Other Articles published in this series Paraneoplastic neurological syndromes. Clinical and Experimental Immunology 2014, 175: 336–48.

Disease-modifying therapy in multiple sclerosis and chronic inflammatory demyelinating polyradiculoneuropathy: common and divergent current and future strategies. Clinical and Experimental Immunology 2014, 175: 359–72. Monoclonal antibodies in treatment of multiple sclerosis. Clinical and Experimental Immunology 2014, 175: 373–84. CLIPPERS: chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids. Review of an increasingly recognized entity within the spectrum https://www.selleckchem.com/products/Roscovitine.html of inflammatory central nervous system disorders. Clinical and Experimental Immunology 2014, 175: 385–96. Requirement for safety monitoring for approved multiple sclerosis therapies: an overview. Clinical and Experimental Immunology 2014, 175: 397–407. Myasthenia gravis: an update for the clinician. Clinical and Experimental Immunology 2014, 175: 408–18. Cerebral vasculitis in adults: what are the steps in order to establish the diagnosis? Red flags and pitfalls. Clinical and Experimental Immunology 2014, 175: 419–24. Multiple sclerosis treatment and infectious issues: update 2013.

Clinical and Experimental Immunology 2014, 175: 425–38. Diagnosis, pathogenesis and treatment of myositis: recent advances 2014, 175: 349–58. Management of disease-modifying treatments in neurological autoimmune diseases of the central nervous system 2014, 176: 135–48. Neuromyelitis selleck chemicals llc optica (NMO, Devic’s syndrome) is an inflammatory disorder of the central nervous system (CNS) that presents typically with relapses of optic neuritis (ON) or myelitis [1-4]. In recent years, the condition has raised enormous interest among scientists and clinical neurologists, fuelled by the detection of a highly specific serum immunoglobulin (Ig)G autoantibody Selleckchem Decitabine (NMO-IgG) targeting the most abundant astrocytic water channel aquaporin-4 (AQP4) [5-8]. NMO-IgG/AQP4-antibodies are

present in up to 80% of patients with NMO [8-11]. This seminal discovery has – together with previous neuropathological work that had already suggested humoral mechanisms to be relevant in the disease pathogenesis [12] – made clear that in most cases NMO is not a subform of multiple sclerosis (MS), as had been assumed for decades, but rather an autoimmune condition with an immunopathogenesis distinct from that of MS despite considerable overlap in clinical presentation and paraclinical findings. AQP4-antibody-positive NMO is part of an expanding spectrum of humorally mediated autoimmune diseases of the CNS that have been identified over the last few years [13, 14]. Several studies suggest that optimum treatment options may differ between NMO and MS, which underscores the necessity for a timely and accurate diagnosis.

Figure 3 shows the mean values of baseline, early peak, nadir, and plateau SkBF. The visual impression conveyed by Figure 2, was confirmed by the statistical analysis of these parameters. From T0 to T2, the mean decrease in the plateau SkBF and increase in early peak were, respectively, −9% to −16% and +10% to +18% of the value at T0 (p values below 0.05 for all conditions). As occurred with the plateau, the nadir tended to be lower at T2 than at T0 in the

four conditions find more tested, but the difference reached statistical significance only in the case of the custom-made chamber probed with LDI. Finally (and not obvious in Figure 2), the baseline SkBF, in all conditions, was slightly and significantly lower at T2, in comparison

with T0. At T2, the higher peak response was associated with a higher mean BP and therefore could reflect a change in perfusion pressure rather than in vascular tone. Against this interpretation, cutaneous vascular conductance (i.e., SkBF divided by mean BP) consistently increased from T0 to T2 (LDI RO4929097 clinical trial custom-made chamber: from 4.7 ± 1.5 to 5.8 ± 1.9 PU/mmHg, p < 0.001; LDI commercial chamber: from 4.0 ± 2.0 to 5.3 ± 2.6 PU/mmHg, p < 0.001; LDF custom-made chamber: from 6.8 ± 4.0 to 8.3 ± 4.7 mV/mmHg, p = 0.001; LDF commercial chamber: from 6.2 ± 2.7 to 7.7 ± 3.4 mV/mmHg, p = 0.001). Finally, the plateau response was somewhat lower with the custom commercial, when compared with the custom-made chamber. Although statistically significant, this effect was minor and could have been related to small differences in heating rate and temperature reached. The present study confirms our previous observation that the repeated application of a local thermal stimulus on the same skin patch,

at least when carried out within two hours, leads to a reduction in the elicited vasodilatory response. However, two studies [4,20] have not noticed this phenomenon. Therefore, the questions that must be asked are the reasons for this apparent discrepancy and whether differences in methods could be involved. The major difference relates to the equipment, both for measuring SkBF (LDF vs LDI) and for local heating (commercially available vs Aldol condensation custom-made chambers, which may not have the same surface area and heating rate). Any of these factors could have contributed to the discrepancy between our previous observations [3] and those made by these other groups [4,20]. However, in the present study, desensitization clearly occurred in all tested conditions, supporting its independency from the measuring equipment and heating system used in the experiment. In the work by Shastry et al., 10 subjects participated, five men and five women. The laser-Doppler flowmeter (PF 5010; Perimed) was single point at 780 nm, based on exactly the same technology as the less recent Perimed 4001 used in the present study.

However, an

unexpected advantage of the Ca2+ restoration was seen as the antigen-specific T cell proliferation was elevated especially in CD4+ T cells, but also in CD8α+ T cells. As both cell separation and wash in our analysis were carried out within 3–4 h after blood sampling, our findings are in good agreement with those of Bull et al. [17] who found that antigen-specific responses to HIV antigen even after cryopreservation was very sensitive to time after blood sampling but not to the type of anticoagulant. Chickens of the MHC haplotypes B13 and B130 (B21 like) were vaccinated against selleck inhibitor NDV. Forty-nine days after the first vaccination, the antigen-specific proliferation was measured. Within chickens of each haplotype, the percentage of proliferated CD8α+ T cells in unstimulated cells varied greatly, while this was not the case for CD4+ T cells. This contrasts the results shown in Fig. 3, as both B13 and B130 chickens in that case varied a lot in CD4+ T cell proliferation also. The discrepancy Selleckchem GS-1101 may be explained by the more uniform set-up in experiment 2. This confirms an NDV vaccine–induced cellular immune response as it was earlier demonstrated in chickens either cyclo-phosphamide-treated or bursectomized [4, 8, 29]. In those cases, it was also shown that the cellular response offered protection although the virus persisted for

a longer time in bursectomized and vaccinated chickens than was the case in control-vaccinated chickens. The fold increase in unstimulated to stimulated cells (SI) was calculated, and for the CD4+ T cells, the MHC difference was significant as the SI in B13 chickens was larger than that in the B130 chickens. The same tendency was seen for CD8α+ T cells although it was not significant. This

is in concordance with an earlier description of the B13 haplotype showing a larger mitogen-induced lymphocyte proliferation activity than the B21 haplotype [30]. In conclusion, we have established and optimized an assay for testing NDV-specific T cell Benzatropine proliferation in chickens upon vaccination. We concluded that it was an advantage to use EDTA as an anticoagulant if the CIS was used simultaneously as serum additive to the culture medium. Ca2+ restoration immediately after cell separation on Ficoll enhanced antigen-specific proliferation especially in CD4+ T cells. The levels of antigen-specific proliferation in chickens vaccinated at least 1 year prior to testing indicated a possible dependence on the MHC haplotype of the chicken. This was finally confirmed as two chicken lines that differed in MHC were subsequently compared. The authors acknowledge financial support from the Danish Poultry Council and from Aarhus University, Denmark. Hanne Svenstrup and Lene R. Dal are thanked for their technical assistance and Karin V. Østergaard for critical review of the manuscript.

67 Recently, a similar trend was reported for ICU patients in a single-centre observational study,68 and has been described in a review of published data predominantly originating from the US.69 Concerning echinocandins, selection of caspofungin-resistant strains has been observed in isolated cases,70 and an increase of C. parapsilosis candidaemia over a 5-year period in parallel to increasing use of caspofungin learn more use was reported from one large tertiary care centre.71 In general, however, current data do not support the notion of broad-scale species shifts or strain selection as a result of pressure exerted by the therapeutic use of echinocandins.

All the same, for convenience selleck products and cost reasons a switch to oral or intravenous treatment with an azole antifungal may appear desirable after stabilisation of the patient. Randomised clinical trials involving echinocandins required 10 days of initial therapy before a switch to an oral agent (usually fluconazole) was allowed.46,48,49 In these studies, 26%, 25% and 21% of the patients initially randomised to a standard-dose echinocandin switched to oral fluconazole after >10 days of therapy. Further prerequisites were confirmed negative blood cultures, defervescence for at least 24 h, improvement of clinical status and demonstration of susceptibility of the initial isolate to the oral agent of choice (fluconazole,

voriconazole). We should add adequate gastrointestinal function to assure crotamiton enteral absorption. A switch earlier than 10 days after initiation of therapy is feasible in individual cases, but it must be emphasised that this procedure is not supported by evidence from randomised

trials. Davis et al. [72] presented a two-period monocentric study comparing a retrospective period 1 with unregulated use of echinocandins (caspofungin or micafungin) for IC vs. an interventional period 2 involving formal in-house recommendations for step down by day 5 from intravenous anidulafungin to an oral azole (fluconazole or voriconazole; the latter to be used in cases with documented C. glabrata infection or unknown species) if certain criteria for oral treatment had been met (negative blood cultures, functional gastrointestinal tract, haemodynamic stability and improved clinical profile including leucocyte counts and body temperature). The rate of patients receiving oral step-down therapy was significantly increased in period 2, the duration of intravenous therapy and the duration of total therapy was decreased, whereas the clinical success rate remained unchanged and hospital mortality showed no significant difference. While the use of historical controls and potential educative effects of the intervention may have biased the results, these data suggest that an early step-down to an oral azole may be feasible in certain patients without compromising outcomes.

This work was funded jointly by British Council (UK) and the Indian Government under the UK-India Education and research initiative (UK-IERI) postgraduate funding scheme. “
“Citation Mason KL, Aronoff DM. Postpartum group A Streptococcus sepsis and maternal immunology. Navitoclax chemical structure Am J Reprod Immunol 2012; 67: 91–100 Group A Streptococcus (GAS) is an historically important agent of puerperal infections and sepsis. The inception of hand-washing and improved hospital

hygiene drastically reduced the incidence of puerperal sepsis, but recently the incidence and severity of postpartum GAS infections has been rising for uncertain reasons. Several epidemiological, host, and microbial factors contribute to the risk for GAS infection and mortality in postpartum women. These include the mode of delivery (vaginal versus cesarean section), the location where labor and delivery occurred, exposure to GAS carriers, the altered immune status associated with pregnancy, the genetic background of the host, the virulence of the infecting GAS strain, and highly specialized immune responses associated with female reproductive tract tissues

and organs. This review will discuss the Idelalisib concentration complicated factors that contribute to the increased susceptibility to GAS after delivery and potential reasons for the recent increase observed in morbidity and mortality. “
“Mesenchymal stem cells (MSCs) inhibit T-cell activation and proliferation but their effects on individual T-cell-effector pathways and on memory versus naïve T cells remain unclear. MSC influence

on the differentiation of naïve and memory CD4+ T cells toward the Th17 phenotype was examined. CD4+ T cells exposed to Th17-skewing conditions exhibited reduced CD25 and IL-17A expression following check MSC co-culture. Inhibition of IL-17A production persisted upon re-stimulation in the absence of MSCs. These effects were attenuated when cell–cell contact was prevented. Th17 cultures from highly purified naïve- and memory-phenotype responders were similarly inhibited. Th17 inhibition by MSCs was reversed by indomethacin and a selective COX-2 inhibitor. Media from MSC/Th17 co-cultures contained increased prostaglandin E2 (PGE2) levels and potently suppressed Th17 differentiation in fresh cultures. MSC-mediated Th17 inhibition was reversed by a selective EP4 antagonist and was mimicked by synthetic PGE2 and a selective EP4 agonist. Activation-induced IL-17A secretion by naturally occurring, effector-memory Th17 cells from a urinary obstruction model was also inhibited by MSC co-culture in a COX-dependent manner. Overall, MSCs potently inhibit Th17 differentiation from naïve and memory T-cell precursors and inhibit naturally-occurring Th17 cells derived from a site of inflammation. Suppression entails cell-contact-dependent COX-2 induction resulting in direct Th17 inhibition by PGE2 via EP4.

VEGF expression did not reveal any correlation with necrosis or bizarre vascular patterns. Supratentorial location is an independent predictor of a poor PFS. Significant coexpression of nestin and VEGF suggests that latter possibly augments stem cell survival. Thus, anti-VEGF therapy may be a good option in future for nestin immunopositive ependymomas. “
“The chromosome 16q22.1-linked

www.selleckchem.com/products/kpt-330.html autosomal-dominant cerebellar ataxia (16q-ADCA) is a form of spinocerebellar ataxia (SCA) common in Japan. It is clinically characterized by late-onset purely cerebellar ataxia. The neuropathologic hallmark of 16q-ADCA is degeneration of Purkinje cells accompanied by an eosinophilic structure which we named “halo-like amorphous materials”. By immunohistochemistry and electron microscopy, the structure has been so far found to contain two components: the somatic sprouts Cobimetinib nmr from the Purkinje cells and presynaptic terminals of unknown origin. As far as we are aware, this peculiar morphological change of Purkinje cells has not been previously described. Further investigations may disclose unique pathological processes in SCA. There is a considerable difference in frequencies of autosomal dominant cerebellar ataxias, also called spinocerebellar ataxia (SCA), in a small country such as Japan. However, overall, Machado-Joseph disease (MJD) and spinocerebellar

Tau-protein kinase ataxia type 6 (SCA6) are the two most prevalent SCAs in Japan. SCA1, SCA2 and dentatorubral-pallidoluysian atrophy (DRPLA), a form of SCA originally identified in Japan, are also present. These SCAs, caused by trinucleotide (CAG) repeat expansions, are diagnosed with relatively simple molecular genetic tests. While these SCAs with CAG repeat expansions are the major fraction of SCA, approximately 10–40% of all SCAs account

for diseases for which mutations have not yet been identified.1 We have been pursuing a form of SCA in which any of the known CAG repeat expansions are excluded from its cause. We started investigation on six such families which showed slowly progressive, seemingly purely cerebellar, ataxia in every generation.2 We embarked on a genome-wide linkage analysis using approximately 300 microsatellite DNA markers to discover in which chromosome the mutation is located. After screening all autosomal chromosomes, we found a significant evidence of linkage to the long arm of chromosome 16 (16q22.1).2 Surprisingly, this locus had been already known for SCA4, a SCA with prominent sensory axonal neuropathy associated with pyramidal tract signs.3 While every SCA4 patient showed prominent sensory axonal neuropathy, none of our patients presented such a remarkable “extracerebellar” dysfunction. In addition, ages of onset were earlier in SCA4 than in our families.

As demonstrated in a flow-diagram of the study (Fig. 1), 1 month after vaccination, four patients Target Selective Inhibitor Library molecular weight were excluded from the levamisole group and two were excluded from the placebo group because of either death or renal transplantation. One month after vaccination, 13 out of 16 (81%) patients in the levamisole group as compared with six out of 18 (33%) patients

in placebo group developed protective anti-tetanus IgG levels (relative risk = 2.44, 95% confidence interval = 1.21, 4.88, P = 0.005) (Fig. 2). From 1 to 6 months post-vaccination, one more patient in the levamisole group and two more patients in the placebo group were excluded because of renal transplantation. None of the excluded patients had protective anti-tetanus IgG levels at 1 month post-vaccination. Moreover, two patients from each group who were seropositive at 1 month post-vaccination became seronegative at 6 months. Therefore, at 6 months post-vaccination, 11 out of 15 (73%) patients in the levamisole group as compared with four out of 16 (25%) patients in the placebo group still had protective anti-tetanus IgG levels (relative risk = 2.93, 95% confidence interval = 1.19, 7.23, P = 0.007) (Fig. 2). While the mean serum levels of anti-tetanus IgG levels

were similar at baseline in the levamisole and placebo groups (0.031 ± 0.025 IU/mL vs 0.027 ± 0.021 IU/mL, P = 0.64), the mean serum levels of anti-tetanus IgG were significantly higher in the levamisole group at 1 month (1.45 ± 1.74 IU/mL vs 0.25 ± 0.36 IU/mL, P = 0.008) PLX4032 and at 6 months (0.61 ± 0.79 IU/mL vs 0.11 ± 0.18 IU/mL, P = 0.012) post-vaccination. Four patients (two from each group) who were seropositive at 1 month but became seronegative at 6 months were older and had lower serum levels of anti-tetanus IgG at 1 month as compared with patients who stayed seropositive from 1 to 6 months (11 in the levamisole and four in the placebo group) (61.3 ± 5.1 years vs 51.7 ± 15.2 years, P = 0.23; 0.58 ± 0.51 IU/mL vs 1.66 ± 1.66 IU/mL, P = 0.27). However, these differences did not reach statistical significance. Other measured factors such as BMI and serum albumin levels were similar between these two groups. In the levamisole group, two patients

developed mild leukopenia (with white blood cell counts of 940 and 1130 cells/mcL, respectively), one patient developed abdominal pain Carnitine palmitoyltransferase II and one patient developed nausea during 12 days of levamisole therapy. In the placebo group, two patients developed abdominal pain and one patient developed nausea during 12 days of placebo therapy. However, these symptoms were not severe enough to stop the treatment and were reversed after 12 days of levamisole or placebo therapy. Although there are studies that showed no enhancing effect of levamisole on haemodialysis patients’ response rates to HBV vaccination,[12] most studies demonstrate that levamisole has a beneficial effect.[8-10] In two recent meta-analyses by Fabrizi et al. and Alavian et al.

, 1998). The Trojan horse mechanism of transport across BBB is considered to play a crucial role in the pathogenesis of viral meningitis in the late phase of AIDS. This model has gained rapid favor; however, recent studies change this model by showing that the vast majority of virions transmitted in trans originate from the plasma membrane rather than from intracellular vesicles (Cavrois et al., 2008). The mechanisms of BBB disruption during retroviral-associated pathologies are not fully understood yet. Most of the studies are focused on the effect

of soluble molecules secreted by infected lymphocytes on BBB functions and intercellular TJ organization. In case of HIV infection, the viral protein Tat has been shown to induce cell apoptosis and disruption of the TJs (Andras et al., 2003). In short, Tat-mediated downregulation find more of claudin-5 plays an important role in altered integrity of BMEC that aids viral transport across BBB (Andras et al., 2005). West Nile virus (WNV)-associated encephalitis is characterized by disruption of the BBB, enhanced infiltration of immune cells into the CNS, microglial activation, inflammation, and eventual loss of neurons (Glass et al., 2005; Sitati et al., 2007). WNV gains entry into the CNS via the transcellular pathway, without compromising

the BBB integrity instead Metformin mw of paracellular pathway (Verma et al., 2009). Tick-borne encephalitis

(TBE) virus causes severe encephalitis with serious sequel in humans. The mechanisms underlying how TBEV gains access to the CNS are not completely elucidated. There are several hypothetical routes for TBEV traversal across BBB. These include (i) cytokine-mediated BBB breakdown, (ii) “Trojan horse” theory, and (iii) viral entry into the BMECs, transcytosis, and the release of virus into the brain parenchyma (Ruzek et al., 2011). Proteins from microbial pathogens are the dominant virulence factors mediating entrance to the CNS; however, various nonproteinous microbial components including lipopolysaccharide, LTA, glycolipids, and hyaluronic acid contribute to breakdown of the BBB. Lipooligosaccharide on the outer membrane is an important inflammatory agent Carnitine dehydrogenase in the CSF. Recent studies have demonstrated that lipooligosaccharide and lipopolysaccharide containing outer membrane vesicles provoke meningeal inflammation, increase concentration of leukocytes, and change permeability of the BBB (Cope et al., 1990). Hyaluronic acid of C. neoformans capsule facilitates the transport via BBB (Jong et al., 2007). Several hyaluronic acid receptors have been identified on various ECs; however, the only receptor on BMEC interacting with hyaluronic acid is CD44, the most common hyaluronic acid receptor in vertebrates. This interaction initiates the events of the entry at the BMEC membrane rafts (Jong et al., 2008).

These two isoforms Ribociclib mw are related closely in structure, but functionally distinct. In the present study we used a specific blocking antibody to FcγRIIB. Moreover, in the present study a different dose of GXM (100 µg/ml versus 50 µg/ml),

different types of cells (MonoMac6 cell line versus monocyte-derived macrophages) and different incubation times (2 h versus 2 days) were used. Our previous observations indicated that active SHIP, in cells treated with GXM, was responsible for reduction of NFκB transcriptional activation and negative regulation of inflammatory cytokines. This effect was mediated via GXM/FcγRIIB interaction [17]. The role of SHIP in FasL up-regulation and in GXM-induced apoptosis remains obscure, but we can assume that in our system SHIP activation induced by FcγRIIB engagement plays a direct role in apoptosis induction. Consistent with this hypothesis, early studies SAHA HDAC have shown a pro-apoptotic role of SHIP1 in several cell types, including B cells, myeloid and erythroid cells [44–46]. Moreover, Liu et al. have

reported that myeloid cells from SHIP−/− mice are less susceptible to programmed cell death induced by various apoptotic stimuli via Akt activation [45]. In addition, a substantial amount of literature provides evidence that SHIP1 is required to inhibit Akt activation [45,47–49]. This inhibition is critical for the activation of JNK [50]. Akt negatively regulates apoptosis signal-regulating kinase 1 (ASK1), which activates JNK and p38 transcriptional events [51], therefore inhibition of Akt could lead to ASK activation with consequent phosphorylation of downstream signalling molecules such as JNK and p38. In this study we demonstrated that GXM induces up-regulation of FasL expression by JNK or p38 signalling, which activate c-Jun independently of each other. In particular, Tacrolimus (FK506) JNK activation seems to be a consequence of GXM interaction with FcγRIIB, whereas p38 activation is also triggered by the binding of GXM with different

pattern recognition receptors (PRRs). However, the capacity of GXM to engage multiple PRRs, such as TLR-4 and FcgRIIB, which simultaneously transmit activating and inhibitory signals, might justify the high level of complexity of these signalling networks. Indeed, more studies are necessary to unravel the complexity of the GXM-induced signalling pathways. A schematic representation of the proposed pathway is shown in Fig. 8. Collectively, our results highlight a fast track to FasL up-regulation via FcγRIIB, and provide evidence for a mechanism involved in the activation of JNK, p38 and c-Jun. Moreover, the present study amplifies the spectrum of FcγRIIB-mediated effects, indicating that this receptor plays a critical role in transducing multiple signallings which contribute to inducing suppressive effects on innate and adaptive immunity.

Mucosal mast cells respond to both IgE-dependent (antigen) www.selleckchem.com/products/mi-503.html and non-IgE-dependent (bacterial toxins, neurotransmitters, etc.) stimulation and release a wide variety of bioactive mediators into adjacent tissues and exert their function in the allergic inflammation and in modulation of the gut function [9]. Besides an increased vascular permeability, mucosal oedema and contraction of smooth muscles, a diminished barrier integrity

was observed leading to an antigen-induced enhanced epithelial permeability [10]. These activated mast cells produce Th2-type cytokines, such as IL-3, IL-5 and IL-13 leading to the accumulation of eosinophils and other inflammatory cells relevant to allergic diseases [11]. The importance of calcium influx in mast cell activation and degranulation has been well recognized [12]. The degranulation of mast cell is Ca2+ dependent, and an increase in intracellular Ca2+ characterized by Ca2+ entry through store-operated calcium channels (SOCs) is essential for granule release [13-15]. Multiple mechanisms are involved in regulation of SOCs activity. It has recently been discovered that the two subunits, STIM1 and Orai1, play a vital role in both the signalling and the permeation mechanisms for Ca2+ influx through Selleck PF01367338 SOCs. Overexpression of STIM1 together with Orai1 caused a

dramatic increase in store-operated Ca2+ entry in RBL cells [16]. Furthermore, SOC activation has been suggested to be linked to PI-3K signalling pathways, as well as reactive oxygen species (ROS) production, despite controversial. However, whether food allergen–induced mast cell activation is related to the regulation of intracellular Ca2+ signalling, and the underlying mechanism remain unknown. In this study, using Brown-Norway rat food-allergic model, we aimed to investigate the involvement of Ca2+ signalling in food allergen–induced

mast cell activation and degranulation and the underlying mechanisms. We found that Ca2+ entry through SOCs was increased in mast cells in the food-allergic animal model. SOC activation was related to PI3K-ROS-induced upregulation of STIM1 and Orai1 expression. Four-week-old female Brown-Norway rats were purchased from Vital Tacrolimus (FK506) River Laboratories (Beijing, China) and housed in groups of four per cage in a controlled environment with a photoperiod of 12-h light/12-h dark and a temperature of 20 ± 2 °C. Sanitary controls were performed for all major rodent pathogens, and the results of these tests were uniformly negative. All the animal experimental procedures were approved by the Animal Care and Use Committee of Shenzhen University and carried out in accordance with the Guide for the Care and Use of Laboratory Animals published by the US National Institutes of Health (NIH publication no. 85-23, revised 1996). Forty Brown-Norway rats were randomly divided into two groups: control group and ovalbumin (OVA, Sigma, USA) group.