Each experimental group contained 20 mice. To investigate the effects of CHIR-99021 IAL treatment, mice were administered 100 μL of IAL subcutaneously 2 h after infection with S. aureus and then at 12-h intervals thereafter for a total of six doses. The control mice were treated with 100 μL

of sterile PBS on the same schedule. For histopathologic analysis, mice were euthanized with anesthesia followed by cervical dislocation. The lungs were placed in 1% formalin. Formalin-fixed tissues were processed, stained with hematoxylin and eosin, and visualized by light microscopy. The experimental data were analyzed with spss 12.0 statistical software. An independent Student’s t-test was used to determine statistical significance, and a P value < 0.05 was considered to be statistically significant. As presented in Table 1, the MIC values for IAL that were tested against S. aureus strains were > 1024 μg mL−1, which indicates that IAL does not inhibit the growth of S. aureus. Four α-toxin-producing S. aureus strains were cultured with increasing concentrations of IAL, and the culture supernatants were tested for the ability to perform hemolysis. As shown in Fig. 2a, treatment with IAL repressed the hemolytic activity in culture supernatants. The hemolytic units (HUs) in drug-free

culture fluids were 42.4, 38.2, 110.7, and 46.4 for S. aureus ATCC 29213, BAA-1717, Wood 46, and 8325-4, respectively. When 8 μg mL−1 of IAL was added to the media, the click here Hydroxychloroquine HUs were 1.2, 4.5, 14.1, and 0.6, respectively. Notably, a dose-dependent (1–8 μg mL−1) attenuation of hemolysis was observed in all the tested strains. Furthermore, drug-free culture supernatants preincubated with 8 μg mL−1 of IAL exhibited no difference in HUs, indicating that the reduction in hemolytic activity was not owing to direct interaction of IAL on α-toxin (data not shown). α-Toxin is the major toxin produced by S. aureus and can cause hemolysis of rabbit erythrocytes. Therefore, S. aureus culture supernatants were subjected to Western blot analysis to determine whether the reduced hemolytic activity was attributed to a decrease in the production of α-toxin. Ten nanograms of purified

α-toxin was used as a positive control. As expected, IAL reduced the production of α-toxin in a dose-dependent manner (Fig. 2b). The addition of 1 μg mL−1 IAL resulted in an undistinguished reduction in α-toxin; however, at 8 μg mL−1, no immunoreactive α-toxin antigen could be detected in the supernatants of the tested strains. The results were confirmed with hemolysis assay. Transcription of hla in S. aureus 8325-4 was measured using real-time RT-PCR. The expression of virulence factors in S. aureus is controlled by several global regulatory systems such as Agr, Sar, Sae, and Rot (Cheung & Zhang, 2002). The accessory gene regulator (Agr) is one of the best-characterized global regulatory systems and is known to regulate α-toxin.

1 About 50 million people travel each

year from industrialized EPZ5676 mouse countries to tropical or subtropical destinations.2 Although estimations on the number of children traveling internationally are limited, travel data for US residents indicate that about 1.5 to 2 million US Americans of age under 16 years travel annually to tropical or subtropical countries.3,4 In the UK, imported diseases account for 2% of pediatric hospitalization.5 Physicians have to be aware that potential pathogens differ in various factors, such as the population of travelers,6,7 the travel destination,8,9 and the incubation period of pathogens typical or specific for the tropics and subtropics.10–12 Travel medicine standards are increasingly based on evidence and moving away from reliance on single expert opinions. Nevertheless, previous studies on pediatric travel-related morbidity were using post-travel questionnaires13,14 or consisted only of small

study populations from single centers with focus on individual diseases.15–20 A certain number of multicentric reviews were performed; however, most of them focused on the demographic characteristics21 and on diagnoses without linking them to the symptoms presented by young patients returning from travel. This study analyzes systematically demographic, travel, and clinical data of travelers of age <20 years returning from tropical and subtropical countries and presenting at the outpatient travel clinic of the Department of Infectious Diseases and Tropical Medicine (DITM) in Munich, Germany. Stratified into age Trichostatin A groups, the study describes the spectrum of imported infectious diseases and syndromes among the study population. Furthermore, it evaluates the risk for acquiring infectious diseases and syndromes

for different travel destinations. From January 1999 through December 2009, 42,863 patients with symptoms or individuals for medical checkup presented at the DITM, including 2,558 (6.0%) individuals of age <20 years. Two criteria were defined to include them into this study: the individuals who had a clinically or laboratory confirmed diagnosis (1,380 subjects fulfilled HA-1077 concentration criteria: 53.9%) and the individuals who had traveled to a tropical or subtropical country before presentation (1,173 subjects fulfilled criteria: 45.9%). Overall, 890 (34.8%) travelers of age <20 years fulfilled both criteria (study population). Among them, 687 (77.2%) individuals had a national health insurance [419 (47.1%) with referrals from physicians of former consultations, 268 (30.1%) individuals without referrals]. The consultation fees of the remaining 203 (22.8%) individuals were paid otherwise (eg, private health insurance, privately, employers of parents, or others). Demographic data [sex, age, and origin (country of birth)] were analyzed for the whole study population of 890 travelers (Table 1).

[41-43] Our results indicate that anticipation also can have a more prevailing effect. An alternative explanation would be viewing the BP increase as a consequence of physical activity associated SP600125 price with travel preparations (eg, packing). However, this seems unlikely considering the limited physical demands associated as well as the morning and evening BP assessment. The continued elevation of diastolic BP suggests increased cardiovascular arousal due to coping with the novel surroundings as found in experimental research.[19] Evidence for increased cardiovascular activity in association with travel and a CoR previously has been found in a study on the prevalence of myocardial infarction

during vacation, which was significantly more common

during the first 2 days.[44] Total average BP increases were 2 to 3 mmHg with no indication of morning–evening differences or heightened responses in certain subgroups. Thus, considering the small magnitude and the transient nature of the BP responses, these cannot be regarded as clinically significant. The return of BP to baseline on day 5 of the stay illustrates the transient nature of the CoR response, but also may be a preliminary reaction to spa-treatment, which tends to lower BP.[45] On the first night at the health resort individuals reported poorer sleep compared to baseline. This finding corroborates the “first-night effect” in sleep research.[12-14] The present result indicates that this phenomenon is not limited to the sleep laboratory, but may be a common reaction to sleeping in any novel environment. However, DNA Damage inhibitor verification with objective sleep measures would be necessary. Morning mood did not respond to the CoR, contrary to our expectation. Several explanations can be put forth to account for this lack of response. First,

mood may not be a measure sensitive to the psychological demands associated with a CoR. Possibly, other variables such as anxiety or perceived tension would have been more adequate. Second, a potential deterioration of mood related to the anticipation of and/or exposure to the novel environment may have been masked by positive expectations, known as the “rosy view” phenomenon, and the curiosity induced by novelty.[46, 47] At this point, a more detailed psychological mapping of the responses to a CoR seems warranted the for future studies. The improvement of mood on the fifth day after CoR is presumably related to a respite from work and the corresponding psychological recovery.[40, 48, 49] The responses to the CoR were not associated with demographic, medical, or travel-related variables except for the retirement status, those retired showing a slightly larger diastolic BP response to the CoR. Whether individuals previously had visited the resort or not also did not affect the responses possibly due to the minimum of 2 years between the current and past visit.

, 1987; Tsuge et al., 2002). One unit of GUS activity was defined as nanomoles of p-nitrophenol released per hour. Simultaneously, the concentration of bacterial proteins per assay was examined. Bacterial cells in 1 mL of culture were pelleted and resuspended with 100 μL of B-PER Bacterial Protein Extraction Reagent (Pierce) to extract bacterial proteins. Protein concentrations were measured using a Protein

Assay kit (Bio-Rad) and bovine serum albumin as a reference. GUS activity of each sample was calculated as U μg−1 bacterial proteins. Total RNA was extracted from bacteria incubated for 16 h using an RNeasy Mini Kit (Qiagen). Two hundred nanograms of each RNA sample was used for the synthesis of cDNA using a reverse-transcriptase ReverTra-Ace (Toyobo), followed by PCR with a DNA polymerase BlendTaq (Toyobo). Amplified fragments were visualized by staining with ethidium bromide after agarose gel electrophoresis. As a control, 16S Ku0059436 rRNA gene was used. The gene-specific primer sets used in this study are listed in Table S2. Xoo strains incubated in XOM2 for 24 h were diluted with the medium to A600 nm=0.3 (c. 108 CFU mL−1). Bacterial cells in 300 μL of diluted culture were

pelleted Bafilomycin A1 and resuspended with 150 μL Laemmli buffer (Laemmli, 1970), then used for SDS-PAGE, followed by Western blot analysis using rabbit anti-Hpa1 (Tsuge et al., 2006) as the primary antibody and alkaline phosphatase-conjugated anti-rabbit IgG as the secondary antibody (Bio-Rad). The Bordetella pertussis calmodulin-dependent adenylate Monoiodotyrosine cyclase (Cya) reporter assay was conducted as described previously (Sory & Cornelis, 1994; Furutani et al., 2009). Bacterial strains with a plasmid harboring an effector gene (xopR) and

cya fusion gene (Furutani et al., 2009) were suspended in distilled water (A600 nm=0.3), and then infiltrated into Nicotiana benthamiana leaves using a needleless syringe. After 3- and 6-h incubations, the translocation of the fusion protein into plant cells was examined by measuring cAMP accumulation using the cAMP Biotrak enzyme-immunoassay system (GE Healthcare). Bacterial strains grown on NBY medium were washed twice and resuspended in distilled water to a concentration of A600 nm=1.0. Samples (1 mL) of the bacterial suspension were added to 25 mL synthetic medium XOM2 containing 0.18% glucose (Originally, we used xylose to induce hrp gene expression, but here, we used glucose for more active growth.) and incubated (120 r.p.m., 28 °C). The bacterial population of cultures (A600 nm) was measured every 12 h after inoculation. A coding region of XrvB, amplified by PCR (Table S2 for primers) and digested with NdeI and EcoRI, was cloned in the expression vector pET28b(+) (Merck), followed by transformation into E. coli BL21(DE3). The transformant was incubated in LB medium for 3 h, and then isopropyl-β-d-1-thiogalactopyranoside. was added for a final concentration of 1 mM, followed by incubation for 1 h.

S3). Analysis of protein extracts from HTS assay such synchronously growing cells showed the presence of LdHAT1 protein at equal amounts in different cell cycle phases of L. donovani promastigotes (Fig. 1b). As the level of LdHAT1 found to be invariable during cell cycle, it would be interesting to study the effect of phosphorylation by the S-phase kinase on its activity. LdHAT1 was shown previously to interact with L. donovani S-phase cyclin LdCyc1 in a RXL-like Cy-motif-dependent manner by peptide competition assay (Maity et al., 2011). To further confirm the contribution of Cy-motif in the interaction, the putative Cy-motif of LdHAT1 was altered (290RRLVVRDDVV, LdHAT1ΔCy), and the mutated protein was used in the

interaction assay. As shown in Fig. 2a, the wild-type protein was found to interact with GST-LdCyc1, whereas the interaction with LdHAT1ΔCy was almost completely abolished, proving the involvement of Cy-motif during direct interaction between the proteins. The observation also confirmed the identity of an active Cy-motif in the molecule. The mutation at the putative Cdk phosphorylation site (394TPEKAPEK, LdHAT1-T394A) of the protein did not affect the interaction

(Fig. 2a), confirming further the specific involvement of Cy-motif in the binding. LdHAT1 was demonstrated to be phosphorylated in vitro by LdCyc1-CRK3 ABT-888 nmr complex (Fig. 2b) (Maity et al., 2011). As the substrate docking on the cyclin moiety was shown to be important for phosphorylation, to investigate the effect of Cy-motif of LdHAT1 on its phosphorylation, LdHAT1ΔCy was used as substrate in a kinase assay of LdCyc1-CRK3 complex. As observed, LdHAT1ΔCy was not efficiently phosphorylated by the kinase complex compared to the wild-type protein (Fig. 2c, lanes 4 and 5). As the mutation in Cy-motif of LdHAT1 was shown to disrupt its interaction with LdCyc1 (Fig. 2a),

the inhibition of the phosphorylation established the requirement of its docking through the Cy-motif on MRAIL-motif on LdCyc1 (Banerjee et al., 2003) for the phosphorylation Tolmetin on the target serine/threonine residue. LdHAT1 was also shown to contain a putative Cdk phosphorylation site on its C-terminal end. To confirm whether Thr-394 in the motif TPEK was phosphorylated by the kinase complex, the threonine residue was changed to alanine, and the mutant LdHAT1-T394A was used as substrate. As shown in Fig. 2c, the phosphorylation was completely abolished because of the mutation (lane 6), suggesting that the S-phase kinase LdCyc1-CRK3 targets Thr-394 for phosphorylation. It is interesting to note that Thr-394 is located very close to conserved catalytically critical Glu residue raising the possibility of regulation of HAT activity because of the incorporation of a phosphate group. Therefore, it is important to study the effect on the activity of LdHAT1 by phosphorylation of the Thr residue by the cell kinase. It was previously implicated that HAT1 from T.

Such recombination processes may significantly influence bacterial diversity (Kobayashi, 2001). R-M systems can also be considered as mobile elements, as suggested by their amplification, mobility, and involvement in genome rearrangements, as well as their mutual competition and regulation of gene expression (Ishikawa et al., 2010). Type II R-M systems are usually located in bacterial

and archaeal chromosomes, although they are sometimes found in plasmids, which may disseminate GSK J4 manufacturer these systems among diverse bacterial populations. In a few cases, R-M modules may play an important role in the biology of bacterial plasmids, since they are able to stabilize these replicons in a bacterial population by eliminating plasmid-less cells at the postsegregational level (e.g. Kulakauskas et al., 1995). The vast majority of plasmid-encoded type II R-M systems have been identified LY294002 ic50 in (1) Enterobacteriaceae (e.g. Klebsiella pneumonia RFL2; Lubys et al., 1999) and (2) lactic acid bacteria (e.g. Lactococcus lactis W56; Kong & Josephson, 2002). Much less is known about the R-M systems of other groups of bacteria. For example,

to our knowledge, only one plasmid-encoded R-M module has been described in the Alphaproteobacteria, whose genomes are known for their multi-replicon structures (Rochepeau et al., 1997). Recently we have performed complex genomic studies of a pool of 17 plasmids residing in bacteria of the genus Paracoccus (Alphaproteobacteria). Detailed analysis of the obtained nucleotide sequences revealed that one of the plasmids (pAMI7 of Paracoccus aminophilus JCM 7686) contains a type II R-M system (Dziewit et al., 2011). In this study we present a molecular and functional characterization of the components of this system. The following bacterial strains were used in this study:

(1) P. aminophilus JCM 7686 (Urakami et al., 1990), (2) Paracoccus pantotrophus KL100 (Bartosik et al., 2002), and (3) Escherichia coli TG1, TOP10 and MC1000 (Casadaban & Cohen, 1980). All strains were grown in lysogeny broth medium (Sambrook & Russell, 2001) at 37 °C (E. coli) or 30 °C (Paracoccus spp.). Where necessary, Alectinib molecular weight the medium was supplemented with antibiotics at the following concentrations: ampicillin – 100 μg mL−1, kanamycin – 50 μg mL−1, rifampicin – 50 μg mL−1, and tetracycline – 20 μg mL−1. The plasmids used in this study are listed in Table 1. The nucleotide sequence of pAMI7 was analyzed using Clone Manager (Sci-Ed8) and artemis software (Carver et al., 2008). Similarity searches were performed using the blast programs (Altschul et al., 1997) provided by the NCBI (http://blast.ncbi.nlm.nih.gov/Blast.cgi) and REBASE (http://rebase.neb.com/rebase/rebase.html). The restriction and modification activity of E.

To determine whether the colonization defect of the mutant lacking both putative MCPs (acfB tcpI) might be

due to a different pattern of colonization within the intestine, we dissected the small intestine into nine equal length segments following colonization of a 1 : 1 mixture of the acfB tcpI mutant and wild-type strains, and measured the bacterial content in each segment Natural Product Library screening (Fig. 4). As has been previously demonstrated (Lee et al., 2001), the wild-type strain shows a preference for colonization of the distal ileal segments. Likewise, the acfB tcpI mutant also preferentially colonized the distal ileal segments in a similar distribution pattern, but the level of mutant recovered was lower than the level of the wild-type strain in all of the segments. These results show that

the spatial distribution of the acfB tcpI mutant within the intestine is similar to that of the wild-type strain. Vibrio cholerae colonization of the intestine leads to the disease cholera. The most important virulence factors expressed by this organism are coordinately regulated by the transcriptional activator ToxT, which is encoded in a horizontally acquired genetic element, the VPI which is almost exclusively found in pathogenic strains. The VPI also encodes the ToxT-regulated tcp genes necessary for the synthesis of the essential colonization factor TCP, as well as regulatory factors necessary for ToxT expression. Additional genes are present within the VPI that have undefined functions, and most of these are also positively regulated by ToxT (Bina et al., 2003). Ivacaftor in vitro Here, we show that two of these ‘undefined’ ToxT-regulated VPI factors, AcfB and TcpI, contribute to V. cholerae intestinal colonization. AcfB and TcpI are putative MCPs. They share significant homology with each other and contain the hallmark motifs found in MCPs, including Cache, transmembrane, HAMP, and MCP domains. We propose that Ureohydrolase these are bona fide MCPs that interact with the V. cholerae

chemotaxis machinery and modulate swimming behavior, and the altered motility/chemotaxis phenotypes associated with V. cholerae strains lacking AcfB and/or TcpI are consistent with this hypothesis. With over 43 putative MCPs encoded within the V. cholerae genome, dissecting the individual contributions of each MCP to chemotaxis is a daunting task, especially if the chemoattractant/repellant is unknown. Moreover, our results suggest that AcfB and TcpI have overlapping functions, in that both needed to be mutated to observe a colonization defect. In addition to this, it has been shown that MCPs form arrays in which one MCP influences signaling through another (different) MCP (Gestwicki & Kiessling, 2002), and so determining the exact contribution of specific MCPs to V. cholerae behavior within the intestinal environment will require further experimentation. Flagellar-mediated chemotaxis plays a critical role in the virulence and infectivity of V.

Studies from two centres have reported that contacts of patients identified as recently infected by RITA show high rates of HIV infection and that a strategy of intensifying contact tracing efforts for this group of patients may be indicated [8, 11]. This survey has a relatively small sample size and results could have been affected by sampling bias, as health professionals with RITA experience were potentially more likely to respond. Nevertheless, analysis revealed that replies were received from clinicians with different levels of clinical and RITA experience and from centres evenly distributed across E&NI. Furthermore, the questionnaire was piloted before launch, in order to reduce any misinterpretation of questions

by participants. Many centres and clinicians GSK J4 clinical trial across E&NI have now incorporated click here RITA into clinical practice with no reported patient adverse events. More collaborative work is required between the HPA, local laboratories and clinics in order to improve clinician and patient access to results. Further evaluation of RITA is underway and national guidance, especially with regard to using RITA as an additional tool for contact tracing, is urgently required. The authors would like to thank A.

M. Geretti and K. Manavi for their detailed feedback on the pilot to this survey and all healthcare professionals who participated. We would also like to thank all clinic and laboratory staff for continuing to support the RITA programme in E&NI. Conflicts of interest: None of the authors has a conflict of interest to declare. ”
“The proportion of people living with HIV/AIDS in the ageing population (> 50 years old) is increasing.

We aimed to explore the relationship between older age and treatment outcomes in HIV-positive persons from the Asia Pacific Dipeptidyl peptidase region. Patients from the Australian HIV Observational Database (AHOD) and the TREAT Asia HIV Observational Database (TAHOD) were included in the analysis. We used survival methods to assess the association between older age and all-cause mortality, as well as time to treatment modification. We used regression analyses to evaluate changes in CD4 counts after combination antiretroviral therapy (cART) initiation and determined the odds of detectable viral load, up to 24 months of treatment. A total of 7142 patients were included in these analyses (60% in TAHOD and 40% in AHOD), of whom 25% were > 50 years old. In multivariable analyses, those aged > 50 years were at least twice as likely to die as those aged 30–39 years [hazard ratio (HR) for 50–59 years: 2.27; 95% confidence interval (CI) 1.34–3.83; HR for > 60 years: 4.28; 95% CI 2.42–7.55]. The effect of older age on CD4 count changes was insignificant (p-trend = 0.06). The odds of detectable viral load after cART initiation decreased with age (p-trend = < 0.0001). The effect of older age on time to first treatment modification was insignificant (p-trend = 0.21).

Differences among means were determined using Fisher’s protected LSD test at P=0.05. All the experiments described were based on the interaction between bacterial cells and the glass surface of the MFCs; however, similar PCI-32765 chemical structure observations were made on polydimethylsilioxane surfaces (not shown). Differences were evident among the wild types and TFP mutants in their ability to adhere to glass as soon as cells were introduced into the MFCs. While M6 and W1 cells attached immediately to the surface, the respective TFP mutants failed to do so (Fig. 1). Blocking medium flow at the main channel for up to 90 min resulted in the accumulation of TFP mutant cells in the field of view. However, when medium flow was resumed (0.25 μL min−1),

all TFP mutants (all M6-M and the majority of M6-T and W1-A cells) were immediately displaced. In contrast to M6-M cells, which, under flow, were unable to adhere to the channel surface regardless of the incubation time, M6-T and W1-A cells showed sporadic attachment after 24 h of incubation. Interestingly, the hyperpiliated M6-T cells attached to the surface not only as solitary cells but also as small clusters of about 5–15 cells (Fig. 2). No apparent differences

were observed between M6 and M6-flg, as both effectively attached to the surfaces (not shown). Adhesion force evaluation assays were conducted to compare the strength of attachment among wild types and mutants. This assay was not performed with mutant M6-M, due to its inability to attach to the surface under tested Selleckchem Lumacaftor conditions. Gradually increasing the flow rate from 0.25 to 16 μL min−1 did not reveal substantial differences between

strains M6 and M6-T in attachment ability. However, following the application of flow rates of 32 and 64 μL min−1, the majority (84%) of the M6-T cells Coproporphyrinogen III oxidase were displaced from the surface (Fig. 2; Supporting Information, Movie S1). Under these conditions, only 37% of the M6 cells were displaced from the surface, and the differences between these strains were significant (P=0.05) (Fig. 2b). Accordingly, wild-type M6 showed a significantly (P=0.01) higher adhesion force (174.8 pN) than M6-T (104.4 pN) (Fig. 2b). For a qualitative assessment of the strength of attachment, the flow rate was increased to 100 μL min−1, equivalent to a drag force of 380 pN (De la Fuente et al., 2007b) for 1 min. Here too, the majority of M6 cells that withstood the previous rate of 64 μL min−1 remained attached to the surface. No significant differences were observed between M6 and M6-flg in adhesion assays (Fig. 2b). Wild-type W1, which, in contrast to strain M6, does not produce polar flagella (Table 1), showed a behavior similar to that of M6, with an average of 49% of the initial cells being displaced from the surface at the end of the assays (not shown). On the other hand, the majority of W1-A cells were quickly removed from the surface following the application of a flow rate of 8 μL min−1.

Under different conditions, for example longer incubation times and anaerobic conditions, nitrite production has been found in some BCG strains

(Weber et al., 2000; Sohaskey & Wayne, 2003; Stermann et al., 2003; Sohaskey & Modesti, 2009). Therefore, different incubation times could explain the discrepancy observed between nitrate reductase test results and intercellular survival. Nitrate reductase activity is not the sole explanation, but we believe it is partly responsible for the survival in host cells, as shown in previous reports (Weber et al., 2000; Sohaskey, 2008) and the present study. Heterogeneity of niacin accumulation was also observed among BCG substrains (Table 1). Recycling of NAD favours the latent infection of M. tuberculosis (Boshoff et al., 2008), and NAD-quinoline reductase is responsible for resistance

to oxidative stress (Akhtar et al., 2006). These reports suggest that the MAPK inhibitor Avasimibe ic50 activity of NAD metabolism is associated with the survival of BCG in macrophages or host cells. Whether the long or short survival of BCG in host cells favours the effectiveness of BCG has not been determined. However, the different characteristics of BCG substrains as reported here provide the basic information for further investigation of immunological characteristics and evaluation. Parker et al. (2007) purified and characterized MPLA. MPLA is associated with cutinase, a serine esterase and catalyses the hydrolysis of lipids including Tween 80. MPLA activity was observed not only in pathogenic M. tuberculosis, but also in BCG-Pasteur. BCG-Pasteur

was weakly positive for Tween 80 hydrolysis (Table 1). In fact, eight of the 14 substrains, namely BCG-Moreau, -Sweden, -Danish, -Connaught, -Montreal, -Phipps, -Australia and -Pasteur, were weakly positive. Mycobacteria are known to use this fatty acid as carbon source at the dormant stage. Therefore, this activity could contribute to survival under starvation conditions during dormancy (Jackson et al., 1989; Deb et al., Amylase 2009). All BCG strains belong to the low-catalase group, although there were variations in the height of bubble column among them (Table 1). It was over 10 mm in BCG-Japan (14.8 mm) and -Birkhaug (11.8 mm) (Table 1). No mutation in the coding region of the ahpC gene among was observed among the substrains (data not shown). The differences between transcription of the genes and the activities have not yet been analysed. Catalase (katG) and peroxidase (ahpC) activities of M. tuberculosis are related to resistance to oxidative killing in human monocytes in vitro (Manca et al., 1999). The expression of katG is partially regulated by ferric uptake regulators (fur), and contributes to the virulence of M. tuberculosis (Lucarelli et al., 2008). Resistance to hydrogen peroxide of M. bovis, BCG-Russia and -Japan was higher than that of other BCG substrains (Fig. 1). This resistance relates well to survival in host cells, THP-1 and BMMs (Fig. 1).