Moreover, in very old patients, the accumulation

of % CST may impair intracellular zinc homeostasis and metallothioneins expression, which itself is linked to an increased number of inflammatory agents, thereby suggesting the existence of a possible causal relationship between % CST and zinc homeostasis. The determination of % CST could be a more reliable means than the simple measure of telomere length as fundamental parameter in ageing to determine whether individuals are still able to respond to stress.”
“Telomeres in somatic cells become shorter with aging, and the shortening is accelerated by pathophysiological conditions. Telomere shortening can be influenced by subtelomeric DNA this website methylation. The telomere length and subtelomeric methylation status in peripheral leukocytes were compared in healthy controls and sarcoidosis patients. The sarcoidosis patients revealed shorter telomeres and a faster attrition of telomere shortening in comparison with healthy controls. Both healthy controls

and sarcoidosis patients showed that long telomeres (> 9.4 kb) decrease and short telomeres (< 4.4 kb) increase with aging, accompanying relative increases of long telomeres with subtelomeric hypermethylation and short telomeres with subtelomeric hypomethylation. This suggested that the aging-related telomere shortening is associated with the surrounding subtelomeric selleck screening library hypomethylation. Furthermore, sarcoidosis patients showed this alteration of the subtelomeric

methylation earlier than controls (in their 60s or later). This altered subtelomeric hypomethylation may correspond to the accelerated telomere shortening in sarcoidosis. This also means that the subtelomeric hypomethylation can be also influenced by certain disease conditions.”
“This study compared measures of chronic during pain, for example, number of pain sites and overall pain severity, in relation to lower extremity function in the older population.

Six hundred older adults (mean age 77.9 years, 64% female) were queried about presence of chronic pain. Number of pain sites was categorized as none, single site, multisite, or widespread. Pain severity was measured in quartiles of the Brief Pain Inventory pain severity subscale. Lower extremity function was assessed by the Short Physical Performance Battery (SPPB), a composite measure of gait speed, balance, and chair stands.

Many older persons reported multisite or widespread pain (40%). Increased pain sites and pain severity were associated with poorer SPPB performance after adjusting for age, sex, height, and weight. With further adjustment for education, comorbid conditions, and depressive symptoms, multisite pain (p < .001) and most severe pain (p < .05) were associated with poorer SPPB performance, but assessed together in the same model, only the association with multisite/widespread pain remained significant (p < .01).

“
“The abilities of wild-type and vpx-defective human immunodeficiency virus type 2 (HIV-2) clones to synthesize viral DNA in human monocyte-derived macrophages (MDMs) and lymphocytic cells were comparatively GSK1838705A in vitro and quantitatively evaluated. While the vpx-defective mutant directed the synthesis of viral DNA comparably to the wild-type virus and normally in lymphocytic cells, no appreciable viral DNA was detected in MDMs infected with the mutant. To substantiate this finding and to determine whether there is some specific region(s) in Vpx crucial for

viral DNA synthesis in MDMs, we generated a series of site-specific point mutants of vpx and examined their phenotypes. The resultant five mutants, with no infectivity for MDMs, showed, without exception,

the same defect as the vpx-defective mutant. Our results here clearly demonstrated that the entire Vpx protein is critical for reverse transcription of the HIV-2 genome in human MDMs.”
“Social behavior in mammals often relies upon the discrimination of same-species individuals via olfactory processing of unique chemosensory signatures. The ability to identify individuals from a different species by their odor (heterospecific discrimination) is less well documented. Here we used a habituation-dishabituation paradigm to demonstrate that rats can discriminate individual cats by their odor. Rats were repeatedly exposed to a collar previously worn by a domestic cat. Strong initial defensive responses (hiding in a small box and vigilant CCI-779 price “”head out”" behavior from the box entrance) habituated

with repeated exposure to the same collar. Brain activation following repeated presentation of the same odor as indexed by c-Fos expression – also habituated in accessory olfactory regions (mitral and granular layers of the posterior accessory olfactory bulb and posteroventral medial amygdala), as well as regions involved in defensive behavior, including the ventromedial and dorsal premammillary hypothalamic nuclei, basolateral amygdala and periaqueductal grey. When a collar taken from a different cat was presented to habituated rats, defensive responses (hiding, vigilance, suppression of grooming) were dishabituated, and c-Fos expression was reinstated in the accessory olfactory system and in defense-related hypothalamic, amygdaloid and brainstem nuclei. Results indicate that G protein-coupled receptor kinase rats may process and store details of the chemosensory signatures of individual predators using the accessory olfactory system. (C) 2008 Elsevier Ltd. All rights reserved.”
“The human immunodeficiency virus type 1 (HIV-1) Nef protein upregulates the expression of the invariant chain (li)/major histocompatibility complex class II (MHC-II) complex at the cell surface. This complex appears to reach the antigen-loading endosomal compartment at least in part via an indirect pathway in which it is internalized from the cell surface via the adaptor protein 2 (AP-2) complex.

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Mol selleck chemical cancer Res 2007, 5 (12) : 1263–1275.CrossRefPubMed 11. Zhang B, Pan X, Cobb GP, Anderson TA: microRNAs as oncogenes and tumor suppressors. Dev Biol 2007, 302 (1) : 1–12.CrossRefPubMed 12. Skaftnesmo KO, Prestegarden L, Micklem

DR, Lorens JB: MicroRNAs in tumorigenesis. Curr Pharm Biotechnol 2007, 8 (6) : 320–5.CrossRefPubMed 13. Calin GA, Liu CG, Sevignani C, Ferracin M, Felli N, Dumitru CD, Shimizu M, Cimmino A, Zupo S, Dono M, Dell’Aquila ML, Alder H, Rassenti L, Kipps TJ, Bullrich CRT0066101 in vitro F, Negrini M, Croce CM: MicroRNA profiling reveals distinct signatures in B cell chronic lymphocytic leukemias. Proc Natl Acad Sci USA 2004, 101 (32) : 11755–11760.CrossRefPubMed 14. Calin GA, Dumitru CD, Shimizu M, Bichi R, Zupo S, Noch E, Aldler H, Rattan S, Keating M, Rai K, Rassenti L, Kipps T, Negrini M, Bullrich F, Croce CM: Frequent deletions and down-regulation of micro-RNA genes miR15 and miR16 at 13q14 in chronic lymphocytic leukemia. Proc Natl Acad Sci USA 2002, 99 (24) : 15524–15529.CrossRefPubMed 15. Nakajima G, Hayashi K, Xi Y, Kudo selleck products K, Uchida K, Takasaki K, Yamamoto M, Ju J: Non-coding MicroRNAs hsa-let-7g and hsa-miR-181b are Associated with Chemoresponse

to S-1 in Colon Cancer. Cancer Genomics Proteomics 2006, 3 (5) : 317–324.PubMed 16. Lanza G, Ferracin M, Gafà R, Veronese A, Spizzo R, Pichiorri F, Liu CG, Calin GA, Croce CM, Negrini M: mRNA/microRNA gene expression profile in microsatellite unstable colorectal cancer. Mol Cancer 2007, 6: 54.CrossRefPubMed 17. Akao Y, Nakagawa Y, Naoe T: let-7 microRNA functions as a potential

growth suppressor in human colon cancer cells. Biol Pharm Bull 2006, 29 (5) : 903–906.CrossRefPubMed 18. Akao Y, Nakagawa Y, Naoe T: MicroRNA-143 and -145 in colon cancer. DNA Cell Biol 2007, 26 (5) : 311–320.CrossRefPubMed 19. Akao Y, Nakagawa Y, Naoe T: MicroRNAs 143 and 145 are possible common onco-microRNAs in human cancers. Oncol Rep 2006, 16 (4) : 845–850.PubMed 20. Ran XZ, Su YP, Wei YJ, Ai GP, Cheng TM, Lin Y: Influencing factors of rat small intestinal epithelial Amylase cell cultivation and effects of radiation on cell proliferation. World J Gastroenterol 2001, 7 (1) : 140–142.PubMed 21. MacPherson I, Montagnier I: Agar suspension culture for the selective assay of cells transformed by polyoma virus. Virology 1964, 23: 291–294.CrossRefPubMed 22. Early DS, Fontana L, Davidson NO: Translational approaches to addressing complex genetic pathways in colorectal cancer. Transl Res 2008, 151 (1) : 10–16.CrossRefPubMed 23. Mangan SH, Campenhout AV, Rush C, Golledge J: Osteoprotegerin upregulates endothelial cell adhesion molecule response to tumor necrosis factor-alpha associated with induction of angiopoietin-2. Cardiovasc Res 2007, 76 (3) : 494–505.CrossRefPubMed 24.

Photosynth Res 96:37–50PubMedCrossRef Böddi B, Lindsten A, Ryberg M et al (1989) On the aggregation states of protochlorophyllide and its protein complexes in wheat etioplasts. Physiol Plant 76:135–143CrossRef Böddi B, Ryberg M, Sundqvist C (1992) Identification of 4 universal protochlorophyllide forms in dark-grown leaves by analyses of the 77-K fluorescence emission-spectra.

J Photochem Photobiol B 12:389–401CrossRef Dehesh K, Ryberg M (1985) The NADPH-protochlorophyllide oxidoreductase is the major protein constituent of prolamellar bodies in wheat (Triticum aestivum L.). Planta 164:396–399CrossRef Dehesh K, van Cleve B, Ryberg M, Apel K (1986) Light-induced changes in the distribution of the 36000-Mr polypeptide of NADPH-protochlorophyllide oxidoreductase within different cellular compartments NVP-LDE225 solubility dmso of barley (Hordeum vulgare L.). Planta 169:172–183CrossRef Ryberg M, Dehesh K (1986) Localization of NADPH-protochlorophyllide oxidoreductase in dark-grown wheat (Triticum aestivum) by immunoelectron microscopy before and after transformation of the prolamellar bodies. Physiol Plant 66:616–624CrossRef Ryberg M, Sundqvist

C (1982) Characterization of prolamellar bodies and prothylakoids fractionated Poziotinib concentration from wheat etioplasts. Physiol Plant 56:125–132CrossRef Ryberg M, Sundqvist C (1988) The regular ultrastructure of isolated prolamellar bodies depends on the presence of membrane-bound NADPH-protochlorophyllide oxidoreductase. Physiol 17-DMAG (Alvespimycin) HCl Plant 73:218–226CrossRef”
“Introduction and instrument methodology Since its introduction, now more than 25 years ago (Schreiber et al. 1986), pulse amplitude modulation (PAM) fluorometry in conjunction with the saturation pulse (SP) method has become a routine tool for non-invasive assessment of photosynthetic electron transport in higher

plants, algae, and cyanobacteria (Schreiber 2004; reviews in Papageorgiou and Govindjee 2004). In particular, PAM-measurements of maximal and effective PS II quantum yields via the fluorescence parameters F v/F m = (F m − F o)/F m and Y(II) = (\( F^\prime_\textm \) − F)/\( F^\prime_\textm \) (Genty et al. 1989) have proven of considerable practical relevance. In most applications, Alvocidib order relative changes of these parameters are of primary interest, e.g., caused by photoinhibition or other types of environmental stress. The same is true for the ETR parameter, derived from Y(II), which provides a relative measure of linear electron transport rate (Schreiber et al. 1994). Determination of absolute values of F v/F m, Y(II) and ETR is complicated by non-PS II fluorescence (e.g., originating in PS I or in the phycobilisomes) and by the difficulty to determine the quantum flux density (or photon fluence rate) of PS II-absorbed actinic light (AL), which depends on chlorophyll content and the PS II absorption spectrum as well as on the color of the applied light.

e., Camarophyllus pallidus (Peck) Murrill, and another that will be raised to species rank [Cuphophyllus pratensis var. pallidus (Cooke) Bon] by Dentinger et al. Furthermore, the basidiomes of C. acutoides var. pallidus

are only pale relative to var. acutoides. Cuphophyllus adonis (Singer) Lodge & M.E. Sm., comb. nov. MycoBank MB804128. Basionym: Camarophyllus adonis Singer 1952, Sydowia 6(1–4): 172, TYPE: ARGENTINA, TIERRA DEL FUEGO, Nueva Argentina, Singer check details M351, LIL. ≡ [Hygrocybe adonis (Singer) Boertm., 2002]. Cuphophyllus aurantius (Murrill) Lodge, K.W. Hughes & Lickey, comb. nov. MycoBank MB804129. Basionym: Hygrocybe aurantia Murrill, 1911, [as ‘Hydrocybe’], Mycologia 3(4): 195. TYPE: JAMAICA: ST. ANDREW PARISH; Morce’s Gap, 5,000 ft. elev.,

Dec. 29–30, 1908, 2 Jan. 1909, W.A. and Edna L. Murrill 743, NY. Cuphophyllus basidiosus (Peck) Lodge & Matheny, comb. nov. MycoBank MB804130. Basionym: Clitocybe basidiosa Peck, Bull. N,Y. St. Mus. Nat. Hist. 1(no. 2):5 (1887), [≡ Camarophyllus basidiosus (Peck) Murrill, N. Am. Fl. (New York) 9(6): 389 (1916)]. Cuphophyllus SAHA HDAC cost bicolor (Dennis) Lodge & S.A. Cantrell, comb. nov. Type: Sandlake. Rensselaer County, New York, August, NYS. MycoBank MB804131. Basionym: Clitocybe bicolor Dennis, Kew Bull 7(4): 490 (1952), [≡ Omphalia bicolor Baker & Dale, illeg. (homonym), Fungi of Trinidad and Tobago, Comm. Mycol. Inst. Mycol. MK-0518 manufacturer Pap. 33:91 (1951), ≡Clitocybe ferrugineoalba Singer, Sydowia 9: (1–6): 371 (1955), superfluous, nom. illeg., ≡ Camarophyllus ferrugineoalbus (Singer) Singer, Beih. see more Sydowia 7: 3 (1973), illeg., = Camarophyllus umbrinus (Dennis) Singer ex Pegler, var. clarofulvus Lodge & Pegler]. Type: TRINIDAD: Omphalia bicolor Baker & Dale, Comm. Mycol. Inst. Mycol. Pap. 33: 91 (1951), coll. TRINIDAD, RED Baker and WT Dale, 1947, ICTA 1494, K. Baker and Dale (1951) described Omphalia bicolor from Trinidad, but it is an illegitimate

later homonym of O. bicolor (Murrill) Murrill (1946). Dennis (1952), cited Omphalia bicolor Baker & Dale as the basionym of a ‘new combination’, Clitocybe bicolor. Because an illegitimate name cannot serve as a basionym, Clitocybe bicolor is treated as a nom. nov. under ICN Art. 58.1, as Clitocybe bicolor Dennis (1952). Singer (1955) replaced the illegitimate Baker and Dale name with Clitocybe ferrugineoalba Singer, but this name is superfluous and hence illegitimate (ICN Art. 52) since the legitimate Clitocybe bicolor should have been adopted under the rules. Cuphophyllus fornicatus (Fr.) Lodge, Padamsee & Vizzini, comb. nov. MycoBank MB804132. Basionym: Hygrophorus fornicatus Fr., Epicr. Syst. mycol. (Upsaliae): 327 (1838) [1836–1838], [≡ Camarophyllus fornicatus (Fr.) P. Karst., 1879, Bidr. Känn. Finl. Nat. Folk 32: 227], ≡ Hygrocybe fornicata (Fr.) Singer, Lilloa 22: 152, ≡ Hygrophorus fornicatus Fr., Epicr. Syst. mycol. (Upsaliae): 327 (1838) [1836–1838].

Common SNPs are locations where all strains in the node share the same base call, which is different from the reference call on the resequencing platform. Unique SNPs are locations where just a single strain in the node has a base call that differs from the reference sequence. Differentiating SNPs are locations at which at least two strains in the node have different VX-661 clinical trial base calls. Maximum SNP separation is the number of base calls separating the two most distant members of the node. Differentiating SNPs and maximum SNP separation are both indicators of the degree of diversity

within the node. The detection of diversity is limited by the extent to which our sample set is representative of the variability within each clade in nature. Refer to Figure 2 for the details of strain clustering. The presence of a large number of differentiating SNPs within each HKI-272 order phylogenetic node suggests that a deeper level of discrimination can be achieved by identifying SNPs unique to individual strains. The smallest number of differentiating

SNPs within a phylogenetic node was 71 (A1b strains). The phylogram (Figure 2B) indicates that the closest clade pairings are between A1a/A1b and B1/B2 which is quantitatively in agreement with the SNP differences as shown in click here Additional File 4. Phylogenetic analyses performed by two independent approaches (Bayesian in Figure 2 and maximum likelihood in Additional File 1) showed some differences only at the level of minor clades in the trees. These did not affect the subsequent analyses. Typing assays based on high quality global SNP C59 chemical structure markers Node pairings that discriminated between F. tularensis subspecies or within subspecies were selected for the development of SNP diagnostic typing assays (Figure 2). The four node pairings were node 4 and node 50, node 52 and node 64, node 39 and node 5, and node 8 and node 23 for discrimination of type A vs. type B, B1 vs. B2, A2 vs. A1 and A1a vs. A1b, respectively. A SNP location was selected to differentiate between two

nodes in the tree when all strains belonging to one node contain the SNP call and all strains belonging to the other node contain the reference call at that location. The location of the 32 in silico identified diagnostic SNP markers in the F. tularensis LVS genome are shown in Figure 4. Fourteen SNP loci were in the forward strand, sixteen in the reverse and two loci were in non-coding intergenic regions. The discriminating nodes, SNP location, locus name, gene symbol with product and the role category is described in the Additional File 5. Figure 4 Location of in silico identified diagnostic SNP markers in the F. tularensis LVS genome. Representation of in silico discriminating SNP markers on the F. tularensis LVS genome. The vertical colored bar represents the position of the SNP marker on the LVS with the relevant node pair indicated by color.

Therefore, it is likely that intracellular blood-borne pathogens A. phagocytophilum and B. microti could be present in higher numbers in the cells even if the patient has coinfection with B. burgdorferi. To determine whether detection of B. burgdorferi will be affected by the presence of higher levels of bacteremia and click here parasitemia due to A. phagocytophilum and B. microti, TPCA-1 clinical trial respectively, we mixed genomic DNA of all three pathogens such that the copy number of BmTPK and APH1387 was 100-fold higher than that of the recA copies of B. burgdorferi. Interestingly, we were able to consistently detect ten copies of recA per

one thousand copies of BmTPK and APH1387 in a multiplex assay (Figure 6B). These results in the Figure 6 demonstrate that irrespective of the levels of each pathogen quantity SAHA relative to the other two pathogens, our

multiplex assay can accurately detect and even quantify each pathogen in the mixture. Differentiation of Lyme spirochetes using denaturation curve analysis The PCR assay for B. burgdorferi described in Figure 2 failed to both amplify and detect B. afzelii and B. garinii amplicons efficiently and differentiate these three Lyme spirochetes. Inefficiency of the PCR amplification for B. afzelii and B. garinii amplicons is likely due to the presence of SNPs found in the RecF and RecR primers binding sites in these two species. RecF and RecR primers were designed based upon B. burgdorferi sequence. Therefore, conserved primers RecF3 and RecR3 were selected for amplification of a 287 bp size amplicon of the recA gene by PCR all three species. These primers amplified the gene

fragment from all three species efficiently. To clearly distinguish three Borrelia species using the denaturation profiles, we conducted asymmetric PCR in which RecR3 primer that synthesizes DNA strand targeted by molecular beacon probe was used in excess. This significantly increases the availability of amplified DNA target for the RecA3 probe to bind. SNPs that are present in the probe-binding region of the amplicon affect the temperature required to denature the probe-target hybrid. Indeed, denaturation profile obtained after asymmetric PCR completion was able to distinguish three Borrelia species, with a melt peak of 66°C for B. burgdorferi, 59°C for B. afzelii, and 55°C for B. garinii (Figure 7). Figure 7 Denaturation profiles can distinguish Casein kinase 1 three major Lyme spirochete species. Amplification of 287 bp amplicons from B. burgdorferi, B. afzelii and B. garinii by real-time PCR using conserved primers was followed by a denaturation profile analysis. SNPs in the molecular beacon-binding region of B. burgdorferi, B. afzelii and B. garinii resulted in at least 4°C melting temperature difference between the species such that RecA3 molecular beacon was able to distinguish all three Borrelia species when first derivative analysis of the denaturation profile was conducted. Real-time PCR can successfully detect low numbers of B.

Figure 7 Hamiltonella and Arsenophonus FISH of T. vaporariorum eggs, nymphs and adults. Secondary symbiont-specific probes for Hamiltonella (green) and Arsenophonus (yellow) were used. A, D and G: FISH of Hamiltonella alone in eggs (A), nymphs (D) and adults (G). B, E and H: FISH of Arsenophonus alone in eggs (B), nymphs (E) and adults (H). C, F and I: double FISH of Hamiltonella and Arsenophonus in eggs (C), nymphs (F) and adults (I). Cardinium showed a dual localization pattern, outside and inside the bacteriocyte, with Portiera in the ZD1839 same B. tabaci individuals (Figure 8). Cardinium, like all symbionts that are confined to the bacteriocyte, is transovarially transferred from the mother to the offspring though the egg.

Thus in the egg’s early

developmental stages, it is confined to the bacteriocyte; however, in older eggs (5-7 days), it is also observed outside the bacteriocyte (not shown), and in later nymphal and adult stages, it occupies most of the body tissues, including the bacteriocyte (Figure 8). Cardinium was not detected in T. vaporariorum. Cardinium has been shown by TEM to localize to the bacteriocytes of the A and Jatropha biotypes of B. tabaci [24]. Our PCR screening assay revealed co-localization of Cardinium in B. tabaci populations (in 15 out of a total 236 individuals tested), mostly with Hamiltonella (10 of the 15 Cardinium-containing individuals also harbored Hamiltonella–66% co-localization). In some cases, multiple infections of Cardinium with two (Wolbachia and Rickettsia) or three (Rickettsia, Wolbachia and Hamiltonella) IACS-10759 cell line symbionts were observed. The localization pattern of Cardinium as seen by FISH was different click here from that of the other symbionts that co-localized with it. Localization of Hamiltonella and Cardinium has also been demonstrated in the bacteriocytes of the A biotype together with Portiera, as shown

here. TEM has revealed the presence of Cardinium in the spermatid cytoplasm, residual bodies, and cyst cell KU-60019 cell line cytoplasm of B. tabaci males [25]. Studies on other hosts have reported the presence of Cardinium in a diverse array of tissues, including the reproductive tract [26], fat bodies, and salivary glands [27, 28], as well as inside bacteriocytes surrounded by oogonia in the apical region of the ovary [29]. Figure 8 Portiera and Cardinium FISH of B. tabaci eggs, nymphs and adults. Portiera-specific probe (red) and Cardinium-specific probe (blue) were used. A, C and G: double FISH of Portiera and Cardinium in eggs (A), nymphs (D) and adults (G) under dark field. B, E and H: double FISH of Portiera and Cardinium in eggs (B), nymphs (E) and adults (H) under bright field. C, F and I are shown only with Cardinium probe to emphasize its location inside the bacteriosome. Wolbachia has been previously shown to localize at the circumference of and inside the bacteriocytes. In adults, Wolbachia can also be seen in the abdomen outside the bacteriocyte [22].

The Abs also specifically reacted with an antigen of high molecular weight (≥250 kDa), which likely corresponds to an oligomeric form of BpaC. Immunofluorescence-labeling of non-permeabilized AZD6094 E. coli cells was used to demonstrate that BpaC is displayed on the surface of recombinant bacteria. As shown in Figure  2B, E. coli carrying pCCbpaC is labeled by α-BpaC Abs while recombinant bacteria harboring the control plasmid pCC1.3 are not. Staining of nucleic acids with DAPI verified that equivalent numbers of bacteria were examined. Figure

2 Analysis of E. coli recombinant strains. Panel A: Whole cell lysates were resolved by SDS-PAGE, transferred to PVDF membranes and analyzed by western blot with Abs against BpaC. Lane 1, E. coli (pCC1.3); lane 2, E. coli (pCCbpaC). MW markers are shown to the left in kilodaltons. Panel B: Non-permeabilized E. coli strains were fixed onto glass slides and fluorescently-labeled with DAPI (blue)

and with α-BpaC Abs (red). Bacteria were visualized by microscopy CFTR inhibitor using a Zeiss LSM 510 Meta confocal system. Representative microscopic fields are shown. Panel C: E. coli strains were incubated with epithelial cells for 3-hr. Cells were then washed to remove unbound bacteria, lysed, diluted and spread onto agar plates to enumerate bound bacteria. The results are expressed as the mean percentage (±standard error) of inoculated bacteria attached to epithelial cells. Asterisks indicate that the increased adherence of E. coli (pCCbpaC), compared to that of E. coli carrying the control plasmid pCC1.3, is statistically significant (P value shown in PI3K inhibitor parentheses). Adherence assays were performed in duplicate on at least 4 independent occasions. Quantitative adherence assays revealed that E. coli expressing BpaC binds to HEp-2 (laryngeal) and A549 (lung) human epithelial cells at levels 7- and 5-fold greater than bacteria carrying pCC1.3, respectively (Figure  2C). BpaC expression was also found to increase adherence by 7-fold to normal human bronchial epithelium (NHBE) cultured in an air-liquid interface system, which has been shown to represent an environment similar to the airway lumen in vivo [54, 63, 64].

These results demonstrate that BpaC mediates adherence to respiratory epithelial cells. Burkholderia pseudomallei and B. mallei are facultative intracellular bacteria that replicate within several eukaryotic cell types. Moreover, autotransporter adhesins BIBW2992 purchase frequently perform additional functions including invasion [1], intracellular motility [11], and survival inside host cells [10]. For these reasons, we examined the ability of E. coli expressing BpaC to invade epithelial cells and survive within murine macrophages. The results of these experiments indicated that BpaC does not substantially increase invasion of epithelial cells, phagocytosis of recombinant bacteria by J774A.1 murine macrophages, or survival inside these immune cells (data not shown).