In a univariate linear regression model, ritonavir boosting (P<0.001) and concomitant use of acid-reducing agents (P=0.027) were associated with ATV plasma concentration, KU-60019 price while a relationship was not detected for sex, country of birth, age, weight, body mass index, hepatitis B virus (HBV) or hepatitis C virus (HCV) coinfection, liver cirrhosis, renal impairment, or concomitant use of tenofovir or CYP3A4-inducing agents (efavirenz, nevirapine or phenobarbital) (Table 2). When all these variables were analysed in a multivariate model, ritonavir boosting, use of acid-reducing

agents and liver cirrhosis showed an independent association with ATV plasma level (see Table 2). A total of 21 patients had more than one measurement available, with a median of 2 samples (range 2–6). Intra-individual variability appeared to be limited (median intra-individual CV 39.7%; IQR 13.7–95.2) and lower than inter-individual variability. Virological response at 24 weeks was observed in 94 of the 115 samples (81.7%). No significant differences in terms of virological response were found between boosted and unboosted regimens (84.2 vs. 76.9%, respectively; P=0.482), between concomitant tenofovir administration and no concomitant tenofovir administration Selleck ABT199 (70.2 vs. 57.1%, respectively;

P=0.368), or between use of acid-reducing agents and no use of these agents (85.7 vs. 81.5%, respectively; P=1.000). We investigated the relationship between ATV C12 h and virological response. ROC curves provided a concentration cut-off of 0.23 mg/L which predicted virological response at 24 weeks (sensitivity 89.4%, specificity 33.3%, positive predictive value 85.7% and negative predictive value 41.2%): samples with a C12 h≤0.23 mg/L showed virological failure in 41.2% of cases (seven of 17), whereas samples with a C12 h>0.23 mg/L showed virological failure in 14.3% of cases (14 of 98) (P=0.021)

(Fig. 2). Moreover, patients with a drug concentration above the C12 h efficacy threshold did not show a higher proportion of grade III/IV hyperbilirubinaemia than those with a concentration below the threshold (21.8 vs. 35.7%, respectively; P=0.433). An ATV concentration below the limit of detection of the assay Thymidine kinase was observed in four of 21 episodes of virological failure (19%), suggesting low adherence as a potential cause of failure. We further investigated predictors of virological response through a logistic regression model (Table 3). Among the studied variables, an ATV concentration above the proposed C12 h threshold, lower baseline viral load, higher baseline CD4 cell count and higher weight were positively associated with virological outcome in univariate analysis; when these variables were analysed in a multivariate model, only ATV C12 h>0.23 mg/L and higher weight were confirmed as independent predictors of virological response. ATV C12 h was weakly correlated with concomitant unconjugated bilirubin levels (r=0.223, P=0.

To ensure correct diagnosis in such cases, a multidisciplinary approach should be adopted: where local expertise and laboratory facilities are available, the diagnosis can be confirmed locally; where they are not available, photographs and samples can be sent off for a remote consultation. Physicians should be encouraged to obtain advice at an early stage in order that such patients with several comorbidities can be offered optimal treatment that provides the best

chance of success. As cases of chronic herpes are not common even in the largest HIV centres, therapeutic prospective and controlled clinical studies have not been conducted. KU-60019 order A new expert consensus on HSV and HIV coinfection would be welcome, 16 years after the first algorithms were proposed during the pre-HAART era [16]. In Z-VAD-FMK nmr particular, such an updated consensus could

integrate the influence of HAART and the immune restoration syndrome. To conclude, chronic mucocutaneous HSV-2 infection in HIV-positive patients remains uncommon in the HAART era. We describe its two main clinical forms, ulcerative and pseudo-tumoral, and emphasize the importance of laboratory confirmation tests not only for diagnosis but also for treatment and follow-up using culture and in vitro HSV sensitivity testing. The long evolution and active viral replication of HSV-2 are linked to dysimmunity and the development of viral resistance to anti-herpetic drugs, and patients with HIV and HSV-2 coinfection therefore require careful and specialized management. We thank Drs Véronique Schiffer, Christian Junet and Joëlle Wintsch for their clinical collaboration in the patient follow-up; Dr Thomas Mckee, Department of Pathology, for his help with the cutaneous biopsies and PCR analyses; and Mrs Delphine Garcia, Laboratory Evodiamine of Virology, for her technical help with the viral

cultures and resistance screening. Conflict of interest: None of the authors has a commercial or other association that might pose a conflict of interest. No funding was obtained for this study. “
“We performed a systematic review and meta-analysis of randomized controlled trials (RCTs) to assess the overall efficacy of new antiretroviral drugs, as well as the factors associated with increased efficacy. We compared CD4 cell count increases associated with chemokine (C-C motif) receptor 5 (CCR5) inhibitors or other new drugs, using indirect comparison. We included RCTs published in 2003–2010 that assessed the 48-week immunological and virological efficacy of adding new antiretroviral drugs vs. placebo to optimized background therapy (OBT) in treatment-experienced subjects. These drugs included maraviroc, vicriviroc, enfuvirtide, raltegravir, etravirine, tipranavir and darunavir. We collected baseline descriptive characteristics, CD4 cell count changes and virological suppression proportions (percentage with HIV RNA <50 HIV-1 RNA copies/mL). We identified 10 studies which included a total of 6401 patients.

Gene blr1516 is predicted to encode a protein of 1050 aa, with 11 predicted transmembrane helices and significant sequence similarity to the RND-type transporters MexD of P. aeruginosa (54%) and AcrB of E. coli (44%), for example. Based on these structural features and the functional data described below, genes blr1515 and blr1516 were termed bdeA and bdeB, respectively, acronyms of the Bradyrhizobium drug exporter. Database searches

revealed that, in addition to BdeAB, the B. japonicum genome encodes 23 further putative RND-type efflux pumps, which are potentially involved in multidrug export. We determined the phylogenetic relationship between these paralogous transporters in B. TGF-beta inhibitor japonicum, and compared them with prototypic RND-type transporters of known substrates (deposited in the Transport Classification Database at http://www.tcdb.org/; Saier et al., 2006, or described in the literature as being present in phytopathogenic bacteria). Phylogenetic analysis revealed that the BdeB membrane transporter is more closely related to orthologs from 17-AAG cell line other Gram-negative bacteria than to any of its 23 paralogs (see Supporting Information, Fig. S1). BdeB

clustered with MexD and MexY of P. aeruginosa, AmrB of Burkholderia pseudomallei and MtrD of Neisseria gonorrhoeae. MexD and MexY have a common basic substrate profile [quinolones, macrolides (e.g. erythromycin), tetracycline, chloramphenicol, and certain β-lactams] that is extended by novobiocin (MexD) and aminoglycosides (MexY) (Masuda et al., 2000; Jeannot et al., 2005). Aminoglycosides and erythromycin are also exported by AmrB (Moore et al., 1999), whereas MtrD was reported to export mainly fatty acids

and bile salts (Hagman et al., 1997). Colonies formed by the ΔbdeAB mutant (strain 9589) on plates were more mucous as compared with those formed by the wild type. Cultures used for all assays Dimethyl sulfoxide performed in this work were inoculated from second-generation precultures in order to minimize the potential risk of exopolysaccharide interference with OD measurements. Heterotrophic growth of the ΔbdeAB mutant cultivated under oxic and micro-oxic conditions in a complex medium was indistinguishable from that of the wild type, and so was growth in minimal medium under oxic conditions (data not shown). The potential susceptibility of the ΔbdeAB strain 9589 to various antimicrobial compounds was tested qualitatively in gradient plate assays (not shown) or, more quantitatively, using agar plate diffusion assays. The deletion of bdeAB resulted in a marked and significant increase of sensitivity to the aminoglycosides kanamycin and gentamicin as compared with the wild type (1.7- and 5.5-fold difference, respectively, based on the size of the inhibition zone; Fig. 2). The complemented strain 9589-38 showed wild-type resistance levels and a largely normal colony morphology.

These partnerships were viewed positively. In school, there were some reports of unwanted absence, resulting from pain and swollen joints, side-effects of medicines, or scheduled appointments. For many young people, arthritis was a ‘hidden’ condition, where medicine-taking was a defining element of its existence. Young people thought carefully about disclosure, especially to peers. There were many accounts showing resilience among young people, detailed

insights about the relative benefit and harm of medicines, and sophisticated medication routines. The rheumatology team was the primary source of information. Pharmacists were not mentioned as a resource, although one young person commented that they felt ‘like a pharmacist’ when managing their medication. Consultations with young people must take account of the psychosocial context in which young people take medicines. The influence of families, school life, and relationships with peers all merit detailed NU7441 price exploration. Understanding a young person’s beliefs about their medicines and condition will help pharmacists to provide relevant and credible advice. Keeping a Cabozantinib datasheet channel open for young people to ask questions would be advantageous, as would providing age- and developmentally-appropriate medicines information at intervals

across this period of rapid change. Better links with local rheumatology teams, in order to understand local prescribing practice of non-steroidal anti-inflammatory drugs and disease-modifying anti-rheumatic drugs used in juvenile arthritis, could provide community pharmacists with the tools to employ MUR and other services to the benefit of young people and their families. 1. Gray N, Keady S, McDonagh J. Care in juvenile idiopathic arthritis (CPD article). The Pharmaceutical Journal 2010; 285: 655–658. 2. Hsieh H, Shannon SE. Three approaches to qualitative content analysis. Qualitative Health Research 2005; 15: 1277–1288. Ahmed Al-Nagar1, Jane

Skinner2, Charlotte Salter2, James Desborough1 1School of Pharmacy, University of East Anglia, Norwich Research Park, Norwich, UK, 2Norwich Medical School, Faculty of Medicine & Health Sciences, University of East Anglia, Norwich, UK A questionnaire was sent to community pharmacists in England exploring their perceptions of consultation skills and training received at undergraduate, Unoprostone pre-registration and post registration training Linear regression was used to explore which factors may predict the number of consultations conducted in a standard working week Self-reported confidence in consultation skills had the largest impact on the number of consultations conducted The role of the community pharmacist has evolved from compounding and dispensing to providing advanced and enhanced services which require more patient interaction. It was assumed that pharmacists had the requisite consultation skills required for the new advanced services whilst evidence suggests that this may not be a fair assumption1.

In absolute terms, cardiovascular PLX4032 events were reported as the most frequent cause of death among Dutch citizens abroad and they occurred mainly in the European region where the majority of Dutch citizens spent their vacations. As might be expected for cardiovascular deaths, the mortality rate increased with age and occurred more frequently in males. It is certainly interesting to note that travel to destinations outside Europe was associated with an even higher mortality risk when the absolute number of travelers to a designated WHO region was taken into account. This finding

was particularly prominent for travelers to Africa. These observations suggest that environmental changes like a tropical climate and changes in physical activity associated with vacation pose a serious challenge to the cardiovascular system of the traveler. These findings are in line with reports of fatalities among American,3,7,8 New Zealand,4,5 Scottish,12 Canadian,10,11 and Australian14 citizens, who also consistently show that cardiovascular problems are the leading causes of

natural deaths abroad. In addition, travel to Africa also carries a higher mortality risk due to a fatal injury or accident. A plausible explanation might be that severe traffic accidents are more common in these regions, given a recent WHO global status report on road safety (available at www.who.int/violence_injury_prevention/road_safety_status/2009/en/index.html). For illustration, over 90% of the world’s fatalities on the roads occur in low-income and middle-income countries, which have less than half of PD0332991 chemical structure the world’s vehicles. In our study, local driving conditions and unfamiliarity with roads were frequently reported as precipitating factors contributing to fatal traffic accidents. Other precipitating conditions that related to injury death were interaction with marine wildlife and adventure activities. These findings are in line with the findings of a study of United Nations Transition Assistance Group

mission in Namibia in which a fatality rate of 0.21 per million km driven was found, which was more than 10-fold higher as the fatality rate recorded in military population in industrialized countries.19 Interestingly, the high fatality rate in Namibia occurred Resveratrol despite the absence of dense traffic. Infectious diseases, although a common cause of illness among travelers, are usually not reported as a frequent cause of death. Nevertheless, travel to Africa and Southeast Asia was associated with a significantly increased risk of death due to a fatal infection as compared with travel within Europe. As in most countries, the prevention of these infections is subject of discussion in our current travel health advice and the success of this approach may be exemplified by the reassuringly low number of fatal infections in our survey and in those of others.

Although

still hypothetical, it looks as if themes arise that may be common pathways leading to or contributing to motor neuron degeneration (see Fig. 5). Intracellular (axonal) transport (motors and cytoskeleton) is one of them (De Vos et al., 2008). KIFAP3 (kinesin), Elp3 (tubulin), UNC13A Ibrutinib nmr (vesicle release) and dynactin (dynein) are examples. Interestingly, mutations in other transport-related proteins have been identified in related motor neuropathies such as Charcot–Marie–Tooth disease (e.g. NEFL; Mersiyanova et al., 2000) and hereditary spastic paraparesis (e.g. KIF5A; Reid et al., 2002). Another emerging theme has to do with RNA processing (TDP-43, FUS/TLS, Elp3), a theme also encountered in spinomuscular atrophy,

senataxin-related motor neuron disease and others (Lemmens et al., 2010). It can be predicted that more RNA-interacting proteins that play an etiologic or mediating role in ALS will be identified. Neurovascular molecules seem to establish another mechanism in ALS (VEGF, angiogenin) and related diseases (e.g. progranulin in FTLD; Lambrechts et al., 2006). The involvement PLX3397 order of ER stress is yet another one (SOD1, VAPB and others; Kanekura et al., 2009). In addition, there is the mechanism of excitotoxicity that comes up in many models generated so far and that could explain the selective vulnerability of motor neurons (Van Den Bosch et al., 2006). Finally, there is the contribution of glial cells to motor neuron death (Ilieva et al., 2009). It remains ID-8 to be seen how these themes will fit together. Most importantly, however, it is uncertain whether they are also at play in human motor neuron degeneration. This is difficult to investigate, as the human material we have is usually from patients in the terminal stages of disease, often poor in quality and, for many researchers, difficult to get hold of. For ∼15 years, ALS research has been limited to mutant SOD1-induced

motor neuron degeneration, as it was the only known cause of this disease. The discovery of other disease-causing mutations and the generation of animal models for them will allow a much broader approach and enable investigators to study compounds with a potential therapeutic effect in several different models. Hopefully these new opportunities will soon yield novel treatment strategies and make a difference for the many patients with ALS, their families and caregivers. A.B. is supported by the Laevers Foundation for ALS research and Fundacao para a Ciencia e a Tecnologia of the Portuguese Government (Postdoctoral grant BPD/SFRH/2009/66777). P.V.D., L.V.D.B. and W.R. are supported by grants from the Fund for Scientific Research Flanders (F.W.O.

, 2006, 2007). Therefore, we suggest that the acdS gene is likely to be horizontally transferred between Mesorhizobium species by exchange of the symbiosis island. This hypothesis is supported by the presence of the acdS gene in the symbiosis island of M. loti R7A, Mesorhizobium sp. MAFF303099,

M. ciceri bv. biserrulae WSM1271, M. australicum WSM2073T, and M. opportunistum WSM2075T, close to the nitrogen fixation genes cluster. Curiously, in strains M. amorphae ACCC19665T and M. huakuii Selleckchem Fulvestrant CCBAU2609T, the acdS gene was not detected. These strains have their symbiosis genes in plasmids (Wang et al., 1999; Zhang et al., 2000) and not in the chromosome on a symbiosis island, as in other Mesorhizobium strains (Kaneko et al., 2000; Sullivan et al., 2002). Analysis of the symbiosis islands of strains M. loti R7A, Mesorhizobium sp. MAFF303099, M. ciceri bv. biserrulae WSM1271, M. australicum WSM2073T, and M. opportunistum Epigenetic inhibitor WSM2075T shows a similar gene organization, suggesting that symbiosis islands may have evolved from a single common

ancestor and that the acdS gene was already present in the symbiosis island at that time. Following extensive gene transfer analysis, Slater et al. (2009) suggested that Mesorhizobium strains may have evolved by plasmid gene integration into the ancestral chromosome. In other members of α-Proteobacteria and in other rhizobial strains, acdS genes are often found on plasmids (Young et al., 2006; Kuhn et al., 2008; Kaneko et al., 2010). Interestingly, in Rhizobium leguminosarum bv. viciae 3841, the acdS gene is located acetylcholine on the pRL10 plasmid near the nitrogen fixation genes cluster (Young

et al., 2006). This arrangement is also observed in Sinorhizobium meliloti BL225C on the plasmid pSINMEB01 (Lucas et al., 2011d). All together these data suggest that the presence of the acdS gene in Mesorhizobium spp. dates to a common ancestor possessing this gene in a symbiosis island. Therefore, the acdS gene appears to be horizontally transferred between different Mesorhizobium species by exchange of the symbiosis island, keeping its regulatory system intact, so that this gene is only expressed in symbiotic conditions under the control of the NifA protein. This work has received funding from Fundação para a Ciência e a Tecnologia (FCT), co-financed by EU-FEDER (PTDC/BIO/80932/2006) and from the European Union Seventh Framework Programme (FP7/2007-2013) under grant agreement no. 247669. C. Brígido acknowledges a PhD fellowship (SFRH/BD/30680/2006) from FCT. We thank G. Mariano for technical assistance. “
“Antibiotic-producing soil bacteria of the genus Streptomyces form a huge natural reservoir of antibiotic resistance genes for the dissemination within the soil community. Streptomyces plasmids encode a unique conjugative DNA transfer system clearly distinguished from classical conjugation involving a single-stranded DNA molecule and a type IV protein secretion system.

Pharmacists also considered their own personal views. This study used hypothetical cases, which may have been handled differently if presented as real scenarios in the pharmacy. This study may have benefitted practice by raising

awareness of the complexity of decision-making, as well as highlighting the impact of personal selleck chemical beliefs and GP relationships on practice. 1. Cooper RJ, Wingfield J, Bissell P. Ethical, religious and factual beliefs about the supply of emergency hormonal, contraception by UK community pharmacists. Journal of Family Planning and Reproductive Health Care 2008; 34: 47–50. 2. Hanna LA, Hughes CM. ‘First, Do No Harm’: Factors that Influence Pharmacists Making Decisions about Over-the-Counter Medication A Qualitative Study in Northern Ireland. Drug Safety 2010; 33: 245–255. Michael Wilcock, Joanna Lawrence Pharmacy, Royal Idelalisib Cornwall Hospitals NHS Trust, Truro, UK Inter-professional collaboration as a means of improving patient care requires that clinical pharmacists have good communication skills. Doctors’ and nurses’ views on how well pharmacists communicate were captured via a brief survey. The results have informed a short tailored training programme on communication

skills for pharmacists and technicians. To ensure that patients receive the optimum level of care it is essential that clinical pharmacists, as members of the healthcare team, can effectively communicate with prescribers and nurses. A recent report acknowledge that the future for pharmacy practice will see the wider

pharmacy team drawing on their individual clinical and communication skills to work with other healthcare professionals and patients to optimise the use of medicines.1 As part of a wider service improvement Urease project, designed to assess and develop the communication skills of the pharmacist team, we undertook a baseline assessment of how clinical staff perceive the pharmacists’ communication skills. Two 3rd year medical students, attached to the pharmacy department for a two week Special Study Unit, undertook a brief survey of doctors and nurses on a range of hospital wards. The survey instrument consisted of 4 closed questions (3 requiring answers on a 5-point Likert scale and the fourth requiring a simple yes/no response), and a final question seeking free text comments. Staff were advised of the broad purpose of the survey (to ascertain how they perceive the ability of the clinical pharmacists to communicate with clinical staff) and reassured that the survey was anonymous. This was deemed service improvement performed to meet specific local needs and ethics approval was not sought. During April 2013, thirty-eight clinical staff (18 junior doctors, 20 nurses) were approached and agreed to answer the survey.

CIA in genetically susceptible strains of mice, rats, rabbits or rhesus monkeys has been used as an experimental model of RA, as it shares many histological and immunological features.[62] In addition to IL-17 and other previously mentioned cytokines, Th17 cells are characterized by expression of IL-6 and TNF.[63] IL-17 plays an important role in the additive/synergistic effects induced together with TNF-α and IL-1, two key cytokines in destructive arthritis.[4, 60, 64] The synergy between monocyte-derived IL-1β and TNF and T cell-derived

IL-17 also causes the Selleck Forskolin up-regulation of CCL20 in RA synoviocytes, a protein involved in the chemotaxis of T cells and immature dendritic cells.[65] Consequently, RA synovium is characterized by elevated levels of IL-17, IL-23, IL-6, TNF and IL-1β, along with nitric oxide (NO) and prostaglandin E2 find more (PGE2).[66] On the other hand, B cell-activating factor (BAFF) as a TNF superfamily member, also plays an important role in humoral immunity and in autoimmune diseases, including RA. Local BAFF gene targeting could inhibit pro-inflammatory cytokine

expression, suppressed generation of plasma cells and Th17 cells, and markedly ameliorated joint pathology.[67] BAFF gene-silenced DCs show defective IL-6 production and display severely impaired capacity, inducing Th17-cell generation in vitro. These results are consistent with previous findings

that APC-produced IL-6 is critically involved in driving Th17 cells to induce T cell reactivity Ergoloid in SKG mice, so that a previously unrecognized role for BAFF in promoting the expansion of Th17 cells was shown and IL-17 was demonstrated as a crucial effector cytokine for BAFF-mediated pro-inflammatory effects during CIA development.[67, 68] Although the increased levels of IL-17A, IL-6, TGF-β, and IFN-γ concentrations in sera and synovial fluid of reactive arthritis (ReA) and undifferentiated spondyloarthropathy (uSpA) compared to RA suggests that Th1 and Th17 cells could be the major cells in RA, it remains unclear whether Th1 and/or Th17 cells are involved in driving disease chronicity and destruction.[69, 70] The differentiation of Th17 cells from naive T cells appears to involve signals in connection with TGF-β, IL-6, IL-21, IL-1β and IL-23. IL-23 is one of the essential factors required for the survival and/or expansion of Th17 cells to promote inflammatory responses.[71] Th17 cells stimulated by IL-23 promote osteoclastogenesis through production of IL-17, which induces receptor activators of nuclear factor (NF)-κ B ligand on mesenchymal cells. The IL-23/IL-17 axis includes Th17 cells and plays a key role in the development of autoimmune arthritis by stimulating receptor activators of NF-κB ligand (RANKL) expression.

, 2010). Vibrio parahaemolyticus was grown at 37 °C in Luria–Bertani medium (10.0 g L−1 tryptone, 5.0 g L−1 yeast extract, 10.0 g L−1 sodium chloride) supplemented with 3% (w/v) NaCl (LBN) and the addition of 1.5% (w/v) agar where appropriate. The Caco-2 cell line (86010202) and the human Burkitt’s lymphoma B cell line, Raji (85011429), were obtained from the European Collection of Animal Cell Cultures, Salisbury, UK. Caco-2 cells were maintained in DMEM supplemented with 10% foetal bovine serum (FBS), Pen-Strep (100 units mL−1 penicillin, 100 μg mL−1 streptomycin) and 1% nonessential amino acids. Raji B cells

were maintained in RPMI supplemented with 10% FBS, Pen-Strep and 1% nonessential amino acids. Both Caco-2 and Raji cells were used between passages 1–10. Medium was changed every ALK inhibitor other day. Caco-2 cells were seeded onto the apical surface of Matrigel™ Basement Membrane Matrix (Becton Dickinson, Bedford, MA)-coated Transwell® inserts (12 mm diameter, 3.0 μm pore size, polyester; Corning, Costar) at a density of 300 000 cells per filter and grown for 21 days at 37 °C/5% CO2, until fully differentiated. Medium was replaced every other day. Raji B cells (resuspended in RPMI : DMEM 1 : 2) were

added to the basolateral compartment of 14- to 16-day-old Caco-2 cell monolayers at a density of 500 000 cells per well and maintained for 5–6 days. Transepithelial resistance (TER) was monitored throughout this period as a measure of monolayer integrity. TER was measured using the EVOM meter and STX2 electrode set (World Precision Instruments, UK). see more Carboxylated latex particles, with mean diameters of 0.5 and 1.0 μm (Molecular Probes) and labelled with FITC and Nile red, respectively, were used in particle transport studies. Latex particles were suspended in Hank’s balanced salt solution

(HBSS) supplemented with 5.5 M glucose RVX-208 and buffered to pH 7.4 with 25 mM HEPES, such that each monolayer was exposed to 2.5 × 108 of 0.5 and 1.0-μm particles. After equilibration, the HBSS on the donor apical side of the monolayer was replaced with prewarmed particle suspension. Particle transport was studied after a 2-h period by receiver basolateral chamber sampling. After establishing standard curves, the number of particles transported across cell monolayers was enumerated by a Dako CyAn ADP flow cytometer (Beckman Coulter). Bacteria were grown to mid-log phase in LBN at 37 °C with agitation. The bacteria were washed with PBS, and OD600 values were measured to determine bacterial numbers (O’Boyle et al., 2013). Inhibitors of the JNK (SP600125), p38 (SB203580) and ERK1/2 (PD98059) pathways were used at the following concentrations: 15 μM SP600125, 5 μM SB203580 and 40 μM PD98059. Inhibitors were added to the apical chamber of the transwell 2 h preinfection and maintained throughout the experiment.