5), the number of cycles at which fluorescence was reached the threshold line was 31.09 on the lipase gene and 5.09 on 16S rRNA, respectively.

In contrast, when we used RNA sample from the cells cultured in NB (3.0) the number of cycles was 28.00 on the lipase gene and 4.98 on 16S rRNA. Consequently, we estimated by the ΔΔCt method that the relative transcriptional level of lipase gene in 3% NaCl is 7.8 times higher www.selleckchem.com/products/midostaurin-pkc412.html than that in 0.5% NaCl. Moreover, as shown in Figure 8, the densities of the samples recovered at 12 and 24  hrs from the culture in NB (3.0) were certainly higher than those from the culture in NB (0.5), showing that the gene for the lipase is well transcribed in A. sobria under the condition of 3.0% NaCl. Transcription of the lipase gene by A. sobria in NB (3.0) at 12 and 24  hrs was more active than in NB (0.5). As shown, the amount of lipase in the culture supernatant from culturing in NB (3.0) was low compared with that in NB (0.5) (Fig. 1); however, transcription of the lipase gene by A. sobria was not suppressed in 3.0% NaCl and the mRNA of the lipase gene was produced well (Fig.  8). We therefore considered that the posttranscriptional process to become mature lipase had been disrupted in NB

(3.0). As shown in Figure 4, lipase expresses esterolytic Selleckchem EPZ 6438 activity; we therefore examined the esterolytic activity of the culture supernatant, using pNpp Bay 11-7085 as the substrate. The supernatant

from the 24  hr culture in NB (0.5) expressed esterolytic activity, but that from the culture in NB (3.0) did not (Fig. 9). These findings suggest that the three-dimensional structure of the lipase differs from that of the active form when A. sobria is cultured in NB (3.0), and that the lipase produced in NB (3.0) is degraded by bacterial intracellular proteases. This explains why the amount of lipase in the supernatant from culture in NB (3.0) was low compared with that in NB (0.5). In this study, we found a protein of A. sobria whose production in the milieu was suppressed by NaCl in the medium. Analysis revealed that this protein is lipase; it degraded tributyrin, and expressed esterase activity against pNp-fatty acyl esters. We then cloned the lipase gene and determined the nucleotide sequence. The lipase substrate binding signature sequence (GLKVHFLGHSLGA) was contained in the sequence (28), supporting the contention that the protein is a lipase. The amino acid sequence deduced from the nucleotide sequence had 78.6% identity with the lipase of A. hydrophila AH-3 (11). Merino et al. have examined the substrate specificity of the lipase from A. hydrophila AH-3 (11). They found that E.

These results suggested that the construct might have been submitted through the germline although no proof for genome integration was obtained. Taken together, Selleckchem GSK2126458 the articles by Heyers et al. and Beckmann et al. (12,18) show proof of principle that it might be possible to enter the germline using transformed miracidia. A further publication by Wippersteg et al. (19) reports the tissue-specific

expression of GFP driven by the promoters of two S. mansoni protease genes cathepsin L1 and cathepsin B2. As predicted from earlier reports (20), the S. mansoni cathepsin L1 promoter drove GFP expression throughout the gut whereas transformation with the SmCB2 (21) construct resulted in GFP fluorescence localized in the tegument. Particle bombardment was also employed by Beckmann et al. (18). Here, different reporter gene constructs using the S. mansoni actin1 regulatory elements and GFP as reporter ABT-263 cost gene were used for transient transformation of adult males and sporocysts. A 445-bp promoter fragment was sufficient for transcription initiation in larvae or adults as confirmed by confocal microscopy. Actin gene characteristic TATA, CArG and CAAT boxes were identified in the promoter, suggesting that it is functionally conserved between vertebrates and invertebrates. However, a vertebrate-specific intron containing an additional regulatory CArG box was not found indicating that

the regulation of SmAct1 transcription depends exclusively on its promoter region. In addition, the authors showed GFP expression in the tegumental area, especially the tubercles, in the muscle tissue

and weakly in the parenchyma of the male worms. The most recent publication describing the transfection of schistosomes Loperamide using biolistic methods was only published last year (22). Here, modified reporter gene constructs containing 5′ and 3′ regulatory regions of protease genes (cathepsins F and D) were used to transfect immature adult worms. The results obtained showed that there was a minor improvement of the intensity and distribution of the reporter signal in constructs containing parts of the ORF and/or 3′ gene-specific genomic fragments. However, reporter signals were found in tissues other than the gut and the authors suggest that this might represent dysregulated transcription which could impact on the utility of biolistics as a tool to accurately profile spatial expression of transgenes. Electroporation as a tool to introduce plasmid-based DNA constructs was tested in S. japonicum and S. mansoni (23,24). Yuan et al., using a commercial plasmid (pEGFP-C1), showed that the cytomegalovirus (CMV) promoter was able to drive EGFP expression in primary cell cultures of S. japonicum. Introduction of the plasmid into schistosomula and adult worms by electroporation led to EGFP expression as demonstrated by RT-PCR, Western blotting and confocal microscopy with EGFP fluorescence detectable along the tegumental surface of the worms (24).

Importantly, adoptive transfer of antigen-loaded DCs stimulated with GLA-SE in vivo was sufficient to induce specific Th1-cell responses in naïve mice. In contrast, DCs stimulated with emulsion alone were unable to prime T cells. Since the DCs also had to express MHCII, this indicates that their T-cell immunizing function required direct presentation of antigen in the mice primed by adoptively transferred DCs. To our surprise, Talazoparib manufacturer antibody responses were unaltered after CD11c+

depletion. In this paper, we only analyzed total IgG responses. Maturation of DCs may still have a role in antibody affinity. The type of immune response that eliminates an infection depends on the type of pathogen. Induction of CD4+ T-cell responses by vaccination was Osimertinib cell line associated with diminished simian immunodeficiency virus (siv) replication after intrarectal challenge and decreased HIV acquisition

in the Thai HIV vaccine trial 44, 45. The results presented here demonstrate that GLA-SE is an efficient adjuvant for the generation of HIV-gag-specific Th1-cell immune response. IFN-γ was produced in large amounts by antigen-specific T cells in both spleen and lymph nodes. HIV-1 vaccines will most likely need to induce mucosal immunity. Mucosal tissues are the major site of natural HIV transmission and the reservoir for HIV replication quickly leading to a rapid loss of T cells in the intestine 46, 47. In addition, Th1 type CD4+ T cells are known to improve the mobilization of the cognate antigen-specific CD8+ T cells to a site of infectious challenge 48, 49. Thus GLA-SE has the capacity to adjuvant a protein vaccine to

induce mucosal immunity that potentially is valuable to limit viral replication and curtail systemic dissemination. Previous studies successfully showed that local immune responses were able to prevent virus spread from the gut mucosa into the systemic circulation 50–52. However, the general belief is that local but not systemic immunization is required to induce robust mucosal responses 53–55. Interestingly, we Methocarbamol found that s.c. injection of the GLA-SE and anti-DEC-HIV gag p24 vaccine was able to induce strong mucosal T-cell responses. Immunization with HIV-gag targeted or untargeted protein plus GLA-SE induced a broad range of different antibody isotypes and therefore a combination of Th1 and Th2-cell responses. This contrast, i.e. with polarized Th1 T-cell responses, may be explained by the different requirement for DC priming. This result is consistent with previous studies where addition of GLA-SE gives a mixed Th1/Th2-cell response but also increases the IgG2/IgG1 ratio to an existent M. Tuberculosis and Influenza vaccine 27, 56.

70,71 This high risk is similar to that seen with essential hypertension and it is held that the maternal vascular adaptation to placental growth is limited in these women and therefore it is a maternal predisposition rather than Erlotinib research buy placental events per se.72 The rate of preeclampsia in women with end stage renal disease approaches 50%.6,73,74 The impact of underlying undiagnosed renal disease was recently explored by looking at the risk of subsequent renal biopsy in

women who had been diagnosed with preeclampsia75 and their risk of end stage renal disease.76 Although the risk was increased, the absolute number of women was small, and this by no means explains the majority of cases of preeclampsia. The overlap with other chronic renal lesions such as focal segmental glomerulosclerosis provides an area of significant diagnostic difficulty.77 Packham et al. showed a very high incidence of underlying renal disease in early severe preeclampsia (resulting in premature delivery).78 learn more The risk of preeclampsia associated with early pregnancy microalbuminura supports these findings.79 The possibility remains that some of the structural changes seen in biopsies after preeclampsia may directly result from the severity of the disease.80 The monitoring of progressive renal function

(serum creatinine) in patients with underlying renal disease is problematic. In the presence of renal disease, proteinuria and hypertension per se are no longer diagnostic features of preeclampsia. It is the presence of other clinical markers such as foetal growth restriction (determined by sequential foetal ultrasound Teicoplanin and regional blood flow), liver function test abnormalities and

disseminated intravascular coagulation (DIC), or maternal symptoms that confirm the diagnosis. A rapid increase in creatinine without any other explanation in women with renal disease may imply superimposed preeclampsia. Similarly, a rapid rise in blood pressure or escalating antihypertensive requirements may imply superimposed preeclampsia in these women. Pregnancies subsequent to kidney donation had previously been thought to confer no increased risk of a hypertensive disorder of pregnancy. Recent work has demonstrated that this may not be the case. Reisæteraet al. conducted a large registry-based retrospective review.81 They demonstrated that the occurrence of preeclampsia was greater after kidney donation (5.7%) compared with women who had pregnancies prior to kidney donation (2.6%). This result was independently confirmed by Ibrahim et al. who undertook a single centre retrospective review.82 They showed that the risk of preeclampsia in women pregnant prior to kidney donation (0.8%) was lower than the rate of preeclampsia post kidney donation (5.5%). Renal transplant donation by women may lead to a higher (three times) baseline rate of preeclampsia despite otherwise normal renal function82 although the baseline rates of preeclampsia were extremely low in the studies quoted.

Currently, belimumab is only approved for treatment for Veliparib molecular weight non-renal SLE. Despite the success of belimumab, the efficacy and safety of antagonism of the TACI receptor needs further evaluation. In this context, the phase III study to examine atacicept (a soluble, fully human, recombinant fusion protein that targets the TACI receptor) in combination with corticosteroids

and mycophenolate mofetil was prematurely terminated due to profound drop in serum immunoglobulins and fulminant sepsis among the study subjects.[51] IL-17 is a type I transmembrane protein isolated initially from a rodent CD4+ T cell cDNA library.[52] This potent pro-inflammatory cytokine is primarily released by activated T lymphocytes (‘Th17 cells’ being the most vibrant producer). As its name implies, these Th17 cells are a subset FK506 nmr of CD4+ T

lymphocytes named for its signature cytokine IL-17. The distinctive features of Th17 lymphocyte include their origination from naïve T cells and its characteristic cytokine profile when aptly primed by exclusive transcription factors. Apart from Th17 lymphocytes, recent data showed that neutrophils, gammadelta T cells and mast cells also abundant express IL-17.[53, 54] A total of six family members (IL-17 A to F) and five receptors (IL-17R A to E) were identified in the IL-17 family.[55] IL-17 possesses potent capacity to recruit monocytes and neutrophils, assist T cell infiltration and upregulate adhesion molecule expressions.[56, 57] Several important cytokines such as IL-6, IL-21 and IL-23 are in intimate association with IL-17. IL-6, when combined with transforming growth factor (TGF)β, was capable of inducing murine naïve T cells to differentiate into Th17 cells.[58, 59] On the contrary, mice deficient in IL-6 would experience defective Th17 differentiation.[58] These observations implied that the presence of an inflammatory

signal is required to transform the naïve T cells to become pro-inflammatory. IL-21 is another factor which exerts a robust influence for Th-17 differentiation. Lonafarnib cell line Unlike IL-6, IL-21 is synthesized by the Th17 cells and T-follicular helper cells but not by antigen presenting cells and, hence, been proposed to act in an auto-amplifier fashion for the Th17 response.[59] Animal studies have also demonstrated that Th17 can be generated from naïve T cells in an IL-23-dependent fashion.[60] In addition, IL-23 elicits IL-17 secretion by memory T cells.[61] Taken together, these findings suggested the IL-23/IL-17 axis may be a novel yet important pathway in the pathogenesis of autoimmune disorders. Although naïve CD4+ T cells can differentiate into Th1, Th2 or Th17 effector subsets, the cytokine milieu characteristic of SLE patients (IL-2 poor but IL-6 and IL-21 rich) favours Th17 expansion.

Thus, a microorganism will only pose a threat to the fetus, if the TLR-negative syncytiotrophoblast layer is breached and the pathogen has entered either the placental villous or the decidual compartments.38,39 TLR expression has also been reported in other types of cells in the placenta. Hofbauer cells, a type of macrophage in the placental villi, were shown to express TLR4 in the term placenta by immunohistochemistry.41 Most recently, PF-01367338 price Ma et al. evaluated the expression of TLR2 and TLR4 in third-trimester placentas by immunohistochemistry.42 They observed stronger expression of TLR2 in endothelial cells and macrophages and weaker expression in syncytiotrophoblast and fibroblast, while staining for TLR4 was most prominent

in syncytiotrophoblast and fibroblast.

These findings suggests that not only immune cells but also trophoblasts and other types of cells within the placenta have a capacity to respond to the invading pathogens and may be involved, similar as the innate immune system, in the physiological protection of the placenta. In contrast to placental tissue, very little is known about the expression of TLRs in the decidua. Recently, two studies described the expression of TLRs in the human decidua. Krikun and coworkers reported the presence of mRNA for all 10 TLRs in first trimester and term decidua. They also demonstrated the protein expression for TLR2 and 4 in first-trimester decidual cells.1 These results were also confirmed by Canavan and Simhan43, using find more immunocytochemistry, described the expression of TLR1-6 in primary cultures of decidual cells isolated from third-trimester pregnancies. As for amnion, one study showed that TLR4 is expressed at the apical side of amniotic epithelium, indicating that TLR4 is poised to monitor amniotic fluid for pathogens.42 Dulay et al.44 demonstrated the presence of soluble TLR2 in amniotic fluid, which may interfere the recognition of TLR2 ligands

by Nutlin-3 mw TLR2. These results suggest that TLR system plays a role in regulating intra-amniotic inflammatory response to microbial pathogens. Given that TLRs are widely expressed at the maternal–fetal interface, not only by immune cells but also by non-immune cells such as trophoblasts, decidual cells and amniotic epithelium, the next question is what is the role of TLRs in these cells and their influence in regulating local and systemic immune responses during pregnancy. Here, we will discuss possible functions of TLRs at the maternal–fetal interface. TLR2 and TLR4 function at the maternal–fetal interface is well described because they are the principal receptors for recognition of bacterial cell wall components. Holmlund et al. firstly reported TLR function in placenta. They showed that stimulation of TLR2 and TLR4 with zymosan and LPS-induced IL-6 and IL-8 production by third-trimester placental cultures, which indicated that trophoblast have a capacity to recognize microorganisms and initiate immune responses by activating immune cells.

It is possible that their reduced inflammatory responsiveness is beneficial in protecting the host from collateral damage that could otherwise result from the presence of large numbers of inflammatory cells. Alternatively, suppression of macrophage responsiveness by targeting TLRs on the HSPCs from which they are produced could be an immune evasion strategy employed by invading organisms. Future

studies will also be required to dissect the mechanisms underlying the specification of myeloid differentiation and function. One key question will be whether TLR signal transduction pathways in HSPCs are similar Y-27632 mouse to those in differentiated cells such as macrophages and neutrophils. It is likely that TLR signaling pathways in HSPCs are at least partially overlapping with differentiated cells, but since TLR signaling in HSPCs uniquely controls myeloid differentiation, it is possible that HSPC TLRs may induce distinct signals in these cells, for example to activate transcription factors and induce Antiinfection Compound Library chromatin modifications that specify myeloid

cell fate choice. Our studies on the functional consequences of exposure of HSPCs to Pam3CSK4, showed that exposed HSPCs produce soluble factors that can act in a paracrine manner to influence the function of macrophages produced by unexposed HSPCs [49]. The identity of these factors is not currently known, but candidates include several cytokines known to be induced by TLRs in differentiated cells, such as type I and II IFNs, TNF-α and IL-6, which have previously been reported to have myelopoietic properties [5, 7, 9, 10]. Thus, it is possible that myeloid differentiation may be specified PtdIns(3,4)P2 by TLRs in HSPCs without the activation of unique signal transduction pathways. The answers to all these questions will provide new insights into the role of TLRs in host–pathogen interactions, emergency myelopoiesis, and the development of immunity against infection,

which may reveal novel targets for antimicrobial intervention. Research in the M. L. Gil laboratory is supported by grants SAF2010–18256 (Ministerio de Economía y Competitividad, Spain) and ACOMP/2013/168 (Generalitat Valenciana, Valencia, Spain). H. S. Goodridge received a Scientist Development Grant from the American Heart Association and an R21 (AI082379) from the NIH. The authors declare no financial or commercial conflict of interest. “
“Citation Iwasawa Y, Kawana K, Fujii T, Schust DJ, Nagamatsu T, Kawana Y, Sayama S, Miura S, Matsumoto J, Adachi K, Hyodo H, Yamashita T, Kozuma S, Taketani Y. A possible coagulation-independent mechanism for pregnancy loss involving β2glycoprotein 1-dependent antiphospholipid antibodies and CD1d. Am J Reprod Immunol 2012; 67: 54–65 Problem  β2glycoprotein1 (β2GP1)-dependent antiphospholipid antibodies (aPL) increase the risk for recurrent pregnancy loss.

Donor proteinuria in the absence of other significant factors influencing organ acceptance, appears to be of little importance in influencing graft outcome. Larger studies are required to further examine this. 254 AMBULATORY VS OFFICE BLOOD PRESSURE MONITORING IN RENAL TRANSPLANT RECIPIENTS J AHMED, V OZORIO, M FARRANT, W VAN DER MERWE North Shore hospital, RGFP966 in vitro Auckland,

New Zealand Aim: To investigate correlation between office (OBPM) and ambulatory (ABPM) blood pressure monitoring in renal transplant recipients (RTR). Background: Hypertension is common post renal transplant and has adverse effects on cardiovascular and graft health. Nocturnal hypertension, which is also implicated in poor outcomes, can only be diagnosed via ABPM. ABPM is increasingly being recognized as a better method of measuring BP with discrepancies between office (oBP) and ambulatory BPs (aBP) being noted in RTR. Methods: We undertook a retrospective analysis of 98 renal transplant recipients (RTR) (40% female, average age 55) in our unit and compared oBP and aBP recordings. Baseline demographic data was recorded along with www.selleckchem.com/products/MDV3100.html eGFR, proteinuria, medications and co-morbidities. Results: ABPM revealed 28.5% and 13.2% had concordant normotension and hypertension

respectively. There was a discordance between OBPM and ABPM in 58% of patients with 53% due to masked hypertension (of which 34% were due to isolated nocturnal hypertension) and 5% had white coat hypertension. Overall mean systolic BP was 3.6 mmHg (0.5–6.5) and diastolic BP 7.5 mmHg (5.7–9.3) higher via ABPM than

OBPM (95% confidence). This was independent of eGFR, proteinuria, transplant time/type and comorbidities. 41% of patients had their management changed after results from ABPM. Conclusions: There is a significant discordance between OBPM and ABPM with a predominance of masked hypertension. The results of ABPM changed management Cobimetinib cost in a significant proportion of patients. ABPM is the only means to diagnose nocturnal hypertension and should be routinely offered as part of hypertension management of RTR. 255 ANNUAL SKIN CANCER INCIDENCE IN RENAL TRANSPLANT RECIPIENTS 1997–2013: A SINGLE CENTRE EXPERIENCE G DAS1, B TAN1,2, K NICHOLLS1,3 Departments of 1Nephrology and 2Dermatology, The Royal Melbourne Hospital, Melbourne; 3Department of Medicine, The University of Melbourne, Melbourne, Australia Aim: To evaluate annual incidence of skin cancers (SC) in renal transplant recipients (RTR) in our hospital (RMH) from 1997 to 2013. Background: ANZDATA data indicates that RTR have a 100 fold increased risk of developing SCC. There is no clear evidence that SC incidence has fallen over time, or with different immunosuppressive regimens. Methods: We retrospectively studied RMH patients transplanted between January 1997 and December 2013, extracting data from medical records, our departmental database, and pathology reports.

However, this observation calls into question the relevance of studying mitochondria from tissue not considered to be a primary target in the disease; selective recruitment suggests the presence of unique mitochondrial spinal cord components interacting with mSOD1 in such a way as to encourage dysfunction see more [69]. Oxidative stress has been implicated as part of the pathogenic process in ALS and may derive from defective oxidative phosphorylation [45]. Investigation of ALS patients has identified: (i) a sporadic microdeletion in the gene encoding a subunit of cytochrome c oxidase, resulting in defective assembly of the holoenzyme

[70]; (ii) evidence of decreased activity of respiratory chain complexes I, II, III, IV in post-mortem central nervous system tissue [71]; (iii) increased levels of oxidized ETC cofactor CoQ10 in SALS cerebrospinal fluid (CSF) [72]; and (iv) increased levels of ROS and lactate in blood [73]. Studies in mSOD1 transgenic mice have supported these observations. A reduction in activity of the individual ETC complexes, beginning with a presymptomatic early decrease in activity of complex I and leading to

decreased function of complex IV after disease onset, has been observed in the ventral horn motor neurones of mSOD1 G93A mice [58,74,75]. Further investigation found this decrease in ETC activity could be rescued with the introduction of exogenous cytochrome c in a reduced state. Thus,

cytochrome c has been implicated this website as a major defective protein in the respiratory chain, specifically in its oxidized form [76]. Defective oxidative phosphorylation leads to the generation of ROS, which is devastating for both the mitochondria and the cell [58,77–79]. Studies of Tyrosine-protein kinase BLK patient CSF have found evidence of this free radical damage, such as an increased concentration of 3-nitrotyrosine, indicative of peroxynitrite mediated nitration of protein tyrosine residues [80]. This has been supported by mSOD1 mouse models, which show evidence of oxidative stress in spinal cord motor neurones, including enhanced oxyradical production, carbonylation of proteins and peroxidation of lipids in the mitochondrial membrane, all resulting in severe consequences for the mitochondria, and indeed, the cell [78]. Peroxidation of the anionic IMM lipid cardiolipin disrupts its hydrophobic and electrostatic interaction with cytochrome c, resulting in high levels of the protein in the IMS [76,81–83]. This renders the cell vulnerable to apoptosis, as well as disrupting oxidative phosphorylation [81–83], and exacerbates the levels of ROS being produced by the mitochondria, resulting in cell toxicity [82]. Impaired calcium buffering by motor neurone mitochondria may be a key factor in the pathogenesis of ALS.

The wztYS-11 was introduced into strain 455, and the changes in the phenotype were observed by SEM. The fragment including the wztYS-11 ORF was amplified by PCR using the primers wzt-EcoF and wzt-PstR (Table 1). An EcoRI site or a PstI site (Table 1, underlined) was introduced into the 5′ end of the PCR product. The reaction

mixture contained 10 ng μL−1 genome DNA of strain YS-11, 1 × PCR buffer, 0.2 mM dNTPs, 0.5 μM each primer, and 25 mU μL−1 KOD dash DNA polymerase (Toyobo, Osaka, Japan), and sterile-distilled water was added to the mixture to a final volume of 50 μL. The reaction conditions were as follows: 94 °C for 6 min, 35 cycles of 94 °C for 1 min, 60 °C for 1 min, and 72 °C for 1 min, and 72 °C for 2 min with a PCR thermal cycler (Takara Bio). The PCR product purified with the QIAquick gel extraction kit (Qiagen) was digested with EcoRI and PstI (Takara Bio), and ligated buy BMN 673 to the plasmid vector pSTV28 (Takara Bio), which was predigested with the same combination of restriction enzymes. Ligation was performed using a DNA ligation kit ver. 2.1 (Takara Bio)

according to the manufacturer’s directions. Escherichia coli DH5α (Invitrogen) was transformed with this ligation solution. Dabrafenib manufacturer The constructed plasmid, named pWZT, was purified from a colony grown on TSAY containing 20 μg mL−1 of chloramphenicol. Ten nanograms of constructed plasmid was added to 50 μL of the competent cell of strain 455, and transformation was carried PAK6 out as described above. Measurement of the viscosity of spent culture media and SEM observation for the presence of meshwork-like surface structures were carried out on the recombinants grown on the TSAY containing 50 μg mL−1 of kanamycin and 20 μg mL−1 of chloramphenicol. The wztYS-11 on the pWZT was fused with the α-peptidase gene on pSTV28 so that the viscosity and the cell surface-associated phenotype were examined under culture conditions with or without 1 mM isopropyl-β-d(−)-thiogalactopyranoside (IPTG; Wako Pure Chemical Industries, Osaka, Japan). Strain 455 with pSTV28 and E. coli DH5α with pWZT were used as controls. The bacterial strains and plasmids used in this study are listed

in Table 2. Escherichia hermannii strains YS-11 and 455-LM with meshwork-like structures were compared with those of strains 455 and ATCC33650 that lacked this phenotype for the ability to induce abscess formation in mice. Bacterial strains were cultured in TSBY for 12 h (early stationary phase). Five hundred microliters of bacterial suspensions (107–109 CFU mL−1) were injected subcutaneously into the inguen of each BALB/c mouse (male, 4 weeks; three mice per strain). Changes in abscess lesions were recorded photographically using a camera (Nikon FIII, Nikon, Japan) set at a fixed magnification for five consecutive days. Stock cultures of YS-11 were inoculated into TSBY and grown for 48 h. The viscosities of the spent culture media were measured using a rotary viscometer.