S chartarum is usually referred to as “toxic mold”; toxicity has

S. chartarum is usually referred to as “toxic mold”; toxicity has been associated with exposure to spores and production of mycotoxins [3–5]. Chk inhibitor In addition, S. chartarum and other indoor molds have been linked to damp building-related illnesses (DBRI) such as allergic reactions of the upper respiratory system (e.g. irritated eyes, nose and throat) [6]. Likewise, cases of idiopathic pulmonary hemosiderosis

have been associated with S. chartarum indoor exposures [7, 8]. Also, S. chartarum may trigger immunologic, neurologic, and oncogenic disorders [5, 7, 9]. Proper risk management decisions are necessary whenever S. chartarum is identified in mold-infested environments for the proper remediation of this mold and minimal exposure of occupational workers to its toxic effects [10, 11]. At present, there are no standardized protocols to identify the need for mold-remediation for indoor built environments. Most of the published mold-remediation guidelines recommend visual inspection for fungal growth as part of the assessment for mold-remediation at damp or water-damaged settings. Usually by the time visible mold growth is observed, it implies that inaccessible areas within the building construction are already mold-contaminated [11, 12]. The implementation of new technologies for close monitoring learn more of secluded, damp spaces is necessary for the early detection of mold growth. Several studies suggested

the use of microbial volatile organic compound (MVOC) profiles as a diagnostic tool to determine mold-related problems in homes and buildings [13–15]. MVOCs are volatile organic chemical emissions associated with mold metabolism and may be linked to some of the adverse respiratory conditions generated by S. chartarum[16–19]. Combinations of MVOC emissions generate characteristic odors; these are detected prior to visual mold growth in buildings where occupants complaint of poor indoor air quality [20, 21]. MVOCs are suitable markers because they easily diffuse through weak barriers

like wallpaper and small crevices [12, 15, 20]. Likewise, they could be used for early detection of mold growth in hidden cavities (i.e. air ducts) and infrequently-visited places such as attics, crawl spaces and basements [12, 22]. Several studies suggest that MVOC emission patterns could be used for the identification and Flavopiridol (Alvocidib) classification of closely related microorganisms [23, 24]. Larsen and Frisvad [25] analyzed the MVOCs emissions pattern of 47 Penicillium taxa and showed and the MVOCs emission profiles were unique enough to classify Penicillium to the species level. In a previous study, our laboratory characterized MVOCs emitted by three toxigenic strains of S. chartarum when grown on Sabouraud Dextrose Agar (SDA) and gypsum wallboard [26]. In the present study, we included seven toxigenic strains of S. chartarum to identify unique MVOCs for this mold to help in the construction of a robust MVOC library.

Blackwell Scientific, Oxford Edwards GE, Huber SC, Ku MSB, Gutier

Blackwell Scientific, Oxford Edwards GE, Huber SC, Ku MSB, Gutierrez M, Rathnam CK, Mayne BC (1976) Variation in photochemical activities in C4

plants in relation to CO2 fixation. In: Burris RH, Black CC (eds) CO2 metabolism and productivity see more of plants. University Park Press Baltimore, MD, pp 83–112 Fleischman DE, Mayne BC (1973) Chemiluminescence as a probe of photosynthetic mechanisms. In: Rao Sanadi D (ed) Current topics in bioenergetics, vol V. Academic Press, New York, pp 77–105 Goldstein LD, Ray TB, Kestler DP, Mayne BC, Brown RH, Black CC (1976) Biochemical characterization of Panicum species which are intermediate between C3 and C4 photosynthesis plants. Plant Sci Lett 6:85–90CrossRef Goltsev V, Zaharieva I, Chernev

P, Strasser RJ (2009) Delayed fluorescence in photosynthesis. Photosynth Res 101:217–232PubMedCrossRef Govindjee, Bazzaz M (1967) On the Emerson enhancement effect in the ferricyanide Hill reaction in chloroplast fragments. Photochem Photobiol 6:885–894 Govindjee, Björn LO (2012) Dissecting photosynthesis: The evolution of the “Z”-scheme for thylakoid reactions, In: Itoh S, Mohanty P, Guruprasad KN (eds) Photosynthesis: overviews on recent progress & future perspective. I.K. Publishers, New Delhi, pp 1–27 Govindjee R, Govindjee, Hoch G (1962) The Emerson enhancement effect in TPN-photoreduction https://www.selleckchem.com/products/ferrostatin-1-fer-1.html by spinach chloroplasts. Biochem Biophys Res Commun 9:222–225CrossRef Govindjee R, Govindjee, Hoch G (1964) Emerson enhancement effect in chloroplast reactions. Plant Physiol 39:10–14PubMedCrossRef Govindjee, Jursinic PA (1979) Photosynthesis and fast changes in light emission by green plants.

In: Smith KC (ed) Photochemical and Photobiological Reviews, vol 4. The Plenum Press, NY, pp 125–205 Govindjee R, Thomas JB, Rabinowitch E (1960) Second Emerson effect in the Hill reaction of Chlorella cells with quinone as oxidant. Science 132:421PubMedCrossRef Govindjee, Owens OvH, Hoch G (1963) A mass-spectroscopic study of the Emerson enhancement effect. Biochim Biophys Acta 75:281–284PubMedCrossRef Hardt H, Malkin S (1973) Oscillations Meloxicam of the triggered luminescences of isolated chloroplasts preilluminated by short flashes. Photochem Photobiol 17:433–440CrossRef Jagendorf AT, Uribe E (1966) ATP formation caused by an acid-base transition of spinach chloroplasts. Proc Natl Acad Sci USA 55:170–177PubMedCrossRef Ke B (2001) Photosynthesis, photobiochemistry and photobiophysics. Advances in photosynthesis, vol 10 (series ed. Govindjee) Kluwer Academic Publishers, Dordrecht Kestler DP, Mayne BC, Ray TB, Goldstein LD, Brown RB, Black CC (1975) Biochemical components of the photosynthetic CO2 compensation point of higher plants. Biochem Biophys Res Commun 66:1439–1448PubMedCrossRef Kok B (1956) On the reversible absorption change at 705 nm in photosynthetic organisms.

In addition, we have also reported an abundant intracellular expr

In addition, we have also reported an abundant intracellular expression of TLR3 INK 128 in a porcine intestinal epithelial (PIE) cell line [22], which is in line with findings of Liu et al. [8] that demonstrated that the non-transformed porcine jejunum epithelial cell line (IPEC-J2) expresses TLR3 constitutively. We characterized the immune response triggered by poly(I:C) challenge in PIE cells and in PIE-immune cell co-cultures, and demonstrated that these systems are valuable tools for studying in vitro the immune response triggered by TLR3/RIG-I on IECs and the interaction between IECs and immune cells [22,

23]. In this study, we therefore aimed to use these porcine in vitro systems to gain insight into the mechanisms involved in the immunomodulatory effect of CRL1505 strain, and concentrated our attention in the crosstalk between L. rhamnosus CRL1505, PIE cells and APCs in order to deepen our knowledge about the mechanisms, through which this strain may help preventing viral diarrhoea episodes. Methods Microorganisms Lactobacillus rhamnosus CRL1505 (Lr1505) and L. rhamnosus CRL1506 (Lr1506) belong to CERELA Culture Collection and were originally isolated from goat milk [11]. These strains were grown in Man-Rogosa-Sharpe (MRS) broth at 37°C. For immunomodulatory assays, overnight cultures

PCI 32765 were harvested by centrifugation, washed three times with sterile PBS, counted in a Petroff-Hausser counting chamber, selleck screening library and re-suspended in DMEM until use. PIE cell monocultures A non-transformed porcine intestinal

epithelial cell line (PIE), characterized by its ability to build a monolayer with a cobblestone and epithelial-like morphology and close contacts between cells was used as described before [22, 23]. Briefly, PIE cells were grown on type I collagen-coated dishes using DMEM (Gibco, Japan) supplemented with 10% fetal calb serum (FCS, Sigma). PIE cells were incubated at 37°C and 5% CO2. Passages were done by treating the monolayer with sucrose/EDTA for 4 min and detaching the cells with 0.04% trypsin. Isolation of adherent population from swine Peyer’s patches (PPs) Suspensions of porcine PP immunocompetent cells were prepared from adult swine intestine. This study was carried out in strict accordance with the recommendations in the Guide for the Care and Use of Laboratory Animals of the Guidelines for Animal Experimentation of Tohoku University, Sendai, Japan. The present study was approved by the Institution Animal Care and Use Committee of Tohoku University with a permitted No. 2011-noudou-5 and all efforts were made to minimize suffering. Swine PPs were cut into small pieces and gently pressed through a nylon mesh to prepare single immune cell suspensions.

Virus titers (plaque-forming units (pfu) mL-1) were determined on

Virus titers (plaque-forming units (pfu) mL-1) were determined on BHK-21, as described elsewhere [48]. Animal experiments Nine 2-month-old pigs and six 1-year-old bovines see more were divided into three groups, each consisting of three pigs and two bovines. All animals were seronegative for FMDV non-structural protein (NSP) antibodies prior to experimental infection.

Two non-RGD recombinant viruses and Asia1/JSp1c8 virus with a titer of 1.6 × 107 pfu mL-1, 1.3 × 107 pfu mL-1, and 1.0 × 107 pfu mL-1, respectively, were used to separately inoculate animals. Each pig was inoculated with 2 mL inoculum via the intramuscular route, each bovine received 1 mL intramuscularly and 1 mL via the tongue. Following inoculation, animals were carefully scored for appearance of lesions at inoculation sites and at other sites. Lesion scores were based on the number of sites affected that were distinct from actual Lumacaftor price injection sites. Scores were calculated as described

by Rieder et al [28]. The viral load in the blood was assessed by real-time quantitative RT-PCR using the RNA Master SYBR green I kit (Roche), as specified by the manufacturer. Quantification was relative to a standard curve obtained with known amounts of FMDV O/CHA/99 RNA, using a procedure that has been described previously [49], except that the primers (patent pending) targeted the 3D non-structural protein were altered. The viral RNA was extracted from vesicular fluid (collected on selected days), selleck reverse transcribed, and sequenced through the entire VP1 region as described above. All animal

studies were approved by the Review Board of Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences (Permission number: SYXK-GAN-2004-0005). All animals used in this study were humanely bred during the experiment and euthanasia was carried out at the end of the experiment to reduce suffering. Statistical analysis Changes in viral titer over time for the in vitro passage experiments were modeled using linear models with virus and time since infection (treated as a factor) as fixed effects. Model selection proceeded by stepwise deletion of non-significant terms (as judged by F-tests) starting from a model including virus, time since infection and an interaction between these factors. Lesion scores over time were modeled using linear mixed models with virus and species as fixed effects and animal identification number as a random effect. Model selection proceeded by stepwise deletion of non-significant terms (as judged by the Akaike information criterion; AIC) starting from a model including virus, species and an interaction between these factors.

hafniense DCB-2 under stressful conditions These qualities would

hafniense DCB-2 under stressful conditions. These qualities would make the strain an attractive bioremediation agent in anaerobic environments that are contaminated with nitrate, metal ions, or halogenated compounds. Methods Culture conditions and genomic DNA

extraction D. hafniense DCB-2 cells were grown fermentatively under strict anaerobic conditions on 20 mM pyruvate in a modified DCB-1 medium supplemented with Wolin vitamins [61]. Cultures were incubated at 37°C without shaking under the headspace gas mixture of 95% N2 and 5% CO2. Cells in mid-logarithmic phase were harvested, and the genomic DNA was isolated according to the procedure of Marmur [86]. Integrity of the genomic DNA and the absence of extrachromosomal DNA elements were confirmed by

pulsed field gel electrophoresis (PFGE) and agarose gel electrophoresis. www.selleckchem.com/products/r428.html Culture conditions for the growth and transcription studies are summarized in Table 2. Cell growth Rapamycin cost under different metal-reducing conditions was monitored by HPLC for consumption of substrates, by optical density that had been previously correlated with the colony forming units and, in the case of some metals, by color change of the culture [25]. Halogenated compounds were added to the fermentatively growing cells (OD600 of 0.1), and the cells were allowed to grow for 6 h before harvest for microarray and northern blot analyses. Cells exposed to oxygen were prepared by exposing fermentatively growing cells (OD600 of 0.1) to filtered air for 3 h with shaking (60 rpm). Autotrophic cell growth was obtained in a carbon fixation medium which is composed of a modified DCB-1 medium, Wolin vitamins, and different gas mixtures as indicated in Table 2 and Figure 3b. The autotrophic cell growth was examined by cell counts after four transfers to a fresh carbon fixation medium with a growth period of 14 days per transfer. For the biofilm study, cells were grown by fermentation and Fe(III)-respiration (Table

2). Two bead types, activated carbon-coated DuPont beads (3-5 mm diameter) and rough-surfaced silica glass Siran™ beads (2-3 mm diameter) Myosin were filled in serum vials. The beads were laid 2.5 cm deep with 1 cm cover of medium, and the medium was refreshed every 2.5 days without disturbing. Biomass and cell size were estimated qualitatively by using light microscopy and scanning electron microscopy from retrieved bead samples. Microarray and northern hybridization Culture conditions for the production of cDNA used on the microarrays are described above and in Table 2. Construction of glass slide arrays and the probe design were performed by the Institute for Environmental Genomics (IEG) at the University of Oklahoma. A total of 4,667 probes covering most of D. hafniense DCB-2 genes were spotted in duplicate on a slide, including probes for positive and negative controls.

On the other hand, cytochemical staining resulted in positive

On the other hand, cytochemical staining resulted in positive selleck kinase inhibitor staining for alkaline phosphatase in the cytoplasm of differentiated HPB-AML-I cells (Figure 4L). Moreover, the differentiated HPB-AML-I cells also secreted calcium, which constitutes the extracellular matrix of the bone, as shown by von Kossa staining (Figure 4M and 4N). These two findings suggested the acquisition of osteogenic characteristics by HPB-AML-I

cells following the induction of osteogenesis. Inhibition of CD3+ T-cell proliferation in the presence of HPB-AML-I cells CD3+ T-cells obtained from peripheral blood were cultured with or without HPB-AML-I cells. The XTT absorbance levels at 450 nm, which show the viability of CD3+ T-cells, decreased selleck in a dose-dependent manner similar to those of UCBTERT-21 (Figure 5). These findings suggested that HPB-AML-I

cells dose-dependently suppress the antigen-driven proliferation of CD3+ T-cells, which is also characteristic of MSCs. Figure 5 Inhibition of CD3 + T-cell proliferation in the presence of HPB-AML-I cells. Mixed lymphocyte culture was performed in the presence or absence of HPB-AML-I cells (white columns). For control, similar experiments were performed with UCBTERT-21 cells (black columns). Results are presented as the XTT absorbance levels at 450 nm, which were normalized to those of the baseline experiments (cell culture in the absence of HPB-AML-I or UCBTERT-21 cells). Means and standard deviations of four independent experiments are shown. *, P < 0.05; **, P < 0.01 compared to the baseline results Discussion Even though HPB-AML-I was established from the PBMCs of an AML-M1 case [12], this cell line presents distinctive morphological features from AML. In terms of cell-surface second antigen expression, multilineage differentiation, and CD3+ T-cell suppression, the characteristics of HPB-AML-I were found to be similar to those of MSCs. Our findings presented here suggest that HPB-AML-I may be a neoplastic

cell line with MSC properties. Few reports have dealt with the establishment of human neoplastic MSC lines. A previous study established F6, a human neoplastic MSC line, from embryonic bone marrow MSCs. Transplantation of F6 cells into the SCID-nude mice resulted in fibrosarcoma formation and tissue metastasis [21, 24]. To the best of our knowledge, however, HPB-AML-I is the first neoplastic MSC line derived from a leukemic case. The appearance of HPB-AML-I cells in suspension phase with their round-polygonal morphology intrigued us. We observed that an increase in the population of HPB-AML-I cells with such morphological patterns occurs in conjunction with the increased confluence of cultured cells. Morphological changes during culturing have previously been described in the case of bone marrow MSCs. Choi et al.

Accordingly, the process of Se(IV) reduction appears to be an NAD

Accordingly, the process of Se(IV) reduction appears to be an NADPH- or NADH-dependent pathway and indicates two possible pathways. One possibility is that Se(IV) did not enter the cytoplasm of strain S44 or only trace levels

of Se(IV) were present in the cytoplasm. The Se(IV)-reducing determinant might have initially been assembled SB203580 mouse in the cytoplasm and then transferred across cytoplasmic and outer membrane. The Se(IV)-reducing determinant would then be only active outside of cells in vivo [21]. Another possibility, and more likely at that, is that Se(IV) was reduced to Se(0) in the cytoplasm and then Se(0) was pumped out of the cells where small SeNPs aggregated into bigger particles. In many cases, the big

and smooth-surface nanoparticles occurred outside of cells [20,21,32]. Here, a large number of SeNPs ranging from 100–200 nm were observed by SEM (Figure 1) and further confirmed by EDX (Figure 3A). In our experiment it was obvious that small selenium particles aggregated into bigger particles as observed by TEM (Figure 3 and Additional file 1: Figure S1). This was different from previous TEM images of a homogeneous density of SeNPs [20,21,32]. In addition, this was not impacted by sample preparation because other strains produced big and homogeneous nanoparticles outside of cells using the same sample preparation and TEM observation technique (Data not shown). Previous

studies confirmed small particles having low negative charges to have a propensity to come together and form aggregates [12]. R788 datasheet In addition, proteins and/or other biomolecules such as polysaccharides and fatty acid may play a key role in controlling selenium nanoparticle size Tyrosine-protein kinase BLK and the morphology of the resultant SeNPs [30]. The bulk of the Se(VI) and Se(IV) reduction to Se(0) was reported to occur on or outside the envelope [21]. This is very different from the reported mechanism where selenium was bound to the assembling protein SefA and then formed nanoparticles which were exported from cells [35]. In most reported cases, Se(VI) reduction occurred under anaerobic condition [36-38]. C. testosteroni S44 has a weak ability to reduce Se(VI) into red-colored selenium under aerobic condition (Figure 5B). The Se(VI) reductase complex was identified as a periplasmic Mo-containing enzyme in T. selenatis [38,39] and B. selenatarsenatis [40]. The Se(VI)-reducing determinant of C. testosteroni S44 also is most likely a Mo-enzyme because tungstate inhibited Se(VI) reduction (Figure 5B). In contrast, the Se(IV)-reducing determinant did not appear to contain Mo because tungstate did not inhibit Se(IV) reduction. Accordingly, Se(VI) reduction is a distinct activity different from Se(IV) reduction. Iron-sulfur (Fe-S) clusters are cofactors for many proteins across all three domains of life.

Weight increased fivefold in this SLN relative to untreated contr

Weight increased fivefold in this SLN relative to untreated controls (Figure 2C). SLN enlargement began 1 day after melanoma cell inoculation. These results implied that before metastasis, SLNs show tumor-reactive lymphadenopathy. Histologically, enlarged SLNs showed remarkable medullary hyperplasia (Figure 2D). The hyperplastic medulla consisted of an increased number of lymphatic sinuses of increased dilatation (Figure 2E) that contained few lymphocytes and macrophages. Figure 2 Non-metastatic cervical sentinel lymph nodes in oral melanoma-bearing mice. (A) Detection of a sentinel lymph node (SLN), showing remarkable enlargement, by injection of Evan’s blue dye. In

contrast, contralateral LN (CLN) is also stained with dye, but shows no enlargement. (B) Photograph of an click here enlarged SLN (arrow) on the left side of the cervix and a normal-like CLN (arrowhead). (C) LN weight is significantly increased in nonmetastatic SLNs relative to control, non-draining LNs as determined by t-test. *, P<0.05. Columns, mean; bar, standard error. (D), (E) Light micrographs of hematoxylin and eosin staining in SLNs. At a lower magnification (D), remarkable enlargement of the medulla (Me) is noted. Dilated sinuses (MeS) are clearly visible in the Me of SLNs (E). ALV, afferent lymphatic vessels; SS, subcapsularsinuse; Co, Cortex; LyN, lymphatic nodule; MeC, medullary cord. Scale bars = 50 μm. Tumor-bearing

SLNs Next, we examined pathological changes in tumor-bearing SLNs. In this model, LN metastases were detected 2 days after inoculation (Figure 3A). By 12 days, rates of metastasis exceeded selleck chemical 90%. Most mice died before 21 days because of eating disorder caused by enlarged tumor of the tongue [21]. Tumor metastasis was indicated macroscopically by the deposition of melanin in SLNs, in addition to LN enlargement

(Figure 3B). After 10 days, some tumor-bearing mice possessed bilateral metastases in cervical LNs (Figure 3C). To elucidate the patterns of invasive patterns of tumor cell invasion into SLNs [22], we analyzed HE-stained sections of nodes (Figure 3D). On day 2 and day 3, most LNs revealed a Grade 1 pattern of invasion, tumor cells were detected from the subcapsular sinus to the follicles. After day 5, tumor-bearing LNs showed Grade CYTH4 2 or 3 invasion, the range of which extended to the paracortex in Grade 2 invasion. In Grade 3 invasion, >60% of LN-areas were occupied by tumors. In addition to tumor-invasion, these LNs showed expansion of the lymphatic medulla. A 2.8-, 4.4-, and 4.2-fold increase was observed in Grade 1, 2, and 3 LNs, respectively, when compared with untreated controls (Figure 3E). Changes in tumor-bearing SLNs were similar to those attributed to tumor-reactive lymphadenopathy in SLNs before metastasis. Figure 3 Tumor-bearing cervical lymph nodes in oral melanoma-bearing mice.

5% of the total scaffold lengths After using both

5% of the total scaffold lengths. After using both Roxadustat chemical structure cDNA/EST and homology-based support to improve the gene models, manual annotation of many genes was completed, and the genome now has a total of 16,709 gene models. There are presently over 300,000 publicly available ESTs that were generated from cDNAs constructed from RNA isolated from cultures of Chlamydomonas exposed to a variety of physiological conditions (Asamizu et al. 1999, 2000; Shrager et al. 2003; Jain et al. 2007). Although in some cases the libraries were normalized to increase the representation of lower abundance transcripts in the EST database, the existing data

set covers a little over half of the predicted protein-coding gene models, with only about half of those covering full-length (or nearly full-length) transcripts. Hence, only ~25% of the protein-coding gene models are accurately computed and verified by transcript maps. Comparisons of the Chlamydomonas gene models to those of the close relative Volvox (shown on the Vista track of the JGI browser) and to available cDNA information, suggest that many JGI models are missing either the entire or part of the 5′ and

3′ UTRs, with several also under-predicted Hydroxychloroquine supplier for the number of exons. Since in-depth sequencing of cDNA libraries may still not capture genes encoding low abundance transcripts and maximizing sequence information from cDNA libraries is neither time-efficient nor cost-effective, present efforts are directed toward the use of next generation transcript re-sequencing technologies (in which cDNA fragments derived from RNAs isolated from various conditions are sequenced without cloning) to generate new gene models and to correct Immune system those that have been previously constructed. The rapid expansion of genomic sequence information for Chlamydomonas has also stimulated the establishment of strong proteomic initiatives (Stauber and Hippler 2004; Wagner et al. 2004, 2008, 2009; Keller et al. 2005; Schmidt et al. 2006; Naumann et al. 2007; Ozawa et

al. 2009; Rolland et al. 2009) and integrative systems databases (May et al. 2008, 2009). Much of our attention has been focused on mechanisms of photosynthetic electron transport and its regulation and identification of specific genes/proteins associated with functional and regulatory aspects of photosynthesis, with an emphasis on acclimation of the photosynthetic apparatus to environmental change. With the genomic sequence information collected for Chlamydomonas and other photosynthetic and non-photosynthetic organisms, we are now in a position to perform comparative genomic analyses to link genes/proteins that have no assigned functions to specific biological processes. The Greencut The photosynthetic eukaryotic lineage comprising the Plantae is thought to have a single evolutionary origin that was initiated with the engulfment of a cyanobacterium by a non-photosynthetic protist.

J Exp Med

J Exp Med Selleckchem Belnacasan 2002, 195:415–422.PubMedCrossRef 18. Zhong W, Gern L, Stehle T, Museteanu C, Kramer M, Wallich R, Simon MM: Resolution of experimental and tick-borne Borrelia burgdorferi infection in mice by passive, but not active immunization using recombinant OspC. Eur J Immunol 1999, 29:946–957.PubMedCrossRef 19. Hodzic E, Feng S, Freet KJ, Borjesson

DL, Barthold SW: Borrelia burgdorferi population kinetics and selected gene expression at the host-vector interface. Infect Immun 2002, 70:3382–3388.PubMedCrossRef 20. Salazar CA, Rothemich M, Drouin EE, Glickstein L, Steere AC: Human Lyme arthritis and the immunoglobulin G antibody response to the 37-kilodalton arthritis-related protein of Borrelia burgdorferi . Infect Immun 2005, 73:2951–2957.PubMedCrossRef 21. Tunev SS, Hastey CJ, Hodzic E, Feng S, Barthold SW, Baumgarth N: Lymphadenopathy during Lyme borreliosis is caused by spirochete migration- induced specific B cell activation. PLoS Pathog 2011, 7:e1002066.PubMedCrossRef 22. Hodzic E, Feng S, Freet K, Barthold SW: Borrelia burgdorferi population dynamics and prototype gene expression during infection of immunocompetent and immunodeficient mice. Infect Immun 2003, 71:5042–5055.PubMedCrossRef 23. Liang FT, Yan J, Mbow ML, Sviat SL, Gilmore RD, Mamula M, Fikrig E: Borrelia burgdorferi changes its surface antigenic expression in response to host immune responses. Infect Immun 2004, see more 72:5759–5767.PubMedCrossRef

24. Probert WS, LeFebvre RB: Protection of C3H/HeN mice from challenge with Borrelia burgdorferi through active immunization with OspA, OspB, or OspC, but not with OspD or the 83-kilodalton

antigen. Infect Immun 1994, 62:1920–1926.PubMed 25. Bankhead T, Chaconas G: The role of VlsE antigenic variation in the Lyme disease spirochete: persistence through a mechanism that differs from other pathogens. Mol Microbiol 2007, 65:1547–1558.PubMedCrossRef 26. Labandeira-Rey M, Seshu J, Skare J: The absence of linear plasmid 25 or 28–1 of Borrelia burgdorferi dramatically alters the kinetics of experimental infection via distinct mechanisms. Infect Immun 2003, 71:4608–4613.PubMedCrossRef 27. Labandeira-Rey M, Skare JT: Decreased infectivity in Borrelia burgdorferi strain B31 is associated with 17-DMAG (Alvespimycin) HCl loss of linear plasmid 25 or 28–1. Infect Immun 2001, 69:446–455.PubMedCrossRef 28. Purser JE, Norris SJ: Correlation between plasmid content and infectivity of Borrelia burgdorferi . Proc Natl Acad Sci USA 2000, 97:13865–13870.PubMedCrossRef 29. Xu Q, Seemanapalli SV, Lomax L, McShan K, Li X, Fikrig E, Liang FT: Association of linear plasmid 28–1 with an arthritic phenotype of Borrelia burgdorferi . Infect Immun 2005, 73:7208–7215.PubMedCrossRef 30. Pal U, Wang P, Bao F, Yang X, Samanta S, Schoen R, Wormser GP, Schwartz I, Fikrig E: Borrelia burgdorferi basic membrane proteins A and B participate in the genesis of Lyme arthritis. J Exp Med 2008, 205:133–141.PubMedCrossRef 31.