Dysbacteriosis of intestinal microflora induces altered immune re

Dysbacteriosis of intestinal microflora induces altered immune responses and results in disease susceptibility. Z-VAD-FMK ic50 Dendritic cells (DCs), the professional antigen-presenting cells, have gained increasing attention because they connect innate and adaptive immunity. They generate both immunity in response to stimulation by pathogenic bacteria and immune tolerance in the presence of commensal bacteria. However, few studies have examined the effects of intestinal dysbacteriosis on DCs. In this study, changes of DCs in the small intestine of mice under the condition of dysbacteriosis induced by ceftriaxone sodium were investigated. It was found that intragastric

administration of ceftriaxone sodium caused severe dysteriosis in mice. Compared with controls, numbers of DCs in mice with dysbacteriosis increased significantly (P = 0.0001). However, the maturity and antigen-presenting ability of DCs were greatly reduced. In addition, there was a significant difference in secretion of IL-10 and IL-12 between DCs from mice with dysbacteriosis and controls. To conclude,

ICG-001 ceftriaxone-induced intestinal dysbacteriosis strongly affected the numbers and functions of DCs. The present data suggest that intestinal microflora plays an important role in inducing and maintaining the functions of DCs and thus is essential for the connection between innate and adaptive immune responses. “
“Laboratory of Mucosal Immunology, Department of Medicine, University of California, La Jolla, CA,

USA Thymic stromal lymphopoietin (TSLP) is constitutively secreted by intestinal epithelial cells. It regulates gut DCs, therefore, contributing to the maintenance of immune tolerance. In the present report, we describe the regulation of TSLP expression in intestinal epithelial cells and characterize the role of several NF-κB binding sites present on the TSLP promoter. TSLP expression can Casein kinase 1 be stimulated by different compounds through activation of p38, protein kinase A, and finally the NF-κB pathway. We describe a new NF-κB binding element located at position –0.37 kb of the promoter that is crucial for the NF-κB-dependent regulation of TSLP. We showed that mutation of this proximal NF-κB site abrogates the IL-1β-mediated transcriptional activation of human TSLP in several epithelial cell lines. We also demonstrated that both p65 and p50 subunits are able to bind this new NF-κB binding site. The present work provides new insight into epithelial cell-specific TSLP regulation. A single layer of columnar intestinal epithelial cells (IECs) physically separates the intestinal lumen from the underlying mucosal immune cells and defects in their barrier function are associated with inflammatory bowel diseases [1, 2].

[28, 29] However, another study showed that infants with DSS had

[28, 29] However, another study showed that infants with DSS had more CD69+ natural killer (NK) cells and CD8+ and CD4+ T lymphocytes compared

to those with DHF without shock syndrome.[30] Hence, the use of CD4+ and CD8+ T-cell counts as predictors of severe dengue require further studies. Different cytokines are produced by DENV-specific T cells in response to the recognition of peptide–MHC selleck chemicals complexes on target cells. The pattern of cytokine production follows a T helper type 1 (Th) or Th0 profile. These T cells may produce IFN-γ, TNF-α, IL-2 and CC chemokine ligand 4 [CCL4; also known as macrophage inflammatory protein-1β (MIP-1β)], whereas the production of Th2 type cytokines, such as IL-4 and IL-13, is less common and less investigated.[31-33] Studies have shown that CD8+ T cells specific to the DENV serotype of a previous infection appear to be preferentially expanded during a secondary infection.[34, 35] Analysis of

the functional phenotypes of CD8+ T cells in DHF cases have revealed that cross-recognition is associated with reduced cytolytic/cytotoxic activity without a significant effect on cytokine production.[32, 35] In addition, activation with peptide variants has been shown to induce different sets of cytokines when compared with stimulation with the original peptide in both CD4+ and CD8+ T cells.[31, 36] Cytokines and chemokines induced by suboptimal activation selleck chemicals llc Obatoclax Mesylate (GX15-070) of T cells may augment vascular permeability leading to plasma leakage in DHF. Indeed, chemokines such as MIP-1β and monocyte chemoattractant protein 1 (MCP-1) are proteins that reduce tight

junctions of vascular endothelium cells in different inflammatory diseases. High concentrations of these proteins have been reported in patients with DHF/DSS.[37, 38] Endothelium exposure to these chemokines can cause injury, amplification of the inflammatory response and finally lead to severe dengue disease.[37] Approximately 90% of DHF/DSS cases are associated with secondary infection by a heterologous serotype, while the remaining 10% result from primary infection. In the context of a heterologous secondary infection, memory B cells generated against the primary infection will respond quickly, producing high titres of antibodies that will potentiate the current infection instead of neutralizing the virus. This response is another important component in immune enhancement, being defined as antibody-dependent enhancement (ADE). Heterologous non-neutralizing antibodies are able to recognize dengue viral epitopes and enhance infectivity in an Fc-dependent manner.[2, 5, 16] Briefly, ADE potentiates infection by linking potentially infective virus to its target cells, essentially monocytes and macrophages. These cells express receptors for the Fc portion of antibodies, in this case FcγR, which binds IgG.

ELISA showed that antisera from four mice were positive, with the

ELISA showed that antisera from four mice were positive, with the highest titer reaching 1:400 (data not shown). However, after booster immunization, the IgG titer of the sera against O. tsutsugamushi Karp increased, with the highest titer reaching 1:1600 as determined by both IFA and ELISA (Tables 3,4). Antibody against O. tsutsugamushi selleck screening library Karp failed to be detected in the sera from controls injected with PBS. Scrub typhus is often misdiagnosed, particularly in rural areas, with other infectious diseases, leading to multi-organ complications and increased mortality

of patients (22). Therefore, development of a rapid, effective diagnostic test for convenient use in rural areas is urgently needed. A more practical approach to the development of a novel serodiagnostic test for scrub typhus is to clone and express the immunodominant genes of O. tsutsugamushi. Many studies indicated that the 56-kDa membrane protein was a type-specific antigen that accounts for 10–15% of the overall protein of the bacterium. The protein proves to be immunogenicity and most people could produce antibodies against it once infected with the bacteria (17–21). In the present study, a recombinant protein with a deletion of 99 amino acid high throughput screening residues at the N terminal and 64 amino acid residues at the C terminal was expressed and purified. The recombinant protein did

not contain the signal peptide or the carboxy-terminal region of the 56-kDa protein, which was predicted to be hydrophobic and embedded in the membrane and showed no reactivity with human IgG and IgM antibodies (23). Previous reports have shown that 56-kDa protein was always produced in the form of inclusion body in E. coli (15–20). However, the recombinant protein was highly soluble in our study. The feature facilitated

performance of the agent in its natural state, without any need for additional manipulation. In the present study, we have observed serological cross-reactivity with rabbit sera against O. tsutsugamushi strains TA763, TH1817 and Kato, B. quintana, A. phagocytophilum and low positive reactivity with sera against E. chaffeensis and B. bacilliformis. Similar cross-reactivity with O. tsutsugamushi strains TA763, TH1817 and Kato was also observed by others, and it was suggested that it may be due to Glycogen branching enzyme homologous 56-kDa sequence (19). In terms of cross-reactivity with other agents, it was speculated that the rabbits used for raising antisera might be infected by P. bacilli that existed broadly in the environment. Cross-reactivity has been documented to occur between OXK antigen P. bacilli and rickettsial antibodies, known as Weil–Felix reactions (24). Another possibility for the cross-reactivity is that the purified protein was not pure enough. The impurity of recombinant protein might cause cross-reactivity by the polyclonal sera used in ELISA testing. With regard to the titer of the polyclonal antibodies, both IFA and ELISA have showed a highest titer of 1:1600.

Laboratory data revealed that our patient did not express donor-s

Laboratory data revealed that our patient did not express donor-specific antibody and the peritubular capillaries did not exhibit C4d immunoreactivity. Upon consideration of both histological and laboratory findings, we diagnosed acute vascular rejection of Banff 2007 class ACR IIA. We commenced 3-day sessions of intravenous steroid

pulse therapy twice weekly and adjusted the trough TAC level to 5–8 ng/mL by varying the TAC dose. We next performed an allograft biopsy and found no evidence of rejection (the S-Cr level was 2.7 mg/dL on April 1 2013). The present case report demonstrates the difficulties associated with management of TAC-based regimens in kidney transplant patients undergoing antituberculosis therapy. We also review the relevant literature. The proportion of Kinase Inhibitor Library supplier kidney allografts that is not rejected has improved dramatically in the era of the calcineurin inhibitor (CNI), but the use of such a strong immunosuppressant increases the risk of infection. Of the various possible infections, tuberculosis is particularly problematic because infection of transplant patients is associated with a higher incidence of mortality than noted Sorafenib manufacturer in the general population. The same antituberculosis agents are recommended for use in both transplant patients and the general population.[1] Rifampicin (RFP) plays a key role in antituberculosis therapy, but the

trough CNI level requires close attention because it is frequently decreased by RFP use. A 29-year-old man was admitted to our hospital in June 2013 for a scheduled biopsy 1 year after primary kidney transplantation. He had been diagnosed with IgA nephropathy at the age of 17 years. He underwent peritoneal dialysis in June 2011. In June 2012, he received a live-donor kidney transplant from his father. The ABO blood types of donor and recipient were compatible, and the HLA alleles were haplo-identical. The standard complement-dependent cytotoxicity cross-match test was negative. Immunosuppressive therapy consisted of tacrolimus (TAC), mycophenolate

mofetil, methylprednisolone and basiliximab. The allograft exhibited excellent early function, associated with an S-Cr Tryptophan synthase level of 1.2 mg/dL. The 1 year protocol biopsy revealed no evidence of rejection. However, our patient was diagnosed with lung tuberculosis. The QFT was positive and the chest CT findings typical of tuberculosis. Standard therapy with antituberculosis agents, consisting of isoniazid (INH) 300 mg, rifampin (RFP) 450 mg, ethambutol (EB) 500 mg and pyrazinamide (PZA) 1500 mg daily, commenced on 9 June 2012. Despite increasing the TAC dose (512 mg, daily) and frequent monitoring of the serum TAC trough level, the serum TAC level decreased gradually from 3.1 ng/dL on 7 July 2012 to 1.6 ng/dL on 1 October 2012.

Recently, we found that reduced expression of Fli-1 protein had a

Recently, we found that reduced expression of Fli-1 protein had a profound effect on disease development in the NZM2410 mice that are a strain derived by intercrossing NZW × NZB F1 mice. Fli-1+/− NZM2410 mice, like Fli-1+/− MRL/lpr mice, had significantly lower serum

autoantibody titres and decreased proteiuniria compared to WT NZM2410 mice. selleck inhibitor Fli-1+/− NZM2410 mice survived significantly longer compared to WT NZM2410 mice (unpublished data). However, Green et al.[25] demonstrated recently that non-haematopoietic factors also contribute to lupus disease development in the α-mannosidase II-deficient mice model. We believe that our data also support an effect of non-haematopoeitic cells on MRL/lpr mice disease development based on the decreased disease in the Fli-1+/− MRL/lpr mice receiving BM from WT MRL/lpr mice. Using mice with specific cell Fli-1 disruption will provide further insight into how Fli-1 affects lupus disease development. We are now generating conditional Fli-1 knock-out MRL/lpr mice for future study. In summary, our data demonstrate that the expression of Fli-1

in BM derived haematopoietic cells has a significant effect on autoimmune disease development in MRL/lpr mice and that decreased expression of Fli-1 in non-haematopoietic cell lineages also probably contributes to the improvement of autoimmune disease development in MRL/lpr mice, These data also indicate that the expression of a single gene in different cell types can have separate but synergistic effects on disease development. This study Sclareol was supported by National Institutes Selleckchem PD0332991 of Health grants (AR054546 to X. K. Z.) and the Medical Research Service, Department of Veterans Affairs (to X. Z. and G. G.). None. “
“Sjögren’s syndrome (SS) is an autoimmune inflammatory disease that primarily affects the lacrimal and salivary glands causing dry eyes and mouth. Antibodies to Ro60 are frequently observed in patients with SS; however, the role of these antibodies in SS initiation and progression remains

unclear. The sequence Ro60 273-289 (Ro274) is a known B cell epitope of Ro60and antibodies to this epitope have been observed in a subset of SS patients and in animals immunized with Ro60 protein. Animals immunized with Ro274 linear peptide develop a Sjögren’s-like illness. We hypothesized that passive transfer of anti-Ro274-specific IgG would induce a Sjögren’s-like phenotype. To evaluate this hypothesis, we adoptively transferred affinity-purified Ro274 antibodies into naïve BALB/c animals then evaluated salivary gland histology, function and IgG localization four days post-transfer. At this timepoint, there was no demonstrable mononuclear cell infiltration and salivary glands were histologically normal, but we observed a functional deficit in stimulated salivary flow of animals receiving Ro274 antibodies compared to animals receiving control IgG.

Likewise, transgenic animals with enhanced expression of particul

Likewise, transgenic animals with enhanced expression of particular genes have been exploited. Novel molecular techniques including real-time PCR for the detection of activated genes and their products, gene sequencing technologies, batteries

of specific reagents for detecting cytokines and their receptors, and the accompanying rapid development of next-generation sequencing and growing field of bioinformatics have all revolutionized the depth of dissection of the host immune response that is now possible. Collectively, all these methods have enabled the individual components of host responses to be documented in a manner that just could not be contemplated in the 1970s–1980s. Advances in our understanding Poziotinib mouse of epigenetics, novel approaches to glycan analysis and post-translational modifications Ceritinib molecular weight of proteins, although slower

in their application to H. p. bakeri than, for example, with viruses [68], in the long-term may turn out to be equally, if not more, important in aiding us to piece together all the threads of the host–parasite relationship of this model system. As explained earlier, the development of protective immunity requires immunization of mice by a single or several priming infections, each abbreviated with an anthelmintic drug to prevent worm burdens accumulating. In this setting, antibody also appears to be essential for expression of protective immunity. B cell–deficient mice cannot expel worms following challenge infections, even though they show marked expression of Th2 cytokines in the intestinal mucosa, but do so when given immune serum by passive transfer [69]. Interestingly, the antifecundity response in immunized B cell–deficient mice is unimpaired, indicating that worm fecundity can be entirely abrogated by mechanisms that do not involve antibody. However, antibody was found to play a role in mediating growth impairment and consequently stunting of the worms. Additionally B cells in this host/parasite system play an important ‘helper’ role

in supporting the expansion and maturation of memory Th2 lymphocytes through secretion Fossariinae of IL-2 [70]. Use of gene-deficient mice demonstrated that IgE does not play an essential role in protective immunity and IgA contributes only to a small extent [55]. By contrast, IgM was not found to play a role in protective immunity as AID-/- strain mice (lacking the RNA editing enzyme AID, [activation-induced cytosine deaminase] [71], and hence unable to undergo isotype class switching, for example from IgM to IgG [55]) failed to reject challenge infections with H. p. bakeri, despite producing enhanced levels of parasite-specific IgM [72]. Taken together, these findings support earlier work showing that the protective capacity of immune serum is largely contained within the IgG fraction [54].


We also observed that the extent of the reduction


We also observed that the extent of the reduction of naive T cells from Stat3-deficient mice was larger than that of memory/effector T cells when compared with the control group (Fig. 3d,e). It is accepted that the homeostasis of naive T cells is maintained by the combination of self-peptide MHC complexes and IL-7 signals.[4, 5] Also, IL-2 plays crucial roles in the differentiation of naive T cells into memory T lymphocytes.[26] Moreover, both IL-2 and IL-7 activate Stat3 in T cells.[19] Hence, we suggest that Stat3 supports the maintenance and expansion of the naive T-cell pool through the IL-7 receptor signals, as well as mediating memory/effector T-cell production via IL-2-induced signal transduction. Consistently,

we showed that both the naive and memory/effector T cells in peripheral lymphoid CYC202 mw organs were significantly deficient in Stat3 knockout mice. Because the mice contain a Cre transgene driven by the distal promoter of Lck gene, Cre-recombinase expression is mainly observed in T cells after T-cell receptor α (Tcra) locus rearrangement and after the process of positive Dorsomorphin nmr selection in thymic cortex.[27] To identify whether the T-cell deficiency in Stat3 knockout mice was attributable to the dysregulation of thymic development, we would have to observe the CD4 and/or CD8 expression pattern in thymocytes from wild-type or Stat3 knockout mice (Fig. 4a). CD4 or CD8 SP cells were unvarying in both groups of mice at 4–8 weeks old (data not shown). However, we observed considerable decreases of both CD4 and CD8 SP cells in thymocytes from Stat3-deficient mice at 6 months old

(Fig. 4a,b). A possible mechanism for this finding is that the failure to compensate the Stat3 G protein-coupled receptor kinase deficiency occurred on the maintenance of the CD4 or CD8 SP population in aged mice, while it works intact at younger age. Stat5, as a candidate molecule for compensating Stat3 deficiency in thymocytes, has been reported to play a crucial role in the thymic development including maintenance of CD4 or CD8 SP thymocytes.[28] Together with the Stat3, Stat5 is a key signal transducer for the IL-2 and IL-7 receptor signalling in T cells.[29] Furthermore, the activity of Stat5 is much reduced in ageing thymus.[29, 30] We therefore speculate that the pro-survival signals delivered from IL-2 or IL-7 receptors successfully lead to the expression of downstream targets such as Bcl-2 and Bcl-xL through Stat5 activation, which is sufficient in young mice even when Stat3 is deficient. However, the expression of Bcl-2 or Bcl-xL might be unable to be maintained in Stat3-deficient mice at an old age because the activity of Stat5 is dramatically decreased in ageing thymocytes. We also demonstrated that the susceptibility to apoptosis was enhanced and the expression of Bcl-2 and Bcl-xL was significantly reduced in thymocytes from Stat3 knockout mice (Fig. 4c,d).

By examination of

By examination of R788 mouse IFA and ELISA, the highest titer of the polyclonal antibodies reaches 1:1600. The recombinant 56-kDa protein in the study is valuable for developing a simple and rapid diagnostic test and vaccine for O. tsutsugamushi. Scrub typhus, also known as tsutsugamushi disease, is an acute febrile illness caused by infection with O. tsutsugamushi and is characterized by fever, rash, eschar, headache and overall

soreness. The disease is endemic in the Asia–Pacific region, including China, Japan, Korea and Thailand (1–4). The incidence of the disease in humans has increased sharply in China during the past 20 years (5–7). Diagnosis of scrub typhus depends generally on clinical presentation and epidemiological history. It is very difficult to differentiate scrub typhus from other acute febrile illnesses such as murine typhus, dengue fever and viral hemorrhagic fevers because of symptom similarities (8, 9). Therefore, underdiagnosis or misdiagnosis of scrub typhus is common and may result in delayed or inappropriate treatment. Current serodiagnostic assays, such as the IFA or micro-immunofluorescent antibody assay require the propagation of Rickettsiae in infected yolk sacs of embryonated chicken eggs or antibiotic-free cell cultures

as well as special equipment such as a fluorescence microscope (10). Isolation and cultivation of O. tsutsugamushi is reliable for diagnosis but is difficult and time-consuming for a non-specialist 3-oxoacyl-(acyl-carrier-protein) reductase laboratory. PCR-based approaches that target specific O. tsutsugamushi genes also require specialist equipment (11). Therefore, a simple, rapid, BI 6727 datasheet sensitive and economic diagnostic

method, especially for use in rural areas, is urgently needed. A more practical serodiagnostic method can be developed by cloning and expressing the immunodominant genes of O. tsutsugamushi in E. coli (12–14). These recombinant proteins offer a considerable advantage over the antigen derived directly from O. tsutsugamushi because the recombinant products can be produced and purified in scalable amounts. They can then be used as antigens for developing a convenient and inexpensive diagnostic method that would greatly reduce the cost, transport expense and overcome the reproducibility problems associated with the present diagnostic tests, which require growth and purification of O. tsutsugamushi (15). Orientia tsutsugamushi is an antigenically diverse microorganism. Ohashi et al. described several antigenic variants, such as the representative strains Gilliam, Karp, Kato and other isolates (16). Most isolates of O. tsutsugamushi in China are identified as serotype Gilliam or Karp. Recent investigations suggested that the major outer membrane 56-kDa protein is a protective antigen that can be produced as a suitable recombinant protein for a diagnostic reagent purpose (15). Kim et al.

“Differences in infant distress and regulatory behaviors b

“Differences in infant distress and regulatory behaviors based on the quality of attachment to mother, emotion Cetuximab purchase context (frustration versus fear), and whether or not mothers were actively

involved in the emotion-eliciting tasks were examined in a sample of ninety-eight 16-month-old infants and their mothers. Dyads participated in the Strange Situation, a limiting task designed to elicit infant frustration, and a novelty task designed to elicit infant fear. Mothers were asked to remain uninvolved during the first minute of each task and then instructed to engage with their infants as they wished for the remaining 3 min. Independent of concurrent maternal sensitivity, resistant infants were significantly more distressed than secure and avoidant infants. Avoidant infants engaged in fewer active mother-oriented regulation behaviors than secure and resistant infants and engaged in more self-soothing in the mother-involved condition than the mother-uninvolved condition. Resistant infants engaged in more physical comfort with their mothers and more venting than both secure and

avoidant find more infants and exhibited a smaller variety of adaptive non-mother-oriented strategies than did secure infants. There were few differences in infant distress and regulatory behaviors as a function of emotion task and maternal involvement. Limitations and implications for future research are discussed. “
“Recent studies demonstrated that in adults and children recognition of Methocarbamol face identity and facial expression mutually interact (Bate, Haslam, & Hodgson, 2009; Spangler, Schwarzer, Korell, & Maier-Karius, 2010). Here, using a familiarization paradigm, we explored the relation between these processes in early infancy, investigating whether 3-month-old infants’ ability to recognize an individual face is affected by the positive (happiness) or neutral emotional expression displayed. Results

indicated that infants’ face recognition appears enhanced when faces display a happy emotional expression, suggesting the presence of a mutual interaction between face identity and emotion recognition as early as 3 months of age. “
“Languages instantiate many different kinds of dependencies, some holding between adjacent elements and others holding between nonadjacent elements. In the domain of phonology–phonotactics, sensitivity to adjacent dependencies has been found to appear between 6 and 10 months. However, no study has directly established the emergence of sensitivity to nonadjacent phonological dependencies in the native language. The present study focuses on the emergence of a perceptual Labial-Coronal (LC) bias, a dependency involving two nonadjacent consonants. First, Experiment 1 shows that a preference for monosyllabic consonant-vowel-consonant LC words over CL (Coronal-Labial) words emerges between 7 and 10 months in French-learning infants.

Enterohemorrhagic Escherichia coli O157:H7 is a food-born pathoge

Enterohemorrhagic Escherichia coli O157:H7 is a food-born pathogen that spreads through fecal-oral transmission. It can cause diarrhea, hemorrhagic colitis, HUS and TTP (1). Sporadic cases and small outbreaks caused by EHEC O157:H7 continue to occur throughout the world. From 1982 to 2002, 350 outbreaks were reported from 49 states in the USA, accounting for 8598 cases of EHEC O157:H7 infection, including 1493 (17.4%) hospitalizations, 354 (4.1%) cases of HUS, and 40 (0.5%) deaths (2). In 1996, 9451 patients were infected by EHEC O157:H7 in Japan; 1808 were hospitalized and 12 died (3).

In 1999, of 20,000 Chinese infected by EHEC O157:H7, 195 developed acute renal failure and 177 died (4). During August and September 2006, outbreaks of EHEC O157:H7 again occurred in the USA, where Dabrafenib clinical trial spinach infected by EHEC O157:H7 caused infection of 199 individuals, of whom 102 required hospitalization, 31 developed

HUS and three died (5). Currently, outbreaks and spread of EHEC O157:H7 continue to occur, posing a great threat to human health and a global public health challenge. The LEE pathogenicity island on the chromosome of EHEC O157:H7 is comprised of LEE1 (ler, escRSTU), LEE2 (escCJ, sepZ, cesD), LEE3 (escVN), LEE4 (espABD, ZD1839 clinical trial escF) and LEE5 (tir, eae, cesT) (6). The size of eae is 2805 bp and encodes Intimin. The eae gene also exists in EHEC, EPEC, and Citrobacter rodentium. There are four distinct intimin subtypes, namely intimin α, β, γ, and δ, intimin γ having commonly been associated with EHEC O157:H7. EHEC O157:H7 adheres to the brush border of epithelial cells of the host large intestine and triggers transmembrane and intracellular signaling cascades, resulting in cytoskeleton rearrangement and aggregation of F-actin filaments Erastin datasheet to form specific A/E lesions (7, 8). These manifest mainly in damage to, or even disappearance of, brush border microvilli, as well as

close adhesion of bacteria to intestinal goblet cell membranes (9). The use of antibiotic therapy against EHEC O157:H7 is limited because, although sensitive to most of them, when damaged by antibiotics these bacteria can release the toxin Stx and promote the initiation of HUS and worsening of symptoms. It has been verified that the C terminal region (IntC280–300) of intimin confers protection from the immune system on these bacteria and that specific anti-intimin serum can block their adhesion to intestinal epithelial cells (10, 11). Anti-adhesin serum produced by animals immunized with a recombinant adhesin protein can block adhesion of EPEC and EHEC to Hep-2 cells and anti-intimin antibody can prevent EHEC O157:H7 from settling into the gut (7). Immunization of mice by feeding them transgenic tobacco expressing elements of C-terminal intimin from EHEC can induce a strong anti-adhesin specific mucosal immune response. After infection by EHEC O157:H7, these mice have reduced EHEC O157:H7 in their feces (12).