Saline was added to make the volume to 11 ml to which 2 ml diethyl ether was added and centrifuged at 10,000 rpm for 10 minutes. This procedure was repeated twice after which the supernatant was discarded and the sediment preserved in sterile containers in normal saline. Ether is classed as an extremely flammable reagent requiring storage in suitable flammable-liquid storage cabinets; therefore, we used ethyl acetate

as an alternative. Formalin was not used as it leads to a reduction in the fluorescence intensity of stained spores and being a Polymerase Chain Reaction (PCR) inhibitor, it may interfere with the molecular study of the parasites to be conducted later [4]. After concentration the saline and iodine find more selleckchem preparations of the samples were microscopically observed as above. Staining The concentrated samples were used for staining. Thin smears from all the samples were prepared on two different slides. The first slide was stained by Modified safranin technique [3]. In this method 3% acid alcohol was used for fixation. Safranin was used for staining and counterstaining was done by Malachite green. Kinyoun’s staining was used to stain the second slide [3]. The smear was fixed with absolute methanol and stained with Kinyoun’s carbol fuschin. Destaining was done by

10% alcohol and the smear was counterstained by Malachite green. At least 200 oil immersion fields of the above smears were examined for the parasites. Fluorescence microscopy A wet mount preparation of the concentrated samples was made and checked for autoflourescence of Cyclospora cayetanensis at 200× magnification with a 330 to 380 nm UV filter. The use of Calcoflour White (Sigma, USA) for fluorescent labeling of Microsporidia spores based on the presence of α-chitin in the inner endospore layer of the spore wall was first introduced by Vávra et al [5]. Calcoflour White stain (10 μl)

was added to the same amount of concentrated samples taken on clean, dry slides. The working solution was prepared by making 1:10 dilution of the stock (1%) and adding 0.05% Evan’s Blue dye. Slides were examined with the help crotamiton of UV fluorescence microscope at an excitation wavelength of 405 nm. A modification of the above method was performed by using a fluorescent probe 4, 6-diamidine-2-phenylindole (DAPI). Equal quantities (10 μl) of stool sample and DAPI (Sigma, USA) were put on a slide and left for 5 minutes. Thereafter, 10 μl of Calcoflour White was added and the slides were air dried. The slides were screened with the help of a fluorescence microscope using 435-485 BA filter. Antigen detection The third part of the unconcentrated stool samples was subjected to sandwich ELISA for Cryptosporidium parvum antigen detection. The procedure was performed as per the instructions given in the commercially available kit (IVD Research Inc. CA, USA).

5 μM of primers PAO1 S AZD2171 in vitro and PAO1 A in combination with agarose gel electrophoresis and ethidium bromide staining and by oprL real-time PCR with 0.5 μM of primers PAO1 S and PAO1 A and 0.1 μM of TaqMan probe oprL TM (Table 3). Table 3 Sequences of primers and probes used Primer/Probe 5′-3′ Sequenced Amplicon size (bp) Reference or source PAO1 Sa PAO1 Aa ACC CGA ACG

CAG GCT ATG-TET CAG GTC GGA GCT GTC GTA CTC 92 TIB Molbiol oprL Fa oprL Ra ATG GAA ATG CTG AAA TTC GGC CTT CTT CAG CTC GAC GCG ACG 504 [13, 28] oprL-LC-FAMb TGC GAT CAC CAC CTT CTA CTT CGA GT-FAM / TIB Molbiol oprL-LC-ROXb ROX-CGA CAG CTC CGA CCT GAA G / TIB Molbiol oprL TMc FAM-AGAAGGTGGTGATCGCACGCAGA-BBQ / TIB Molbiol a Primers b HybProbes c TaqMan Probe. d TET, FAM and ROX are fluorescent labels. BBQ: BlackBerry quencher The DNA-extraction protocol, which enabled the most sensitive detection as assessed by these two PCR formats, was used to compare different PCR and real-time PCR formats. PCR and real-time PCR formats Depending on the type of PCR,

detection of P. aeruginosa was done using two primer sets (Table 2 and Table 3). Both primer sets are targeting the oprL gene because available sequences of different isolates show that this gene is highly conserved http://​www.​pseudomonas.​com/​related_​links.​jsp#alleles. A total of six PCR formats (incl. 4 real-time PCR formats) LY3023414 mw were compared. Conventional PCR, using the Veriti 96-Well Thermal Cycler (Applied Biosystems, Foster City, Ca.), was done with primers PAO1 S (TET-labeled) and PAO1 A, whereby PCR products

were subsequently visualized either with agarose gel electrophoresis and ethidium bromide staining or with fluorescent capillary electrophoresis. Agarose gel electrophoresis was carried out at 100 V on an agarose gel of 2.5% (w/v), containing 1 mg/ml ethidium bromide and visualized on a UV transilluminator at 540 nm. For capillary electrophoresis, 1 μL of PCR product was added to a mixture of 12 μL deionised formamide, 0.3 μL ROX-labeled GS-400 high-density size standard and 0.2 μL ROX labeled GS-500 size standard. This mixture was then electrophoresed on an ABI PRISM 310 (Applied Biosystems), as described O-methylated flavonoid previously [35]. Of the four real-time PCR formats, three were carried out on the LightCycler 1.5 Instrument (Roche) using three different LightCycler real-time PCR kits, all with an optimized MgCl2 concentration, i.e. LightCycler FastStart DNA MasterPLUS SYBR Green I (Roche), LightCycler FastStart DNA MasterPLUS HybProbe (Roche) and LightCycler Taqman Master (Roche) and one was carried out on the ABI7000 instrument, using the commercially available TaqMan Pseudomonas aeruginosa detection kit (Applied Biosystems). For all of these PCR formats, the PCR mixes were prepared as recommended by the manufacturer and also the PCR programs were carried out as prescribed by the manufacturer.

The concept of enhancement and the two light reactions arose from these experiments. In the same review, p. 209, Vernon and Avron also said that part of “the evidence for two pigment systems in photosynthesis was Blinks’s Ulva work (Haxo and Blinks 1950; Yocum and Blinks 1950, 1954; Blinks 1957, 1959) which caused a pulse of oxygen evolution, the height and duration of which depend on the history of the cell.” In a review on phycobilins

and phycobilisomes, Tandeau de Marsac (2003) stated: About 60 years later, however, the major role of the different phycobilins from red algae and cyanobacteria Vactosertib mouse in light-harvesting for photosynthesis was largely confirmed and quantitatively MDV3100 nmr established by several groups (Emerson and Lewis 1942; Blinks 1954a, b; Brody and Emerson 1959; Lemasson et al. 1973).

Tandeau de Marsac also mentioned: The discovery of two spectrally slightly different phycoerythrins in primitive red algae of the order of Bangiales (Bangiophyceae) B-phycoerythrin (Airth and Blinks 1956) and the b-phycoerythrin (Gantt and Lipschultz 1974); the nomenclature of “R” for red algae was no longer valid. Consequently, these prefixes no more refer to the type of source organisms but denote their specific spectral characteristics. In reevaluating Blinks’s contributions, Raven and Giraud-Bascoe (2001, p. 946) concluded: The second investigation of the Emerson [Enhancement] effect (Emerson et al. 1957;

Emerson and Chalmers 1958)… was ‘found’ in the work of Blinks (1957, 1960a, b) on chromatic transients, involving sequential rather than simultaneous supply of the irradiation of different wavelengths to marine macroalgae. Blinks was forced to use sequential rather than simultaneous irradiations because Idelalisib he had used only one monochromator. However, Blinks’s approach allowed him to confirm that enhancement did not necessarily involve simultaneous irradiation and so involved interaction between the different wavelengths at the level of chemical products of photochemistry rather than at the level of excitation energy or photochemistry. According to Govindjee (pers. commun.), Emerson et al. (1957) used a shaking vessel, and the two light beams he used were also absorbed by the cells with some time delay; thus, they were also not quite ‘simultaneous’. Further, the two light effect was clearly shown to be not in respiration, as Blinks had thought: (a) R. Govindjee et al. (1960) discovered a two-light effect in a benzoquinone Hill reaction in Chlorella cells, where benzoquinone had inhibited respiration; (b) Govindjee et al. (1963) showed, using mass spectroscopy, that the effect was in photosynthesis, not in respiration. Later, Govindjee and R.

PubMed 11. Knirel YA, Moll H, Helbig JH, Zahringer U: Chemical characterization of a new 5,7-diamino-3,5,7,9-tetradeoxynonulosonic acid released by mild acid hydrolysis of the Legionella pneumophila serogroup 1 lipopolysaccharide. Carbohydr Res 1997,304(1):77–79.PubMedCrossRef 12. Neumeister B, Faigle M, Sommer M, Zahringer U, Stelter F, Menzel R, Schutt C, Northoff H: Low endotoxic GF120918 in vitro potential of Legionella pneumophila lipopolysaccharide due to failure of interaction with the monocyte lipopolysaccharide receptor CD14. Infect Immun

1998,66(9):4151–4157.PubMed 13. Goon S, Kelly JF, Logan SM, Ewing CP, Guerry P: Pseudaminic acid, the major modification on Campylobacter flagellin, is synthesized via the Cj1293 gene. Mol Microbiol 2003,50(2):659–671.PubMedCrossRef 14. Schoenhofen IC, McNally DJ, Brisson JR, Logan SM: Elucidation of the CMP-pseudaminic acid pathway in Helicobacter pylori: synthesis from UDP-N-acetylglucosamine by a single enzymatic reaction. Glycobiology 2006,16(9):8C-14C.PubMedCrossRef 15. Hopf PS, Ford RS, Zebian N, Merkx-Jacques A, Vijayakumar S, Ratnayake D, Hayworth J, Creuzenet C: Protein glycosylation

in Helicobacter pylori: beyond the flagellins? PLoS One 2011,6(9):e25722.PubMedCrossRef 16. Lewis AL, Desa N, Hansen EE, Knirel YA, Gordon JI, Gagneux P, Nizet V, Varki A: Innovations in host and microbial sialic acid biosynthesis revealed by phylogenomic prediction of nonulosonic acid structure. Proc Natl selleck kinase inhibitor Acad Sci U S A 2009,106(32):13552–13557.PubMedCrossRef 17. Rangarajan ES, Proteau A, Cui Q, Logan SM, Potetinova Z, Whitfield D, Purisima EO, Cygler M, Matte check details A, Sulea T, et al.: Structural and functional analysis of Campylobacter jejuni PseG: a udp-sugar hydrolase from the pseudaminic acid biosynthetic pathway. J Biol Chem 2009,284(31):20989–21000.PubMedCrossRef 18. Schoenhofen IC, Vinogradov E, Whitfield DM, Brisson JR, Logan SM: The CMP-legionaminic acid pathway in

Campylobacter: biosynthesis involving novel GDP-linked precursors. Glycobiology 2009,19(7):715–725.PubMedCrossRef 19. Morrison JP, Schoenhofen IC, Tanner ME: Mechanistic studies on PseB of pseudaminic acid biosynthesis: a UDP-N-acetylglucosamine 5-inverting 4,6-dehydratase. Bioorganic Chemistry 2008,36(6):312–320.PubMedCrossRef 20. Schoenhofen IC, Lunin VV, Julien JP, Li Y, Ajamian E, Matte A, Cygler M, Brisson JR, Aubry A, Logan SM, et al.: Structural and functional characterization of PseC, an aminotransferase involved in the biosynthesis of pseudaminic acid, an essential flagellar modification in Helicobacter pylori. J Biol Chem 2006,281(13):8907–8916.PubMedCrossRef 21. Schoenhofen IC, McNally DJ, Vinogradov E, Whitfield D, Young NM, Dick S, Wakarchuk WW, Brisson JR, Logan SM: Functional characterization of dehydratase/aminotransferase pairs from Helicobacter and Campylobacter: enzymes distinguishing the pseudaminic acid and bacillosamine biosynthetic pathways. J Biol Chem 2006,281(2):723–732.PubMedCrossRef 22.

[16, 28–33]. Interestingly, a study in the Balearic Islands, showed a higher risk of AEs, some more severe in intensity as a consequence of the decision to administer ARV FDCs as separate components to reduce

costs. Many of these AEs were neuropsychiatric disorders possibly related to EFV in stable patients who previously tolerated this drug. As a result, unlike the desired objective of cost saving, the disruption of ARV FDCs led to an increase of health care expenditure [34]. Selonsertib in vitro Adherence is also a cornerstone of persistence. Persistence is the length of time patients remain on a specific ARV regimen and is a key tenet to achieve long-term treatment success. NNRTI-based regimens exhibited greater persistence than PI-based ones. Among the specific regimens, TDF/FTC/EFV provided the longest persistence [35]. As successive ARV regimens have exhibited progressively shorter durability, optimizing the duration of the first regimen in treatment-naïve patients is of utmost importance. OD regimens had greater

longevity than those taken BID or more frequently and the shift to newer, more convenient Selleck Vactosertib and better-tolerated therapeutic options has induced, over the last few years, a remarkable increase in the durability of first regimens [36]. STR and Quality of Life (QoL) As cART options have increased and HIV-infected patients are living longer, the improvement or maintenance of health-related QoL has become an HAS1 increasingly important goal of the management of chronic HIV infection. The maintenance of QoL passes through HIV medications use [37]. Simplification of cART has been shown to maintain or increase the QoL. Switching virologically suppressed subjects from their existing PI-based or NNRTI-based regimen to TDF/FTC/EFV STR was associated with maintained QoL and better treatment adherence. Patients referred

an improved ease of use and an increment of treatment satisfaction after the switch to STR that was associated to a sustained improvement of several commonly encountered HIV-related symptoms [5]. One of the secondary objectives of the ADONE study was to verify the effect of the simplification strategy on QoL. The results confirmed an improvement of QoL over time from 68.8% to 72.7% (p = 0.042) and this change was significantly associated with the perception of health status and presence, number and intensity of reported AEs (p < 0.0001). Also, QoL significantly influenced adherence (p < 0.0001) [21]. The switching boosted PI to rilpivirine (RPV) in combination with truvada as a STR (SPIRIT) study evaluated the switch from a PI-based cART to a STR (TDF/FTC/RPV) in chronically suppressed HIV patients. The study explored several patient-reported outcomes mostly dealing with symptoms often related to chronic therapies.

In the present study, a representative sample of 45 isolates was chosen to characterize their IncA/C plasmids. The code labels of the strains were designed to include relevant information about their isolation. The first two letters indicate the state: YU, Yucatán; SL, San Luis Potosí; MI, buy GANT61 Michoacán; and SO, Sonora. The third and fourth letters indicate the isolation source: HS, human;

PUS, pork meat; RES, beef meat; POLS, chicken meat; RAPUS, pork intestine; and RARES, beef intestine. The first two numbers indicate the year of isolation (from 2002-2007), and the last numbers are the isolate numbers. Plasmid DNA extraction and plasmid profiles Plasmid profiles were obtained by a modified alkaline lysis procedure [29] and were visualized by electrophoresis in 0.7% agarose gels subjected to 60 V for 8 hours. Plasmid profiles of E. coli V157 [30], E. coli E2348/69 [31] and E. coli AR060302 [6] were used as molecular markers for large plasmids, and supercoiled DNA ladders (Invitrogen) were used for smaller plasmids. To resolve plasmids larger than 50 kb, we performed S1 restriction PFGE. Briefly, total DNA was embedded in agarose plugs, and slices were treated with 8 U of nuclease S1 (Promega) at 37°C for 45 min. The PFGE running conditions were 6 V/Cm at 14°C for 15 hours, and switching times

ranged from 1 sec to 25 sec. Blebbistatin ic50 The Low Range PFG Marker was used as the reference standard (New England Biolabs). Plasmid transformation and antimicrobial susceptibility testing Plasmid DNA was introduced into E. coli DH5α and TOP10 through electroporation. Transformants were selected on Luria-Bertani (LB) agar containing either 2-μg/ml ceftriaxone for the CMY+ isolates or 15-μg/ml chloramphenicol second for the CMY- isolates. Susceptibility testing was performed by disk diffusion according to Clinical and Laboratory Standards Institute (CLSI) recommendations [32]. The following commercially purchased disks (Becton, Dickinson and Company, Sparks, MD, USA) were used: ampicillin (A), 10 μg; chloramphenicol (C), 30 μg; streptomycin (S), 10

μg; sulfonamides (Su), 250 μg; tetracycline (T), 30 μg; ceftriaxone (Ax), 30 μg; gentamicin (G), 10 μg; trimethoprim-sulfamethoxazole (Sxt), 1.25/23.75 μg; kanamycin (K), 10 μg; nalidixic acid (N), 30 μg. Resistance to ceftriaxone was confirmed by agar dilution using a breakpoint of ≥4 μg/ml. Plasmid Pst I restriction and Southern hybridization Plasmid restriction analysis with Pst I has been used for the classification of CMY+ plasmids according to Giles types [12, 20]. Giles type A has been correlated with IncA/C plasmids carrying a single bla CMY-2 copy, type B with IncI1 plasmids, and type C with IncA/C plasmids carrying two bla CMY-2 copies [6, 19]. Plasmid DNA was treated with 15 U of Pst I (Invitrogen) at 37°C for 6 hours and was electrophoresed in 0.7% agarose for 3 hours at 100 V.

The regulation of adpA gene expression is complex and various mechanisms have been described [17]. AdpA represses its own gene expression in S. griseus[18] whereas it activates its own transcription in S. coelicolor[16]. In several Streptomyces species, the binding of γ-butyrolactones to a γ-butyrolactone PARP inhibitor receptor represses the adpA promoter [19, 20]. In S. coelicolor, BldD represses adpA expression [21]. At the translational level, a feedback-control loop regulates levels of AdpA and AbsB (a RNAse III) in S. coelicolor[22, 23]. A positive feedback loop between AdpA and BldA, the only

tRNA able to read the UUA codon present in all adpA mRNA, has been demonstrated in S. griseus[22, 23]. In S. coelicolor, adpA expression is constant during growth in liquid media [4] whereas on solid media, adpA is strongly expressed before aerial hyphae formation and AdpA is

most abundant during the early aerial mycelium stage [4, 16]. Even though AdpA plays a major role in development of Streptomyces spp., little is known about the pathways it controls in S. lividans, a species closely related to S. coelicolor and whose genome has recently been sequenced [24]. We have recently shown that in S. lividans AdpA directly controls sti1 and the clpP1clpP2 operon, encoding important factors for Streptomyces differentiation; this website we also found interplay between AdpA and ClpP1 [25]. Here, we report microarray experiments, quantitative GPX6 real-time PCR (qRT-PCR), in silico analysis and protein/DNA interaction studies that identify other genes directly regulated by AdpA in S. lividans. Finally, in silico

genome analysis allowed the identification of over hundred genes that are probably directly activated or repressed by AdpA in S. lividans. These findings and observations reveal new AdpA-dependent pathways in S. lividans. Methods Bacterial strains, growth conditions and media S. lividans 1326 was obtained from the John Innes Culture Collection. In this S. lividans background, we constructed an adpA mutant in which adpA was replaced with an apramycin-resistance cassette [25]. Streptomyces was grown on NE plates [26] and in YEME liquid medium [27] in baffled flasks. MS medium was used for sporulation experiments [27]. Apramycin was added to final concentrations of 25 μg mL-1 to solid media and 20 μg mL-1 to liquid media as appropriate. Microarray experiments S. lividans microarrays were not available, so S. coelicolor oligonucleotide arrays covering most open reading frames (ORFs) of the genome (for array coverage and design, see [28, 29]) were used. Aliquots of 60 mL of liquid YEME medium were inoculated with about 108 spores and incubated at 30°C with shaking at 200 rpm until early stationary phase (about 30 h of growth). Samples of 12 mL of culture (at OD450nm = 2.3, corresponding to time point T on Figure 1a) were then collected and RNA extracted as previously described [30]. RNA quality was assessed with an Agilent 2100 Bioanalyser (Agilent Technologies).

Therefore, replication of all mycoplasma plasmids is likely to be driven through a rolling-circle mechanism by a Rep protein of the pMV158 family type. Mosaic structure of the mycoplasma plasmids is indicative of recombination events In spite of a conserved structure, multiple pair-wise DNA sequence comparisons indicated that mycoplasma plasmids are in fact a mosaic of rep, dso, copG, and sso blocks. This was evidenced by the occurrence of several local regions of homology detected by using the BLAST program (Figure 5). Pairs of plasmids that show a high level of identity for the Rep sequence (e.g. pKMK1 and Ganetespib research buy pMG1B-1; pMG2D-1 and pMG2B-1) do not necessarily share a high degree of identity

for the region upstream of copG. Interestingly, high sequence identity for the region spanning sso was found to be indicative of plasmids being hosted by the same mycoplasma species. For instance, the following plasmid-pairs, pADB201 and pKMK1, pMG1B-1 and pMG2D-1, and pMG2B-1 and pMG2F-2 were isolated from Mmc, Mcc, and M. yeatsii, respectively (Figure 5). This result is consistent

with the fact that during replication this region interacts with chromosome-encoded components [18]. Further degrees of mosaicism were found in particular cases such as for pMG2D-1, in which two putative dso showing sequence heterogeneity are found. Other examples of genetic variability are the small size of pBG7AU and the unusual location of the dso in pMG2F-2. Such a mosaic structure is clearly indicative of successive recombination

events between replicons. Figure 5 Analysis of plasmid Selleck SHP099 content of Mycoplasma yeatsii type strain GIH (TS). A. Agarose gel electrophoresis of total DNA. Lanes were loaded after twofold dilution series of the DNA preparation obtained as described in Methods. Bands corresponding to the chromosome and the 2 plasmids are identified. Lane M, DNA ladder. B. Estimated plasmid copy number of pMyBK1 and pMG2B-1 as estimated by gel assay (Panel A) and relative real-time PCR as described in Methods. pMyBK1 is a unique representative of a new replicon family As indicated above, M. yeatsii strain GIH TS was the only strain that yielded a banding pattern of extrachromosomal DNA that suggested the presence of two distinct Lepirudin plasmids (Figure 5A). The small plasmid, pMG2B-1, was shown to belong to the pMV158 family like all other mycoplasma plasmids (Figure 3). In contrast, the larger plasmid (3,432 bp) named pMyBK1 (GenBank Accession number EU429323; [25]) has a genetic organization that sets it apart from the other mycoplasma plasmids. Initial database searches using pMyBK1 sequence as a query indicated low identity with other plasmids and prompted us to further analyze this plasmid that might represent a new family of replicons. First, the relative copy number of each plasmid of M.

putida indicating that these targets may also be regulated by directly by Crc [34]. Besides the role that CRC plays in the bioremediation activities of P. putida, little else is known about the control that CRC imposes on the ecological functions of Pseudomonads other than for virulence-associated functions in Pseudomonas aeruginosa. A crc mutant of P. aeruginosa PA14 was defective in biofilm

formation and type IV pilus-mediated twitching motility [36]. and a crc mutant of P. aeruginosa PAO1 displayed increased susceptibility to some antibiotics as well as defects in type III secretion, motility and expression of quorum sensing-regulated virulence factors [27]. Given the range of ecological functions that Pseudomonas may perform there is great scope for Crc to be Proteases inhibitor a significant regulator beyond JNK inhibitor mouse the realm

of primary metabolism. For instance, glucose metabolism is subject to CRC and gluconate is a product of glucose metabolism. Gluconate itself is linked to phosphate solubilisation [9] and biocontrol [37] and there is a link between the ability to produce gluconate and the levels of antimicrobial compounds produced such as 2,4-diacetylphloroglucinol and pyoluteorin [38]. Additionally, recent evidence indicates that there is a link between primary metabolism and secondary metabolism controlled by the GacS/Rsm system [39]. This suggests that there is great potential for

CRC to interact with other regulatory networks, at least indirectly, and it is therefore a high priority to better understand the Crc regulon. Based on the size of the Crc product and the proposed mechanism of action, it is thought that Crc binding must occur within -70 to +16 bp relative to the origin of translation [18]. There remain, however, very few known direct targets of Crc: only benR [33], alkS [18], xylR and xylB [34] mRNAs from P. putida and amiE mRNA [17] (product of the amidase gene amiE), in P. aeruginosa have been demonstrated to bind Crc. To extend the number of direct targets known, we carried out a bioinformatic analysis using genome information from sequenced Pseudomonas strains. By identifying the specific targets from in pathways that are known to be regulated by CRC, it will be possible to determine precisely how different Pseudomonads control nutrient uptake and utilisation. Furthermore, the analysis is expected to identify new pathways and processes, not previously known to be CRC-regulated. A better understanding of how Pseudomonas species use CRC will enhance knowledge of the ecology of these bacteria and will facilitate efforts to exploit the metabolic capacity of these bacteria in industrial and environmental microbiology.

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