The emergence of pandemic influenza A(H1N1) a few months before the 2009 Hajj season was the most recent of these pandemics.9 The lack of an available, effective, and publicly acceptable vaccine in time was just one of

the challenges.10 Restricting age groups at higher risk of complications from attending Hajj activities, as happened for the 2009 Hajj because of the H1N1 influenza threat,10 or even applying Trametinib cost a ban on individuals from certain countries during the maximum incubation period as happened with severe acute respiratory syndrome (SARS),11 was considered at length, though not fully implemented, and may be imperative for a future Hajj or other mass gathering events to combat future epidemics. This study was conducted to better document whether the several recommendations that were put into practice before the launch of 2009 Hajj season10 were effective in reducing the spread of pandemic influenza A(H1N1) and other viruses among pilgrims. The study’s primary objective

was to determine whether pilgrim attendance at Hajj venues increased risk of acquiring influenza (or other respiratory viruses). An additional Selleck SB203580 objective was to assess compliance with influenza immunization and other recommended preventive measures. Our study uses data collected from pilgrims participating in the 2009 (1430H) Hajj. The main religious activities of the 2009 Hajj season started on November 25, 2009 and continued for 5–6 days, according to each pilgrim’s plan. The 2009 Hajj, similar to the Hajj in other years, included Muslims from all over the world, was one of the world’s largest yearly mass gatherings, and was culturally very diverse, including males and females of different ages, races, educational levels, and socioeconomic levels. Two cross-sectional surveys were conducted at the King Abdulaziz International Airport in Jeddah. It is the main airport used by pilgrims and the Hajj terminal is only used by pilgrims. The first survey was conducted during the week before Hajj activities began on November 25, 2009. As the survey was conducted during a declared influenza A(H1N1) pandemic, all pilgrims arriving at the King Khalid international

Hajj terminal were screened by thermal cameras ID-8 and questioned about flu symptoms. This was documented in the incoming survey, and results were included in the final analysis; however, departing pilgrims were not questioned about flu symptoms. The primary sampling units were incoming flights. It proved impractical to select flights by probability sampling; instead, survey teams, after finishing one flight, generally selected the next arriving flight. After deplaning, pilgrims waited in an arrival room (a separate one for each flight) before immigration formalities began, grouped around rows of seats. Interviewers randomly selected a row, a person around the row, and a clockwise or counterclockwise direction, and then interviewed pilgrims successively until the room cleared.

Such a synergistic function by the TARP family is also indicated from a study using stg/γ-3-DKO mice (Menuz et al., 2008). γ-3 is highly expressed in cerebellar Golgi cells (Fukaya et al., 2005), and its sole gene ablation did not affect cerebellar contents of AMPA receptors or AMPA receptor-mediated responses in Golgi cells. In stg/γ-3-DKO mice, PLX4032 research buy however, all four AMPA receptor subunits, particularly GluA2 and GluA3, were severely reduced in the cerebellum, and AMPA receptor-mediated responses were reduced to nearly

10% in Golgi cells (Menuz et al., 2008). Multiple TARP members, being expressed with differential combination and stoichiometry in given neuronal populations, may regulate AMPA receptor expression in a cooperative manner. In quantitative Western blot analysis, we found severe reductions in GluA2 and GluA3 and mild reductions in GluA4 in γ-2-KO cerebellum. GluA2–GluA4 were further reduced in γ-2/γ-7-DKO cerebellum. Light-microscopic immunohistochemistry gave a

closely similar result, which was also consistent with their severe reductions at almost all cerebellar click here synapses examined by postembedding immunogold. In γ-7-KO mice, reductions in AMPA receptor subunits were more modest, i.e., mild reductions in GluA3 at the parallel fiber–Purkinje cell and parallel fiber–interneuron synapses and moderate reduction in GluA4 at the mossy fiber–granule cell synapse. As to GluA1, we found mild reductions at the parallel fiber–Purkinje cell and climbing fiber–Purkinje cell synapses

in γ-2-KO mice, and found no reduction at any synapses examined in γ-7-KO mice. Nevertheless, following the ablation of both TARPs, GluA1 was reduced severely at climbing fiber–Purkinje cell synapse and moderately so at the parallel fiber–Purkinje cell and parallel fiber–interneuron synapses. These results suggest that γ-2 or γ-7 per se preferentially promotes synaptic expression of GluA2–GluA4, and that they come to promote GluA1 expression too, when expressed together. AMPA Idoxuridine receptors containing an edited GluA2 exhibit either linear or outwardly rectifying current–voltage (I-V) relationships and have low permeability to Ca2+, whereas those lacking GluA2 show strong inward rectification and high Ca2+ permeability (Hollmann et al., 1991; Hume et al., 1991; Verdoorn et al., 1991; Mosbacher et al., 1994; Tsuzuki et al., 2000). In Purkinje cells, AMPA receptors exhibit a linear I-V relationship and thereby little Ca2+ permeability (Tempia et al., 1996; Momiyama et al., 2003), indicating that GluA2-containing receptors are the major form in this neuron. Consistent with this notion, high levels of GluA2 mRNA are expressed together with GluA1 and GluA3 mRNAs in Purkinje cells (Keinänen et al., 1990; Pellegrini-Giampietro et al., 1991; Lambolez et al., 1992).

The inability to utilize nitrogen sources from carrot agar may have resulted in immature ΔareA ascospores. The total nitrogen content of carrots agar is low, and the major nitrogen compounds

are nitrate and proteins, which ΔareA strains cannot use (Międzobrodzka et al., 1993; U.S. Department of Agriculture, 2010). When we supplemented carrot agar with 5 mM urea, the sexual development of ΔareA strains was restored to the level of the wild-type strain, suggesting that the deletion mutants exhausted all available nitrogen sources during early sexual development and therefore could not complete development. In conclusion, the global nitrogen regulator areA is required for nitrogen metabolism, virulence, secondary metabolism, vegetative Roscovitine growth, and sexual development in G. zeae. This study is the PI3K inhibitor first report to account for the functions of an areA orthologue in sexual development of filamentous fungi. The detailed mechanisms of how areA regulates fungal development with other regulators would be exciting topics for future studies of G. zeae. This work was supported by a grant (2012-0000575) by the National Research Foundation funded by the Korean government (MEST). “
“Plant pathogens usually promote pathogenesis

by secreting effector proteins into host plant cells. One of the secreted effectors of Pseudomonas syringae pv. phaseolicola, the causative agent of halo-blight disease in common bean (Phaseolus vulgaris), HopF1, activates effector-triggered immunity (ETI) in a bean cultivar containing R1 resistance gene, but displays

virulence function in a bean cultivar without the R1 gene. The virulence mechanism of the effector remained SPTLC1 unknown, although it was identified more than a decade ago. Here we demonstrated that HopF1 can inhibit pathogen-associated molecular pattern-triggered immunity (PTI) in a susceptible bean cultivar Tendergreen. HopF1 directly interacted with two RPM1-interacting protein 4 (RIN4) orthologs of bean, PvRIN4a and PvRIN4b. Like RIN4 in Arabidopsis, both PvRIN4 orthologs negatively regulated the PTI responses in bean. However, the virulence function of HopF1 was enhanced in Tendergreen silencing PvRIN4. Furthermore, silencing PvRIN4a compromised the avrβ1-induced hypersensitive response (HR), which previously was reported to be suppressed by HopF1. Together, these results demonstrated that PvRIN4 orthologs were not the virulence target of HopF1 for inhibiting PTI, but probably for interfering with ETI. Plant pathogens usually employ a type III secretion system to deliver type III secreted effectors (T3SEs) into plant cells, where they interact directly with host substrates to modulate defense pathways and promote disease. Plants rely on an elaborate immune system to counteract pathogens (Boller & He, 2009).

The inability to utilize nitrogen sources from carrot agar may have resulted in immature ΔareA ascospores. The total nitrogen content of carrots agar is low, and the major nitrogen compounds

are nitrate and proteins, which ΔareA strains cannot use (Międzobrodzka et al., 1993; U.S. Department of Agriculture, 2010). When we supplemented carrot agar with 5 mM urea, the sexual development of ΔareA strains was restored to the level of the wild-type strain, suggesting that the deletion mutants exhausted all available nitrogen sources during early sexual development and therefore could not complete development. In conclusion, the global nitrogen regulator areA is required for nitrogen metabolism, virulence, secondary metabolism, vegetative selleck chemicals growth, and sexual development in G. zeae. This study is the PLX4032 in vitro first report to account for the functions of an areA orthologue in sexual development of filamentous fungi. The detailed mechanisms of how areA regulates fungal development with other regulators would be exciting topics for future studies of G. zeae. This work was supported by a grant (2012-0000575) by the National Research Foundation funded by the Korean government (MEST). “
“Plant pathogens usually promote pathogenesis

by secreting effector proteins into host plant cells. One of the secreted effectors of Pseudomonas syringae pv. phaseolicola, the causative agent of halo-blight disease in common bean (Phaseolus vulgaris), HopF1, activates effector-triggered immunity (ETI) in a bean cultivar containing R1 resistance gene, but displays

virulence function in a bean cultivar without the R1 gene. The virulence mechanism of the effector remained Rolziracetam unknown, although it was identified more than a decade ago. Here we demonstrated that HopF1 can inhibit pathogen-associated molecular pattern-triggered immunity (PTI) in a susceptible bean cultivar Tendergreen. HopF1 directly interacted with two RPM1-interacting protein 4 (RIN4) orthologs of bean, PvRIN4a and PvRIN4b. Like RIN4 in Arabidopsis, both PvRIN4 orthologs negatively regulated the PTI responses in bean. However, the virulence function of HopF1 was enhanced in Tendergreen silencing PvRIN4. Furthermore, silencing PvRIN4a compromised the avrβ1-induced hypersensitive response (HR), which previously was reported to be suppressed by HopF1. Together, these results demonstrated that PvRIN4 orthologs were not the virulence target of HopF1 for inhibiting PTI, but probably for interfering with ETI. Plant pathogens usually employ a type III secretion system to deliver type III secreted effectors (T3SEs) into plant cells, where they interact directly with host substrates to modulate defense pathways and promote disease. Plants rely on an elaborate immune system to counteract pathogens (Boller & He, 2009).

This careful control of metalloprotein assembly may well be Torin 1 mw the Tat pathway’s main raison d’être and demonstrates a critical role for the Tat pathway in the biosynthesis of noncytoplasmic metalloproteins. Amongst the putative Tat substrates in cyanobacteria, several are predicted or known to bind metals and examples include FeS cluster containing proteins, such as PetC, molybdopterin-containing oxidoreductases, Mn-dependent superoxide dismutase and the zinc-dependent carbonic anhydrase. Each of these proteins must acquire its metal cofactor within the cytoplasm

before translocation can occur. The recent publication of complete genome sequences of a number of cyanobacterial species has opened the door to new and detailed genomic and proteomic investigations of protein targeting in cyanobacteria. Given their significance in terms of global photosynthetic activity and primary production, a fundamental understanding of cell function in general will be of great benefit. The use of advanced

bio-imaging techniques and proteomics should help us to unravel the secrets of protein sorting in cyanobacteria whose unique cellular organization amongst prokaryotes provides an intriguing layer of complexity. The significance of the Tat pathway in metalloprotein assembly selleck chemical and export is also beginning to be unravelled and recent advances in bioinorganic chemistry, including metalloproteomics, are opening new avenues of enquiry. The authors acknowledge the support of the Leverhulme Trust. “
“Bc1245 is a monocistronic chromosomal gene of Bacillus cereus ATCC 14579 encoding a putative protein of 143 amino acids identified in this study to have a spore-related function in B. cereus. Bc1245 is highly conserved in the genome of members of the B. cereus group, indicating

an important function of the gene in this group of bacteria. Quantitative PCR revealed that bc1245 is transcribed late in sporulation (upon formation of phase-bright spores) and at the same time as the mother cell–specific transcription factor σK. The σK regulon Adenosine triphosphate includes structural components of the spore (such as coat proteins), and it is therefore plausible that bc1245 might encode a structural outer spore protein. This was confirmed by detection of BC1245 in exosporium extracts from B. cereus by immunoblotting against BC1245 antiserum. Bacillus encompasses species capable of forming highly resistant dormant endospores as a response to environmental stress such as nutrient deprivation (Setlow & Johnson, 2007, and references therein). When receiving a specific signal (nutrient or nonnutrient derived), spores are able to come back to life as vegetative cells in an irreversible process called germination and subsequent outgrowth (Moir et al., 2002; Setlow, 2003).

14,19 Treatment strategies for GAE will include combinations of critical care techniques to reduce increased ICP, craniotomy for biopsy or excision of mass lesions, and combination pharmacotherapy with antifungals, anti-protozoal agents, synergistic antibiotics, and several experimental therapies that have shown promise in vitro, such as phenothiazines. Although case fatality rates in GAE are very high (90%–94% in acanthamoebiasis and ≥90% in balamuthiasis), successful drug treatment combinations in acanthamoebiasis have included intravenous pentamidine isethionate, flucytosine (5-flurocytosine), amphotericin B, the benzimidazole

antifungals (albendazole), the triazole antifungals (itraconazole and fluconazole), the synergistic antibiotics, rifampin and trimethroprim/sulfamethoxazole (TMP/SMX) (or amikacin or oral sulfadiazine), and topical ketoconazole 17-AAG molecular weight or miltefosine for skin ulcers.26,34–37 In 2008, Aichelburg and colleagues in Vienna reported treating a patient successfully with disseminated tuberculosis and acanthamoebiasis

SCH 900776 chemical structure with topical and oral miltefosine, a phosphocholine analog used to treat visceral leishmaniasis, and a combination of intravenous fluconazole, TMP/SMX, synergistic antibiotics (amikacin), and four tuberculostatic drugs.22 Successful intravenous drug treatment combinations in balamuthiasis have included azoles (albendazole, fluconazole, or itraconazole), flucytosine, pentamidine, sulfadiazine, and synergistic macrolide antibiotics (azithromycin or clarithromycin) Thymidylate synthase and phenothiazines (thioridazine or trifluoperazine).29,31 In 2004, Schuster and Visvesvara demonstrated that the phenothiazines demonstrated in vitro efficacy against B mandrillaris in clinical specimens.34 The optimum duration of drug therapy for GAE is unknown, but most survivors have been treated for many weeks to months.29–31,35–37 In 2010, Martinez and coworkers reported the successful treatment of B mandrillaris-confirmed GAE in a patient with extensive cutaneous and neurological

involvement with prolonged therapy with albendazole, fluconazole, and miltefosine.38 A genetic predisposition to B mandrillaris GAE has now been identified in American Hispanics, who appear less able to produce effective antibodies against the free-living amebae, and may be predisposed by more frequent contact with Balamuthia-contaminated soils and aerosols in agricultural occupations.39,40 Prevention and control strategies for GAE should include (1) consideration of GAE in organ transplant and immunocompromised patients with encephalitis and skin ulcers not improving with standard therapies; (2) recognition of genetic risk factors for acanthamoebiasis and balamuthiasis in Hispanics less able to produce antibodies against causative free-living amebae; and (3) recognition of other soil or stagnant freshwater risk factors in both immunocompetent and immunosuppressed patients with skin ulcers and unexplained meningoencephalitis.

We therefore evaluated the effect of selective tibial branch nerve transfer on behavioural recovery in animals following acute transection of the deep peroneal nerve. The results indicate that not only can hindlimb nerve transfers be successfully accomplished in a rat model but that these animals display a return of skilled locomotor function on a par with

animals that underwent direct deep peroneal nerve repair (the current gold standard). At 2 months, ground reaction force analysis demonstrated that partial restoration of braking forces occurred in the nerve transfer group, whereas www.selleckchem.com/products/Neratinib(HKI-272).html the direct repair group had fully restored these forces to similar to baseline levels. Ankle kinematic analysis revealed that only animals in the direct repair group significantly recovered flexion during the step cycle, indicating a recovery of surgically induced foot drop. Terminal electrophysiological and myological assessments demonstrated similar levels of reinnervation, whereas retrograde labelling studies confirmed that the peroneal nerve-innervated muscles were innervated by neurons from the tibial nerve

pool in the nerve transfer group. Our results demonstrate a task-dependent recovery process, where skilled locomotor recovery is similar between nerve transfer and direct repair animals, whereas flat surface locomotion is significantly better in direct repair animals. “
“Endocytosis at the presynaptic terminal is initiated by Ca2+ influx through voltage-gated Ca2+ channels. At Selleckchem Atezolizumab the Drosophila neuromuscular junction, we demonstrated two components of endocytosis linked to distinct Ca2+ channels. A voltage-gated Ca2+ channel blocker, (R)-(+)-Bay K8644 (R-BayK), selectively blocked one component (R-BayK-sensitive component) without affecting exocytosis, while low concentrations of La3+ preferentially depressed the other component (La3+ -sensitive component). In a temperature-sensitive mutant, shibirets, at non-permissive

temperatures, dynamin clusters were found immunohistochemically at the active zone (AZ) during the R-BayK-sensitive endocytosis, while they were detected Galactosylceramidase at the non-AZ during the La3+-sensitive endocytosis. Immunostaining of the Ca2+ channel α2δ subunit encoded by straightjacket (stj) was found within the AZ, and a mutation in stj depressed the R-BayK-sensitive component but enhanced the La3+ -sensitive one, indicating that the α2δ subunit is associated with the R-BayK-sensitive Ca2+ channel. Filipin bound to the non-AZ membrane and inhibited the La3+ -sensitive component, but not the R-BayK-sensitive one. We concluded that the R-BayK-sensitive component of endocytosis occurred at the AZ and termed this AZ endocytosis. We also concluded that the La3+ -sensitive component occurred at the non-AZ and termed this non-AZ endocytosis.

the triple therapy arms in their primary efficacy analyses at week 48 [5, 7]. However, longer term analyses showed a slightly higher

risk of low-level viraemia for patients taking DRV/r monotherapy [6, 8]; so far, the patients with low-level viraemia have not developed phenotypic resistance to PIs. More detailed analyses of these trials may help to identify patients GSK2118436 datasheet at the lowest risk of viraemia during monotherapy treatment, who could be most suitable for treatment with DRV/r monotherapy. In the MONOI trial, patients with low-level viraemia at baseline, problems with adherence or higher HIV DNA levels at baseline were more likely to show elevations in HIV RNA up to week 96 [9]. In a similar analysis of the Only-Kaletra-04 (OK-04) trial of lopinavir/ritonavir monotherapy, patients with poor adherence, lower nadir CD4 cell counts and lower baseline haemoglobin levels were

most likely to lose virological suppression over Selleckchem Birinapant 96 weeks of randomized treatment [10]. In other studies of standard triple combinations of antiretroviral treatment, coinfection with hepatitis C virus (HCV) has been a consistent predictor of lower HIV RNA suppression rates [11-15]. This trend has been seen across trials of PIs [12, 13, 15] and nonnucleoside reverse transcriptase inhibitors [11, 14]. Coinfection with HCV may be associated with prior or current injecting drug use, which could affect adherence to study medication. In addition, the efficacy endpoint used in these HIV clinical trials – the time to loss of virological response (TLOVR) – can be difficult to interpret. This endpoint classifies virological failure as any confirmed elevation above

50 copies/mL, occurring at any time during the trial. However, these elevations in HIV RNA may be low level, may not be associated with drug resistance and may occur for short time periods, with subsequent resuppression of HIV RNA by the Grape seed extract end of the trial. The results of the MONET trial were analysed at the final week 144 time-point, to assess whether there were baseline factors affecting the efficacy in the two treatment arms. In addition, the efficacy data were analysed by a strict intent-to-treat (ITT) (switches not considered failures) endpoint, which classified patients as success or failure depending on their HIV RNA levels at the end of the trial, regardless of transient elevations in HIV RNA at earlier time-points. The MONET trial recruited patients who had HIV RNA levels below 50 copies/mL at screening, while on a stable triple antiretroviral regimen, for at least 24 weeks, and no history of virological failure since first starting antiretrovirals. The trial methodology has been described previously [5]. Briefly, patients were randomized to receive DRV/r 800/100 mg once daily, either as monotherapy (monotherapy arm) or with two investigator-selected NRTIs (triple therapy arm).

In all experiments, cells were infected at a multiplicity of infection (MOI) = 5. Bacteria CH5424802 clinical trial were added to the apical chamber of the inserts, and monolayers were incubated at 37 °C for 1 h with agitation. Following incubation, all basolateral medium was removed and replaced

with prewarmed DMEM minus Pen-Strep. The monolayers were incubated at 37 °C for a further hour with agitation, and the basolateral medium was again collected. The basolateral medium was serially diluted and plated on LBN. TER was measured at 0-, 1- and 2-h time points. All LBN plates were incubated at 37 °C overnight. Colony-forming units (CFU) were counted for each experimental parameter. Data were analysed using Graph Pad Prism® software. All experiments were carried out three times in duplicate or triplicate, unless otherwise stated. Data are expressed as mean ± standard error of mean (SEM). Significances buy R428 of differences between mean values were assessed using the two-tailed, unpaired Student’s t-test or one-way anova with Tukey post hoc test where

appropriate, with significance set as P < 0.05 *, P < 0.01 **, P < 0.001 ***. The passage of V. parahaemolyticus across the M cell-like co-culture model vs. Caco-2 monolayers was investigated. First, the translocation of fluorescently labelled particles across both the monolayers and co-cultures was investigated to confirm in vitro induction of the M-like phenotype in the latter. After 2 h, an 18- and 16-fold increase in 1- and 0.5-μm particle transcytosis, respectively, were observed in the co-cultures, when compared to transcytosis across the Caco-2 monolayer (Fig. 1a). PLEKHB2 These values are in agreement with the reported value of 14-fold for similarly sized particles in former studies (Martinez-Argudo et al., 2007). These data highlight the significant sampling ability of M-like cells, thereby confirming the successful induction of the co-culture model in vitro. Examination of the transcytosis

of V. parahaemolyticus indicated an increase in bacterial translocation across the co-cultures compared to the Caco-2 monolayers following 1 and 2 h of infection (Fig. 1b). One hour postinfection, transcytosed bacterial numbers were 3.3-fold higher in the co-cultures with a 3.2-fold difference between Caco-2 monolayers and co-cultures observed following 2 h of infection. Comparison of translocation of V. parahaemolyticus across the co-culture and control demonstrated a 5.7- and 5.8-fold increase, respectively, between the 1- and 2-h time points. The data indicate that while V. parahaemolyticus has the ability to translocate across both the control and co-culture models 1 h postinfection with a dramatic increase in translocation observed 2 h postinfection, it translocates across the co-culture model in significantly increased numbers when compared to passage across the Caco-2 monolayer.

In all experiments, cells were infected at a multiplicity of infection (MOI) = 5. Bacteria Adriamycin nmr were added to the apical chamber of the inserts, and monolayers were incubated at 37 °C for 1 h with agitation. Following incubation, all basolateral medium was removed and replaced

with prewarmed DMEM minus Pen-Strep. The monolayers were incubated at 37 °C for a further hour with agitation, and the basolateral medium was again collected. The basolateral medium was serially diluted and plated on LBN. TER was measured at 0-, 1- and 2-h time points. All LBN plates were incubated at 37 °C overnight. Colony-forming units (CFU) were counted for each experimental parameter. Data were analysed using Graph Pad Prism® software. All experiments were carried out three times in duplicate or triplicate, unless otherwise stated. Data are expressed as mean ± standard error of mean (SEM). Significances X-396 solubility dmso of differences between mean values were assessed using the two-tailed, unpaired Student’s t-test or one-way anova with Tukey post hoc test where

appropriate, with significance set as P < 0.05 *, P < 0.01 **, P < 0.001 ***. The passage of V. parahaemolyticus across the M cell-like co-culture model vs. Caco-2 monolayers was investigated. First, the translocation of fluorescently labelled particles across both the monolayers and co-cultures was investigated to confirm in vitro induction of the M-like phenotype in the latter. After 2 h, an 18- and 16-fold increase in 1- and 0.5-μm particle transcytosis, respectively, were observed in the co-cultures, when compared to transcytosis across the Caco-2 monolayer (Fig. 1a). cAMP These values are in agreement with the reported value of 14-fold for similarly sized particles in former studies (Martinez-Argudo et al., 2007). These data highlight the significant sampling ability of M-like cells, thereby confirming the successful induction of the co-culture model in vitro. Examination of the transcytosis

of V. parahaemolyticus indicated an increase in bacterial translocation across the co-cultures compared to the Caco-2 monolayers following 1 and 2 h of infection (Fig. 1b). One hour postinfection, transcytosed bacterial numbers were 3.3-fold higher in the co-cultures with a 3.2-fold difference between Caco-2 monolayers and co-cultures observed following 2 h of infection. Comparison of translocation of V. parahaemolyticus across the co-culture and control demonstrated a 5.7- and 5.8-fold increase, respectively, between the 1- and 2-h time points. The data indicate that while V. parahaemolyticus has the ability to translocate across both the control and co-culture models 1 h postinfection with a dramatic increase in translocation observed 2 h postinfection, it translocates across the co-culture model in significantly increased numbers when compared to passage across the Caco-2 monolayer.