutant strain. (B) Bacterial suspensions of X. citri,

the hrpB − mutant and the hrpB − c strains were inoculated at 108 CFU/ml into the intercellular spaces of fully expanded tomato, cotton and pepper leaves. A representative photograph of a leaf is shown after 1 day of inoculation. (C) As in B, bacterial suspensions at 107 CFU/ml were inoculated into the intercellular spaces of fully expanded citrus leaves. A representative photograph of a leaf is shown after 8 days of inoculation. (D) RT-qPCR to determine Buspirone HCl CsLOB1 expression levels in leaves after 48 hours of infection with X. citri, the hrpB − mutant and hrpB − c strain. Bars indicate the expression levels relative to buffer infiltrations. Values are the means of four biological replicates with three technical replicates each. (PDF 137 KB) Additional file 2: Figure S2: Swimming and swarming assays. Representative photographs of Petri dishes with X. citri, the hrp mutants and the hrpB − c strain after 2 days of inoculation. Scale bars: 10 mm. (PDF 819 KB) Additional file 3: Table S1: Oligonucleotides used in RT-qPCR assays. (PDF 7 KB) References 1.

During surgical intervention, the following signs are of greatest

During surgical intervention, the following signs are of greatest importance for the NF diagnosis: grayish necrotic deep fascia, a lack of resistance of normally adherent

muscular fascia to blunt finger dissection (“”Finger test”"), lack of bleeding from the fascia and the presence of dish-water pus [6, 36]. Based on our surgical practice we also recommend an early and very aggressive debridement of all involved Selleckchem Bafilomycin A1 tissue that can be easily elevated off of the fascia with gentle find more pressure or finger spreading. The surgical intervention in which we removed all infected tissue in a single operation, rapidly improved the clinical course of the infection. All deep fascia and muscle should be inspected for potential involvement with streptococcal myositis or clostridium infection. We believe that the mass and the extension of soft tissue that must be initially excised GS-7977 mw depend on the body region in which the infection appeared. Nevertheless, the extent of debridement should not be needlessly limited because the novel plastic surgical techniques can cover every wound defect

size. Special attention should be paid to the upper and lower extremities, AW with intra-abdominal infection such as secondary peritonitis, and on the CW with persisting sternum infection and mediastinitis [8, 11, 26]. The extent of debridement is very important on the extremities. In cases with compromised viability and compartment syndrome additional fasciotomies of all fascio-cutaneous spaces should be performed [36]. A suspected case of clostridial myonecrosis requires early

surgical exploration and extensive debridement of all involved muscle structures [36]. A tourniquet should be used during the limb surgery to reduce blood loss and offer better examination [36]. The incision proceeds proximally from the infected area in a longitudinal manner, until healthy fascia adherent to the overlying subcutaneous tissue and underlying muscle is encountered. In that moment, the tourniquet should be deflated, the Montelukast Sodium wound checked to confirm tissue viability, and then meticulous hemostatis should be performed [36]. Still, controversy exists regarding how much tissue should be initially excised because the skin may often appear normal. Andreasen et al. [22] investigated the normal-appearing tissue microscopically, and found that soft tissue had extensive vascular micro-thromboses as well as vasculitis. Their finding indicated that this tissue, which has a normal external appearance, has a high risk of full thickness necrosis [22]. Poor prognostic indicators for limb amputation very often include old age, peripheral vascular disease and diabetes [36, 44, 45]. Amputation must be obligatory considered if the extent of infection includes a large joint and most muscle groups or if the infection is rapidly spreading towards the torso [36, 46]. Postoperative wound management consists of serial dressing changes, until the wound becomes free of recurrent or progressive skin and soft tissue necrosis.

pylori and L acidophilus determined by the percentage of LDH lea

acidophilus determined by the percentage of LDH leakage (in triplicate) and non-stained trypan blue (single) Bacteria and MOI Cytotoxicitya (% LDH) Viable cell count (× 106) Cell only for 4 and 8 hours 18.0, 18.0

1.36 H. pylori for 4 hours     MOI 100 18.1 selleck kinase inhibitor 1.00 Lactobacillus for 8 hours     MOI 1 18.4 1.00 MOI 10 18.0 1.11 MOI 100 18.7 1.24 MOI 1000 24.2 0.77 aAll cytotoxicity data were presented with mean value of three tests H. pylori stimulated IL-8 and TNF-α but not TGF-β1 production in vitro In MKN45 cells incubated with H. pylori (MOI 100) at various time periods, the IL-8 level increased from the 4th to the 8th hour after co-incubation, as determined by ELISA (MCC950 in vivo Figure 1A). For TNF-α, the post-incubation level rose after the 4th hour and maintained a plateau until the 8th hour (Figure 1B). However, the TGF-β1 level did not increase after H. pylori incubation for 4 hours (data not shown). Figure 1 (A) IL-8 and (B) TNF-α concentrations in the supernatant of MKN45 cells culture after variable duration of H. pylori and L. acidophilus

infection (MOI = 100). Data were expressed as means ± standard deviation (SD) (in triplicate). HDAC inhibitor In contrast, L. acidophilus did not induce IL-8, TNF-α, and TGF-β1 expressions of MKN45 at least within the 8-hour co-incubation period. Pre-treatment of L. acidophilus attenuated H. pylori-induced IL-8 Because the IL-8 level of MKN45 cells could be induced by H. pylori challenge for 4 hours, the time- and dose-dependent effects of probiotics in reducing pro-inflammatory cytokines and TGF-β1 on the 4th hour were

studied. The IL-8 and TGF-β1 concentrations were PD184352 (CI-1040) shown for MKN cells challenged by H. pylori and with variable doses of L. acidophilus pretreatment for 8 hours (Figure 2). Compared to the control group, L. acidophilus pre-treatment with higher bacterial colony count (MOI 100) reduced H. pylori-induced IL-8 expressions in MKN45 cells (P < 0.05). The TGF-β1 level did not change (P > 0.05). Figure 2 The concentrations of IL-8 (blank column) and TGF-β1 (black column) in the supernatant of MKN45 cells pre-treated with different MOI (0: control; 1: 1 × 10 6 c.f.u.; 10: 1 × 10 7 c.f.u.; 100: 1 × 10 8 c.f.u.) of L. acidophilus. The cells were washed thrice with PBS to remove the L. acidophilus and then infected with H. pylori (MOI = 100) for 4 hours. Data are expressed as means ± SD (in triplicate). Statistical analysis was performed in each measurement with comparisons to the controls (cells treated H. pylori only; IL-8 2034 ± 865 pg/ml and TGF-β1 587.2 ± 39.8 pg/ml) (*P < 0.05). L. acidophilus reduced H. pylori-induced NF-κB by increasing IκBα The study determined that MKN45 cells (MOI 100) incubated with H. pylori led to a peak increase of nuclear NF-κB production within one hour. Thus, nuclear NF-κB levels of MKN45 cells co-incubated with H. pylori, after prior pre-treatments by various MOIs (1-100) of L.

Genomics 1998, 54: 145–148 CrossRefPubMed 34 Yatsuoka T, Sunamur

Genomics 1998, 54: 145–148.CrossRefPubMed 34. Yatsuoka T, Sunamura M, Furukawa T, Fukushige S, Yokoyama T, Inoue H, Shibuya K, C188-9 nmr Takeda K, Matsuno S, Horii A: Association of poor prognosis with loss of 12q, 17p, and 18q, and concordant loss of 6q/17p and 12q/18q in human pancreatic ductal adenocarcinoma. Am J Gastroenterol 2000, 95: 2080–2085.CrossRefPubMed 35. Harada T, Okita K, Shiraishi K, Kusano N, Furuya T, Oga A, Kawauchi S, Kondoh S, Sasaki K: Detection of genetic alterations in pancreatic cancers by comparative genomic hybridization coupled with tissue microdissection and degenerate oligonucleotide primed polymerase chain reaction.

Oncology 2002, 62: 251–258.CrossRefPubMed Competing interests The authors declare that they have no competing 17DMAG interests. Authors’ contributions KN conceived of the study and performed immunohistochemical studies and measurements of serum metastin. RD conceived of the study, and participated Pitavastatin manufacturer in its design and coordination and helped to draft the manuscript. FK and TI conceived of the study and performed immunohistochemical studies. AK and MK conceived of the study and performed measurements of serum meatstin. TM, YK, KT, SO and NF conceived of the study and performed

experiments on pancreatic cancer tissues. SU conceived of the study, and participated in its design.”
“Background The A-type lamins (predominantly lamins A and C, two alternatively spliced products of the LMNA gene), along with B-type lamins (members of the intermediate filament

proteins), are the most principal components of the nuclear lamina-a proteinaceous meshwork of 10 nm diameter filaments lying at the interface between chromatin and the inner nuclear membrane. The nuclear lamina is thought to be a principal determinant of nuclear architecture. Downregulation or specific mutations in lamins cause abnormal nuclear shape, changes in heterochromatin localization at the nuclear periphery, global chromatin reorganization and possibly specific changes in the positions of genes NADPH-cytochrome-c2 reductase [1]. It is possible that changes in the nuclear lamina and in nuclear shape affect chromatin organization and gene positioning, respectively, and in this way alter patterns of gene expression, contributing to transformation [2]. Lamin A/C is important in DNA replication, chromatin anchoring, spatial orientation of nuclear pore complexes, RNA Pol II-dependent transcription and nuclear stabilization [3]. With regard to the multiple functions of A-type lamins, mutations in the human LMNA gene cause a wide range of heritable diseases collectively termed laminopathies [4]. Importantly, numerous studies suggest that reduced or absent lamin A/C expression is a common feature of a variety of different cancers, including small cell lung cancer (SCLC), skin basal cell and squamous cell carcinoma, testicular germ cell tumour, prostatic carcinoma, leukemia and lymphomas.

The above data showed that

the expression of the two gene

The above data showed that

the expression of the two genes played an important role in the occurrence and development of the breast carcinoma; and the changes of BCL-2 and BAD occured in the early stage of the breast carcinoma. This study showed that the expression of BCL-2 and the expression of ER and PR were highly correlated. In the ER and PR-positive groups, the expression of BCL-2 was significantly higher than that of its negative group;But the expression of BAD showed no significant correlation with the expression of ER and PR. Compare with the BCL-2 negative group, the expression Of ER and PR were higher in the BCL-2 positive group. When the expression of BCL-2 and BAD were positive, at the same time the expression of ER and PR were especially high. Milella [7]. also confirmed that the expression of BCL-2 was #C646 randurls[1|1|,|CHEM1|]# regulated by estrogen. The expression of BCL-2 most confined to the ER-positive breast cancer cells, ER-positive was a necessary condition in endocrine therapy; the patient with BCL-2 high expression having a good prognosis, maybe more sensitivity to endocrine therapy. The expression of BCL-2 and BAD can be used as prognosis factors of breast cancer. Detecting the expression of the BCL-2 protein expression level, in particular the combined detection

AZD4547 of the expression of BCL-2 and BAD as well as ER and PR were helpful in the prognosis of breast carcinoma. Chemotherapy is an important treatment means of breast cancer. When we choose chemotherapeutic agents in clinical there still have certain blindness. By using the same chemotherapy, the curative effect of different individuals have large difference. If we did not know the sensitivity

of chemotherapeutic agents and utilized them blindly, there would be a lot of side effects. To avoid the side effects we needed to understand the sensitivity of chemotherapeutic agents before the chemotherapy start, and let the treatment individualization. Therefore, before chemotherapy the drug sensitivity, to forecast it becomes necessary, especially. Most chemotherapeutic agents killed tumor cells through inducing apoptosis, thus to investigate the regulatory factor in the procession of apoptosis will provide Urocanase us a insight to know mechanism of the drug resistance. BCL-2 and the members of this family plays an important role in regulating the process of cell apoptosis. BCL-2 is the anti-apoptotic gene, its mechanism is not yet clear, and it may affect Ca2 + into cells, thereby regulating cell signal transduction, disturbing the adversed function of free radical and so on [8]. The expression product of BAD can formed heterodimer with the expression product of the anti-apoptotic members of BCL-2 gene family, thereby reversed the function of them.

Their compositions in the SSBs in question are less than in the E

Their compositions in the SSBs in question are less than in the EcoSSB, at 61.0%. Moreover, the FpsSSB and PinSSB have a lower content of these residues, at 54%, than the TteSSB3, at 56%. The composition of the small and

tiny PF-6463922 residues in the PprSSB, at 50%, and the PtoSSB, at 52%, is even less than in the TmaSSB, at 53%. Aromatic amino acid residues are known to play an important role in stabilizing the three-dimensional structure of proteins. Psychrophilic proteins usually display a decrease in these amino acids. The psychrophilic SSBs deviate from this rule; all of proteins investigated MK-4827 in vivo show a higher content of these residues than the EcoSSB, at 6.6%. The FpsSSB has the same number of aromatic amino acids in its sequence as the TteSSB3, namely 9.3%. It was also observed that, in psychrophilic proteins, the number of hydrophobic

amino acids is lower than for their mesophilic counterparts. The content of hydrophobic amino acid residues in the DpsSSB, CB-5083 in vivo FpsSSB, ParSSB, PcrSSB, PinSSB, PprSSB, and PtoSSB is 44.2%, 39.9%, 46.5%, 44.2%, 42.0%, 46.0% and 41.7%, respectively. The number of these residues in the psychrophilic SSB proteins is less than in the EcoSSB, at 52.7%. Moreover, the aromatic residue content in the ParSSB and PprSSB is close to that of the TmaSSB, at 46.9%. Analysis of the amino acid sequence of the DpsSSB, FpsSSB, PinSSB and PtoSSB shows the presence of cystein residues to a number of 1, 2, 1, and 3, respectively. To date, these amino acid residues have not been found in any known SSBs.

A residue such as proline or cystein has a significant impact on the stability and rigidity of the conformational structure of proteins. The presence of cystein residues in psychrophilic SSBs may affect their stability, particularly if disulphide bridges are formed. Single strand DNA binding proteins have the property of causing the destabilization of duplex DNA and the same is true of the psychrophilic SSBs under study. The greatest decrease in dsDNA melting temperature was observed in the presence of the PtoSSB, at 17°C, which was a more substantial change than in the presence of the EcoSSB, TaqSSB or TthSSB, at 13°C in each case [40–42]. Studies of other SSBs have Thalidomide often shown that the size of the binding site depends on the salt concentration. At least two distinctly different DNA-binding modes have been described for the EcoSSB, for example [3]. In high salt concentrations, 65 nucleotides bind per EcoSSB tetramer, with a fluorescence quench of almost 90% whereas, in low salt concentrations, 35 nucleotides are sufficient to saturate the protein and quench its fluorescence by only 53%. Our current study has demonstrated that the binding site size of the DpsSSB, ParSSB, PcrSSB, PinSSB, PprSSB and PtoSSB has a constant value of approximately 30–32 nucleotides per tetramer, with one, salt-independent, DNA-binding mode.

reinhardtii cells, PAM fluorometry, 77-K fluorescence emission, a

reinhardtii cells, PAM fluorometry, 77-K fluorescence emission, and chlorophyll fluorescence induction experiments (Wykoff et al. 1998), as well as spectrophotometric measurements of absorbance differences to determine the concentrations of functional PSII and PSI reaction centers

or cytochrome f in isolated thylakoid membranes (Melis et al. 2000) (see below). Other methods were utilized in order to analyze the H2 metabolism. The three indicators for GANT61 in vitro the latter are usually in vitro hydrogenase activity assays as described above, in vivo assays (see below), and the analysis of the gas phase of the cells by GC. However, for all these experiments, the samples are usually taken from a culture vessel to be analyzed in different devices. This always perturbs the

equilibrium of the system, since a volume is extracted from the incubation vessel, and the click here sample itself will be exposed to air to a certain extent. Therefore, optimal experimental conditions combine the recordings of several relevant data in one sample, preferably in the culture vessel or the photobioreactor itself. Such systems, measuring pH, dissolved O2, redox potential, and chlorophyll fluorescence simultaneously in one photobioreactor have been described (e.g., GM6001 manufacturer Kosourov et al. 2002; Antal et al. 2003), and they allow the direct relation of photosynthetic parameters such as PSII chlorophyll

fluorescence with other indicators such as dissolved O2 concentration and redox potential. Using such a photobioreactor setup, Antal et al. (2003) could demonstrate a clear relationship between a rapid drop of PSII efficiency and the onset of anaerobiosis, and could further find evidence that the hydrogenase enzyme provided a sink for electrons in the absence of the usual electron-consuming pathways such as CO2 fixation. A very convenient system to study the exchange of gases in C. reinhardtii Adenosine triphosphate cell suspensions is a so-called Membrane Inlet Mass Spectrometer (MIMS). The setup is very useful to study the production or exchange of gases in liquid samples in general, e.g., in aqueous PSII solutions (Messinger et al. 1995; Shevela et al. 2008; Konermann et al. 2008), and it is described in detail in the article by Beckman et al. (On-line Mass spectrometry: Membrane Inlet sampling) in this issue. A MIMS has been established, for instance, in a research group at CEA Cadarache, France (Laurent Cournac, Gilles Peltier, Départment d’Ecophysiologie Vegétale et de Microbiologie, CEA Cadarache, France) (Dimon et al. 1988; Lindberg et al. 2004). Here, a measuring chamber of the Hansatech DW2/2 type (Hansatech, Norfolk, England, www.​hansatech-instruments.​com/​index.

As processing plants receive milk from the same dairies over time

As processing plants receive milk from the same dairies over time, it is likely that the same herds and even the same animals were sampled multiple times. Major temporal changes in prevalence and genotypes should

be detectable. Indeed, minor genotypes were detected among the goat milk samples, indicating ephemeral emergence of different types. Conversely, subtle changes may be masked by the milk pooling process and the ability of a single infected animal to contaminate large quantities of milk. Indeed, other studies suggest that there is evidence of seasonality: In cows, shedding in milk is not associated with parturition [39] although seroprevalence is highest in the Autumn [40]. In goats, C. burnetii are highly ICG-001 abundant

(up to 109 organisms/g of placental tissue) Tipifarnib in birth tissues [41] and more likely to be shed after parturition [42]. Human infections are therefore likely to be more common during livestock birthing seasons [43], suggesting that infection variation among goat herds might also be seasonally linked. Seasonality is often associated with a boom and bust cycle of transmission, and the lack of strong seasonal patterns may increase disease persistence. As pathogens are dispersed across the landscape, elapsed time allows for cellular replication and opportunities for genetic mutations to Fer-1 solubility dmso accumulate, providing genetic signatures to identify the patterns and speed of dissemination. The presence of the same genotypes among samples from across the country and the world is indicative of rapid dispersal of particular gentoypes and subsequent ecological establishment across these regions. While a paucity of historical samples and sampling efforts prevents us from

estimating when these STs became dominant, no ST20 isolates were collected in the U.S. before 2007 [20]. Interestingly, the only U.S. C. burnetii samples isolated from milk with a known date were obtained from cows in California (1947) and Ohio (1958) [20]. Both samples Interleukin-3 receptor are ST16/26, showing that the dominant genotype among cows may have recently changed. Higher resolution genotyping will be important for discerning dissemination patterns and mechanisms of these C. burnetii genotypes as dispersal may be due to long distance aerosol spread, trade, or other anthropogenic means. For example, sexual transmission through semen [44] from the small stock of infected breeding bulls used to breed Holstein cows throughout the world could result in shared genotypes. However, additional resolution among ST20 and ST8 samples has been shown with MLVA [27] and demonstrates that dissemination speed and patterns may have allowed for the accumulation of genetic differences and thus discerning patterns, mechanisms and barriers to dispersal may be possible.

Microbiol 2010, 156(Pt 2):555–560 CrossRef 10 Calix JJ, Nahm MH:

Microbiol 2010, 156(Pt 2):555–560.CrossRef 10. Calix JJ, Nahm MH: A new pneumococcal serotype, 11E, has a variably inactivated wcjE gene. J Infect Dis 2010, 202(1):29–38.PubMedCentralBIX 1294 PubMedCrossRef 11. Calix JJ, Porambo RJ, Brady AM, Larson TR, Yother J, Abeygunwardana C, Nahm MH: Biochemical, genetic, and serological characterization of two capsule subtypes among Streptococcus pneumoniae Serotype 20 strains: discovery of a new pneumococcal serotype. J Biol Chem

2012, 287(33):27885–27894.PubMedCentralPubMedCrossRef 12. Kolkman MA, van der Zeijst BA, Nuijten PJ: Diversity of capsular polysaccharide synthesis gene clusters in Streptococcus pneumoniae . J Biochem 1998, 123(5):937–945.PubMedCrossRef 13. Garcia E, Llull D, Munoz R, Mollerach M, Lopez R: Current trends in capsular polysaccharide biosynthesis of Streptococcus pneumoniae . Res Microbiol 2000, 151(6):429–435.PubMedCrossRef Smad inhibitor 14. Morona JK, Paton JC, Miller DC, Morona R: Tyrosine phosphorylation of CpsD negatively regulates capsular polysaccharide PF477736 biosynthesis in Streptococcus pneumoniae . Mol Microbiol 2000, 35(6):1431–1442.PubMedCrossRef 15. Morona JK, Miller DC, Morona R, Paton JC: The effect that mutations in the conserved capsular polysaccharide

biosynthesis genes cpsA , cpsB , and cpsD have on virulence of Streptococcus pneumoniae . J Infect Dis 2004, 189(10):1905–1913.PubMedCrossRef 16. van der Windt D, Bootsma HJ, Burghout P, van der Gaast-de Jongh CE, Hermans PW, van der Flier M: Nonencapsulated Streptococcus pneumoniae resists extracellular human neutrophil elastase- and cathepsin G-mediated killing. FEMS Immunol Med Microbiol 2012, 66(3):445–448.PubMedCrossRef

17. Martin M, Turco JH, Zegans ME, Facklam RR, Sodha S, Elliott JA, Pryor JH, Beall B, Erdman DD, Baumgartner YY, Sanchez PA, Schwartzman JD, Montero J, Schuchat A, Whitney CG: An outbreak of 3-mercaptopyruvate sulfurtransferase conjunctivitis due to atypical Streptococcus pneumoniae . N Engl J Med 2003, 348(12):1112–1121.PubMedCrossRef 18. Crum NF, Barrozo CP, Chapman FA, Ryan MA, Russell KL: An outbreak of conjunctivitis due to a novel unencapsulated Streptococcus pneumoniae among military trainees. Clin Infect Dis 2004, 39(8):1148–1154.PubMedCrossRef 19. Porat N, Greenberg D, Givon-Lavi N, Shuval DS, Trefler R, Segev O, Hanage WP, Dagan R: The important role of nontypable Streptococcus pneumoniae international clones in acute conjunctivitis. J Infect Dis 2006, 194(5):689–696.PubMedCrossRef 20. Beiter K, Wartha F, Hurwitz R, Normark S, Zychlinsky A, Henriques-Normark B: The capsule sensitizes Streptococcus pneumoniae to alpha-defensins human neutrophil proteins 1 to 3. Infect Immun 2008, 76(8):3710–3716.PubMedCentralPubMedCrossRef 21. Nelson AL, Roche AM, Gould JM, Chim K, Ratner AJ, Weiser JN: Capsule enhances pneumococcal colonization by limiting mucus-mediated clearance.