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There is no universally accepted uniform research to classify the severity of allergic reactions triggered by different food allergens. We established a food allergy model based on repeated intragastric administrations of proteins from peanut, egg, milk, or soybean mixed with cholera toxin followed by oral food challenges with a high dose of the sensitizing proteins. Increased specific IgE, specific IgG1, allergic symptom scores, histamine, murine mast cell proteases-1, vascular leakage, Th2 cytokines, and mast cell infiltration in the lungs and intestine were found in the allergic groups

Introduction: The increase in high-fat diet (HFD)-induced obesity and food allergy leads to an assumption that the 2 are related. This study aims to (1) systematic verification of HFD-induced obesity aggravates food allergy and (2) explore the correlation and molecular mechanisms of HFD-induced obesity promotes food allergy. Methods: Female BALB/c mice are divided into the control group (control), the ovalbumin (OVA)-sensitized group (OVA), the HFD-induced obesity group (HFD), and HFD-induced allergic obesity group (HFD + OVA). Results: In vivo data showed that HFD feed enhance clinical symptoms and intestinal mucosa villi shed on allergic mice. Moreover, we found that HFD and OVA irritation enhanced levels of mast cell degranulation and Th2 humoral response. Additionally, Western blot analysis showed the potentiation of peroxisome proliferator-activated receptor γ (PPAR γ) remarkably reduced on intestinal in HFD and OVA group, thereby inhibiting the expression of nuclear factor kappa B (NF-κB)/PPAR γ signal the phosphorylation of NF-κB P65. Conclusions: Overall, our results suggest that HFD-induced obesity is a potential risk factor for food allergy, which related to intestinal barrier destruction and inflammation through the PPAR γ/NF-κB signaling pathway.

As an essential indicator of allergic reactions, mast cell (MC) activation involves FcεRI-mediated signaling and the release of allergic mediators. In FcεRI signaling, CaIn vitro experiments used immunoglobulin E (IgE)/antigen (Ag)-induced activation of rat and mouse MCs in vitro. The levels of MC degranulation mediators were used to evaluate the effect of exCaIn vitro experiments revealed that exCaOur study provides an essential theoretical basis for targeting Ca

Over the past three decades, the number of obese people has risen steadily. The chronic low-grade inflammatory state and the non-specific activation of the immune system have contributed greatly to the development of obesity-related immunology. Food allergy as a kind of inflammatory disease with abnormal immune response may be associated with obesity. This review begins with the pro-inflammatory immunological effects of adipose tissue in obesity, and explains the possible effects of obesity on food allergy. In short, obesity not only directly causes imbalance of allergic-related immune cells in adipose tissue, but also indirectly causes this consequence through affecting expression of adipocytokines and peroxisome proliferator-activated receptor gamma (PPARγ) in adipose tissue. As a result, circulating levels of pro-inflammatory factors which are partly derived from adipose tissue increase, which might cause intestinal barrier injury. Therefore, obesity may increase the risk of food allergy.

Crustacean allergy, especially to shrimp, is the most predominant cause of seafood allergy. However, due to the high flexibility of immunoglobulin E (IgE), its three-dimensional structure remains unsolved, and the molecular mechanism of shrimp allergen recognition is unknown. Here a chimeric IgE was built in silico, and its variable region in the light chain was replaced with sequences derived from shrimp tropomyosin (TM)-allergic patients. A variety of allergenic peptides from the Chinese shrimp TM were built, treated with heating, and subjected to IgE binding in silico. Amino acid analysis shows that the amino acid residue conservation in shrimp TM contributes to eliciting an IgE-mediated immune response. In the shrimp-allergic IgE, Glu98 in the light chain and other critical residues that recognize allergens from shrimp are implicated in the molecular basis of IgE-mediated shrimp allergy. Heat treatment could alter the conformations of TM allergenic peptides, impact their intramolecular hydrogen bonding, and subsequently decrease the binding between these peptides and IgE. We found Glu98 as the characteristic amino acid residue in the light chain of IgE to recognize general shrimp-allergic sequences, and heat-induced conformational change generally desensitizes shrimp allergens.

(1) Background: The use of antibiotics affects the composition of gut microbiota. Studies have suggested that the colonization of gut microbiota in early life is related to later food allergies. Still, the relationship between altered intestinal microbiota in adulthood and food allergies is unclear. (2) Methods: We established three mouse models to analyze gut microbiota dysbiosis’ impact on the intestinal barrier and determine whether this effect can increase the susceptibility to and severity of food allergy in later life. (3) Results: The antibiotic-induced gut microbiota dysbiosis significantly reduced Lachnospiraceae, Muribaculaceae, and Ruminococcaceae, and increased Enterococcaceae and Clostridiales. At the same time, the metabolic abundance was changed, including decreased short-chain fatty acids and tryptophan, as well as enhanced purine. This change is related to food allergies. After gut microbiota dysbiosis, we sensitized the mice. The content of specific IgE and IgG1 in mice serum was significantly increased, and the inflammatory response was enhanced. The dysbiosis of gut microbiota caused the sensitized mice to have more severe allergic symptoms, ruptured intestinal villi, and a decrease in tight junction proteins (TJs) when re-exposed to the allergen. (4) Conclusions: Antibiotic-induced gut microbiota dysbiosis increases the susceptibility and severity of food allergies. This event may be due to the increased intestinal permeability caused by decreased intestinal tight junction proteins and the increased inflammatory response.

Hypersensitivity occurs when the body is stimulated by an antigen, resulting in an immune response, and leads to a physiological disorder or abnormal tissue trauma. Various immune cells, cytokines, and inflammatory mediators are involved in the immune responses related to allergic diseases, which are the core of anaphylaxis. Estrogen receptors are widely distributed in immune cells, which combine with estrogen and participate in allergic responses by affecting immune cells, cytokines, and inflammatory factors. We aimed to summarize the association between estrogen and allergic reactions to provide a scientific basis for understanding and studying the mechanisms of allergic diseases.

It has been established that lanatoside C, a FDA-approved cardiac glycoside, reduces proliferation of cancer cell lines. The proliferation of fibroblasts is critical to the pathogenesis of pulmonary fibrosis (PF), a progressive and fatal fibrotic lung disease lacking effective treatment. In this study we have investigated the impact of lanatoside C on a bleomycin (BLM)-induced mouse model of PF and through the evaluation of fibroblast proliferation and activation in vitro. We evaluated explanted lung tissue by histological staining, western blot analysis, qRT-PCR and survival analysis, demonstrating that lanatoside C was able to protect mice against BLM-induced pulmonary fibrosis. The proliferation of cultured pulmonary fibroblasts isolated from BLM-induced PF mice was suppressed by lanatoside C, as hypothesized, through the induction of cell apoptosis and cell cycle arrest at the G2/M phase. The Akt signalling pathway was involved in this process. Interestingly, the production of α-SMA, fibronectin, and collagen I and III in response to TGF-β1 in healthy mouse fibroblasts was suppressed following lanatoside C administration by inhibition of TGF-β1/Smad signalling. In addition, TGF-β1-induced migration in lung fibroblasts was also impeded after lanatoside C treatment. Together, our data revealed that lanatoside C alleviated BLM-induced pulmonary fibrosis in mice via attenuation of growth and differentiation of fibroblasts, suggesting that it has potential as a candidate therapy for PF patients.

Currently, the weight loss effects of piperine have gained considerable attention; however, the underlying mechanism needs to be comprehensively elucidated. In the present study, we aimed to investigate the relationship between the weight loss effects of piperine and intestinal function. Based on the obtained results, piperine inhibited intestinal fatty acid absorption in both cellular and animal models. The underlying mechanism may be related to the downregulation of fatty acid absorption-related genes, fatty acid-binding protein 2 and cluster of differentiation 36, but not fatty acid transport protein 4. In addition, piperine repaired the tight junction damage induced by obesity by downregulating jejunal tumor necrosis factor-α and reducing lipopolysaccharide-induced damage on intestinal cell proliferation, thus enhancing intestinal barrier function, which is beneficial in reducing chronic inflammation associated with obesity. In conclusion, the anti-obesity effect of piperine is related to the enhancement of intestinal barrier function and inhibition of intestinal fatty acid absorption.

In recent decades, a rapid increase in the prevalence of food allergies has led to extensive research on novel treatment strategies and their mechanisms. Mouse models have provided preliminary insights into the mechanism of epicutaneous immunotherapy (EPIT)-induced immune tolerance. In EPIT, antigen applied on the skin surface can be captured, processed, and presented in the lymph nodes (LNs) by Antigen-presenting cells (APCs). In the LNs, induction of regulatory T cells (Treg cells) requires both direct contact during antigen presentation and indirect mechanisms such as cytokines. Foxp3+CD62L+ Treg cells can exhibit the characteristics of hypomethylation of Foxp3 TSDR and Foxp3-LAP+ Treg cells, which increase the expression of surface tissue-specific homing molecules to exert further sustained systemic immune tolerance. Studies have shown that EPIT is a potential treatment for food allergies and can effectively induce immune tolerance, but its mechanism needs further exploration. Here, we review Treg cells’ role in immune tolerance induced by EPIT and provide a theoretical basis for future research directions, such as the mechanism of EPIT and the development of more effective EPIT treatments.

Aims Epidemiology shows that gender affects the incidence of food allergy. However, there is a lack of evidence of gender differences in food allergies and little is known about the mechanisms. The aim of this study was to excavate potential reasons for gender differences in food allergy based on estrogen. Main methods Female and male BALB/c mice sensitized with ovalbumin (OVA) were established to analyze the difference in food allergy. The systemic anaphylactic, including OVA-specific IgE, OVA-specific IgG, histamine, and cytokines, was assessed using an enzyme-linked immunosorbent assay (ELISA). ELISA also detected the estradiol in serum. Western blotting and immunofluorescence were used to detect the estrogen receptor. Peroxisome proliferator-activated receptor gamma (PPARγ) implicated in immune homeostasis and nuclear factor kappa-B (NF-κB) were determined by western blotting. Immunohistochemistry and hematoxylin-eosin (H&E) staining were used to detect zonula occludens-1 (ZO-1), tryptase, forkhead box protein P3 (Foxp3), and intestinal morphology, respectively. Key findings Female mice were more vulnerable to food allergy. Female mice treated with OVA did exhibit more serious systemic anaphylaxis than male mice. We observed increased levels of estradiol in serum, estrogen receptor, NF-κB, and decreased levels of PPAR γ in female mice. Furthermore, the intestinal mucosal integrity and intestinal permeability were more impaired in female mice treated with OVA than male mice. Significance Clarify the mechanism of gender differences in food allergies can provide targets in female mice and provide personalized diagnosis, management, and treatment of food allergy for female mice.

As a ligand-activated transcription factor, peroxisome proliferator-activated receptor gamma (PPAR-γ) plays a crucial role in allergic inflammation. Recently, the nuclear factor kappa B (NF-κB) pathway and PAK1 have been indicated to be associated with allergic diseases. However, the effect of PPAR-γ on NF-κB and PAK1 production in food allergies is not known. This study aims to 1) systematically validate that the activation of PPAR-γ attenuates allergic reactions and 2) elucidate the mechanism by which PPAR-γ regulates mast cell degranulation. Brown Norway rats were separated into control, ovalbumin, ovalbumin + rosiglitazone, and ovalbumin + GW9662 groups. In vivo experiments demonstrated that rosiglitazone administration markedly inhibited the clinical symptoms and the serum levels of immunoglobulins E and G1. In addition, cytokine release was regulated by activated PPAR-γ and characterized by increased levels of IFN-γ and decreased levels of IL-4, IL-5, and TNF-α. Our data showed that activated PPAR-γ has the potential to alleviate food allergies by enhancing intestinal mucosal integrity and tight junctions. Moreover, we found that PPAR-γ activation inhibited mast cell degranulation both in vivo and in vitro. Our in vitro findings also showed that the activated PPAR-γ signal could inhibit PAK1 phosphorylation and the expression of p65. Furthermore, the interaction between p65 and p-PAK1 during ovalbumin treatment was attenuated after PPAR-γ activation. Collectively, these results demonstrate that PPAR-γ is an important regulator of mast cell degranulation and the Th2-type response, which sheds new light on the importance of PPAR-γ in food allergies.

Introduction: Biological rhythm is inextricably linked to the physiological mechanisms of allergic diseases, but the exact mechanisms are still poorly understood. Clinical studies have reported rhythmic fluctuations in allergic diseases. The search for natural and harmless active ingredients based on biological rhythm with which to regulate allergic diseases is essential for the control of food allergy. Methods: In this study, mice were treated at different time points to determine the link between the severity of allergic reactions and the circadian clock genes. The mice were treated with lentinan, either continuously or discontinuously, to assess their clinical symptoms, vascular permeability, immune cells, cytokines, and clock genes. Specifically, rat basophilic leukemia (RBL-2H3) cells were treated with lentinan and the rhythmic changes of cell degranulation were measured. Results: The results in different models showed that the allergic reactions in mice treated at different time points were significantly different and thus related to fluctuations in biological rhythm. Treatment with lentinan was found to reduce the amplitude of changes in the clock genes, such as the activation of Per and Cry proteins in allergic mice, as well as to regulate biological rhythm in cells, inhibit the activation of Th2 cells, and alleviate allergic reactions. Furthermore, lentinan changed the rhythm of degranulation in RBL-2H3 cells. Conclusion: Lentinan was, therefore, determined to successfully alleviate allergic reactions by reducing the amplitude of changes in the body’s biological rhythm, inhibiting the activation of Th2 cells, and affecting the immune microenvironment.

Idiopathic pulmonary fibrosis (IPF) is a chronic and irreversible inflammatory disease with a high mortality rate and limited therapeutic options. This study explored the potential role and mechanisms of Dehydrocostus lactone (DHL) in the inflammatory and fibrotic responses in a bleomycin (BLM) induced model. Treatment with DHL significantly reduced pathological injury and fibrosis, the secretion of BLM-induced pro-fibrotic mediators TGF-β and α-SMA, and components of the extracellular matrix (fibronectin). Additionally, in the early stages of inflammation, DHL administration inhibited the infiltration of inflammatory cells and downregulated the expression of TGF-β, TNF-α, and IL-6, indicating that DHL treatment effectively alleviated BLM-induced pulmonary fibrosis and inflammation in a dose-dependent manner. Furthermore, BLM induced the production of IL-33 in vivo, which initiated and progressed pulmonary fibrosis by activating macrophages and enhancing the production of IL-13 and TGF-β. In contrast, a significant decrease in the expression of IL-33 after DHL treatment in vitro showed that DHL strongly reduced IL-13 and TGF-β. Regarding the mechanism, BLM-induced phosphorylation of JNK, p38 MAPK, and NF-κB were significantly reduced after DHL treatment, which further led to the down-regulation of IL-33 expression, thereby decreasing IL-13 and TGF-β. Collectively, our data suggested that DHL could exert its anti-fibrosis effect via inhibiting the early inflammatory response by downregulating the JNK/p38 MAPK-mediated NF-κB signaling pathway to suppress macrophage activation. Therefore, DHL has therapeutic potential for pulmonary fibrosis.

The flavone apigenin is widely distributed in vegetables and fruits and has a variety of pharmacological effects. However, there is no definitive scientific evidence that apigenin could act as a phytoestrogen and exert exerting estrogenic or antiestrogenic efficacy in vivo. Therefore, this study was established an ovariectomy (OVX) and estrogenized mouse model to evaluate the effects of apigenin on reproductive target tissues. Our data demonstrated that apigenin could exert a double-directional adjusting estrogenic effect in vivo. Specifically, treatment with apigenin reversed the weight changes caused by abnormal estrogen levels and altered the status of vaginal epithelial cells via the estrogen receptors. In addition, we found that apigenin exhibited a significant estrogenic activity, as indicated by the reversal of uterine atrophy. Apigenin treatment could also regulate the target tissue coefficient changes and estrogen disorders caused by excessive estrogen. Importantly, the administration of apigenin could upregulated the estrogen receptor (ER) α and ER β expression as a partial agonist. Our results demonstrate that apigenin has a double directional adjusting function in different physiological environments.

Aims Cholera toxin is often used to induce food allergies. However, its exact mode of action and effect remain ambiguous. In this study, we established a BALB/c mouse cholera toxin/ovalbumin-induced food allergy model to determine the molecular basis and signaling mechanisms of the immune regulation of cholera toxin during food allergy. Materials and methods The adjuvant activity of cholera toxin was analyzed by establishing mouse allergy model, and the allergic reaction of each group of mice was evaluated. The effect of cholera toxin on Th1/Th2 cell differentiation was analyzed to further explore the role of cholera toxin in allergen immune response. We stimulated bone marrow-derived dendritic cells (BMDCs) with cholera toxin in vitro to investigate the effect of cholera toxin on Notch ligand expression. BMDCs and naive CD4+T cells were co-cultured in vitro, and their cytokine levels were examined to investigate whether cholera toxin regulates Th cell differentiation via the Jagged2 Notch signaling pathway. Key findings The results showed that in the presence of allergens, cholera toxin promotes Th2 cell differentiation and enhances the body's immune response. Cholera toxin induces expression of the Notch ligand Jagged2, but Jagged2 Notch signaling pathway is not required to promote BMDCs-mediated differentiation of Th2 cells. Significance This study initially revealed the mechanism by which cholera toxin plays an adjuvant role in food allergy, and provides reference for future related research.

The antitumor activity of zero-valent selenium (Se0) nanoparticles stabilized by chitosan and its oligosaccharides having molecular weights 3 k, 65 k, and 600 k Da, was investigated. The nanoparticles stabilized with high molecular weight chitosan not only released selenium more easily compared with low molecular weight chitosan, but were also taken up by HepG2 cells more easily through electrostatic effect. Moreover, these were more efficient in inhibiting HepG2 cell viability. High ROS levels of cancer cells could easily induce selenium release from these nanoparticles, and oxidize the less toxic Se0 to highly toxic Se4+. The latter could not only consume antioxidant enzymes, but also cause mitochondrial dysfunction and cell apoptosis. Study of antitumor efficacy and side effect on a HepG2 xenograft BALB/c nude mice model exhibited that CS-Se0NPs had a higher selectivity for cancer cells; however, their effect on normal cells, which have relatively lower ROS levels, was limited.

The whey protein β-lactoglobulin (BLG) is a major milk allergen which is absent in human milk. Here, we for the first time generated DNA-free BLG bi-allelic knockout cow by zinc-finger nuclease (ZFNs) mRNA and produced BLG-free milk. According to the allergenicity evaluation of BLG-free milk, we found it can trigger lower allergic reaction of Balb/c mice including the rectal temperature drop and the allergen-specific immunoglobulin IgE production; BLG free-milk was easily digested by pepsin at 2 min, while BLG in control milk was still not completely digested after 60 min, and the binding of IgE from cow’s milk allergy (CMA) patients to BLG free-milk was significantly lower than that to the control milk. Meanwhile, the genome sequencing revealed that our animal is free of off-target events. Importantly, editing animal genomes without introducing foreign DNA into cells may alleviate regulatory concerns related to foods produced by genome edited animals. Finally, the ZFNs-mediated targeting in cow could be transmitted through the germline by breeding. These findings will open up unlimited possibilities of modifying milk composition to make it more suitable for human health and also improve the functional properties of milk.

Food allergy includes sensitization phase and effect phase, and effect cells degranulate and secrete cytokines in the effect phase, causing allergic clinical symptoms. We have demonstrated that Notch signaling plays an important role in the sensitization phase, but its role in effect phases still remains unclear. In this study, we investigated the role of Notch signaling in degranulation and cytokine production of the effect phase response. A RBL-2H3 cell model was used and Notch signaling was induced by priming with Notch ligands. Our results showed after priming with Notch ligand, Delta-like1(Dll1)-Fc, β-hexosaminidase release, and cytokines production, including TGF-β, IL-1β, IL-4, IL-6, and IL-13, were increased significantly, and the enhancement was abolished after DAPT treatment, a γ-secretase inhibitor, indicating that Dll1 Notch signaling enhanced RBL-2H3 cell degranulation and cytokine production. Western blot analysis showed that Dll1 Notch signaling augmented high-affinity IgE receptors-mediated phosphorylation of MAPKs through suppressing the expression of downstream tyrosine kinases 1 (Dok-1). Besides, a passive systemic anaphylaxis mouse model was used to confirm the role of Notch signaling. And our data showed that allergic clinical features of mice were alleviated, and the level of degranulation was decreased significantly after inhibiting Notch signaling in vivo. Therefore, we demonstrated Notch ligand Dll1 enhanced RBL-2H3 cell degranulation and cytokine production through a novel Notch/Dok-1/MAPKs pathway, suggesting Notch signaling played a key role in the effect phase of food allergy.

Glycyrrhizic acid (GA), the major bioactive triterpene glycoside of glycyrrhiza, has been shown to possess a wide range of pharmacological properties, including anti-inflammatory and anti-viral properties. However, few studies have examined the anti-allergic activity and exact mechanism of action of GA. In the present work, the anti-allergic activity and possible mechanisms of action of GA on an immunoglobulin (Ig) E-mediated allergic reaction has been studied using three models of allergic reaction in vivo and in vitro. Active systemic allergic reaction in Balb/c mice showed that GA can suppress the increased level of IL-4 to restore the immune balance of TH1/TH2 cells in a dose-dependent manner. Additionally, GA attenuated significantly the B cells producing allergen-specific IgE and IgG1 partly because of the low levels of TH2 cytokines. Both passive cutaneous anaphylaxis in vivo and an RBL-2H3 cell-based immunological assay in vitro indicated that GA acted as a “mast cell stabilizer”, as it inhibited mast cell degranulation and decreased vascular permeability by inhibiting the expression of Orai1, STIM1 and TRPC1, which blocked extracellular Ca2+ influxes. The current study suggests that GA may serve as an effective anti-allergic agent derived from food for the prevention and treatment of IgE-mediated allergic reaction.

The present pharmacotherapy for eosinophilic esophagitis (EoE) fundamentally depend on inhaled corticosteroids. Despite the fact that oral intake of topical steroids can be successful in restricting EoE-related inflammation, there are concerns with respect to the long term utilization of steroids, especially in kids. In the current research, we assess the effect of quail egg, which is reportedly a known serine protease inhibitor, on symptomatology and immune responses in a peanut-sensitized mouse model of food allergy induced EoE. Daily oral treatment with quail egg attenuated mice symptomatology and immune response. Treatment with quail egg inhibited antigen-prompted increments in mouse tryptase and eosinophil cationic protein (ECP) in serum and eosinophil in inflamed tissues like oesophagus, lung, and digestive system. Quail egg treatment resulted in decreased antibody specific IgE and IgG1 and a variety of inflammatory genes that were abnormally expressed in EoE. Other effects included increased IL-10, decreased PAR-2 activation and NF-kB p65 in inflamed tissues. Our results suggest that quail egg treatment may have therapeutic potential in attenuating the symptoms of food allergy induced EoE like disease through regulating PAR-2 downstream pathway by blocking the activation of the transcription factor NF-kB p65 activity.

Notch signaling regulates proliferation, differentiation, and function of dendritic cells, T cells, and mast cells, as well as many other immune cells, which act as important parts in food allergy, Notch signaling may play an important role in food allergy.To investigate the role of Notch signaling in IgE-mediated food allergy.An ovalbumin-induced food allergy mouse model was built (cholera toxin as adjuvant) and Notch signaling was blunted by FLI-06 and MW167, which inhibited Notch receptor-expressing phase and the γ-secretase-affecting phase, respectively. Then food allergy indicators, including levels of serum antibodies, cytokines, and degranulation, were examined. Meanwhile, clinical features, such as vascular permeability changes, intestinal permeability changes, body temperature changes, and symptoms, were also observed.After blunting Notch signaling, the levels of serum ovalbumin specific IgE and IgGFood allergy was inhibited by blunting Notch signaling through suppressing T

Food allergy is an important public health problem that affects an estimated 8% of young children and 2% of adults. With an increasing interest in genetically-engineered foods, there is a growing need for development of sensitive and specific tests to evaluate potential allergenicity of foods and novel proteins as well as to determine allergic responses to ensure consumer safety. This review covers progress made in the field of development of cell models, specifically that involving a rat basophil leukemia (RBL) cell-based immunoassay, for use in allergen identification, diagnosis, and immunotherapy. The RBL assay has been extensively employed for determining biologically relevant cross-reactivities of food proteins, assessing the effect of processing on the allergenicity of food proteins, diagnosing allergic responses to whole-food products, and identifying anti-allergy food compounds. From the review of the literature, one might conclude the RBL cell-based assay is a better test system when compared to wild-type mast cell and basophil model systems for use in allergen identification, diagnosis, and analyses of potential immunotherapeutics. However, it is important to emphasize that this assay will only be able to identify those allergens to which the human has already been exposed, but will not identify a truly novel allergen, i.e. one that has never been encountered as in its preferred (humanized) configuration.

To assess inhibition mechanisms of a Phellinus igniarius (PI) extract on cancer, C57BL/6 mice were orally treated with PI extractive after or before implanting H22 (hepatocellular carcinoma ) or B16 (melanoma) cells. Mice were orally gavaged with different doses of PI for 36 days 24h after introduction of H22 or B16 cells. Mice in another group were orally treated as above daily for 42 days and implanted with H22 cells on day 7. Then the T lymphocyte, antibody, cytokine, LAK, NK cell activity in spleen, tumor cell apoptosis status and tumor inhibition in related organs, as well as the expression of iNOS and PCNA in tumor tissue were examined. The PI extract could improve animal immunity as well as inhibit cancer cell growth and metastasis with a dose-response relationship. Notably, PI's regulation with the two kinds of tumor appeared to occur in different ways, since the antibody profile and tumor metastasis demonstrated variation between animals implanted with hepatocellular carcinoma and melanoma cells.

The classification of food allergens based on the structure and function of proteins contributes to the study of the relationship between bioinformatics and potential allergenicity of allergens. Food allergens always share sequence similarity with the allergens in the same allergen families. For that reason, food proteins from different allergen families may induce different patterns of immune responses in animal models. Female Balb/c mice (3-4-weeks-old) were sensitized with food proteins once per week for 4 weeks, and then challenged 2 weeks later (on Day 42 of study). Blood was collected (to obtain serum levels of histamine and protein-specific IgG1 and IgE antibodies) and measures of vascular permeability were performed 20 min after the challenge. Five food proteins (11S globulin, OVA [ovalbumin], HAS [human serum albumin] and LRP [lysine-responsive storage protein] of different allergen families, and Cry 1Ab/Ac [crystal protein]) were used to assess patterns of immune responses for each allergen family and then bioinformatics and digestive stability in simulated gastric fluid were employed to assess the overall utility of the Balb/c. The assay results indicated that, in this model, histamine and protein-specific IgE antibody levels and vascular permeability could be used to identify allergenicity of 11S globulin, OVA, and PAP (potato acid phosphatase) only. However, the results of the protein-specific IgG1 measures could only distinguish allergic food proteins with negative control. Based on bioinformatic analyses, the five different food proteins clearly induced distinct patterns of immune responses in the Balb/c model.

There is currently no validated animal model for evaluating the potential allergenicity of food proteins. This study aimed to compare the allergic reactions between BN and Wistar rats after oral exposure to ovalbumin (OVA) by studying immune responses and clinical manifestations. Female BN and Wistar rats were orally exposed to OVA on days 1 and 14, and thereafter daily from day 15 to day 42. Sera and plasma were screened for OVA-specific antibodies and histamine. On day 49, all the OVA-sensitized animals were orally challenged with OVA before blood pressure was measured. One day later (on day 50), histopathology and differential cell counts were performed. The results indicate that oral exposure of BN rats to OVA yielded IgE, IgG, and IgG(2a) antibody responses that were generally of higher levels than those observed in Wistar rats (p0.05). However, the Wistar rats presented with more serious clinical manifestations and histopathologic changes that could have serious implications for any OVA-induced anaphylaxis. The studies here proved that OVA-sensitized BN and Wistar rats evinced different immune responses and clinical manifestations; these outcomes suggested that the two rat strains might differ in their immunologic mechanisms of allergy and that there was no correlation between immune responses and the severity of clinical symptoms. To be clear, the data from these studies should be viewed as 'preliminary', as only a single protein allergen was examined. Accordingly, further studies are needed to compare the allergic reactions between BN and Wistar rats by using purified strong-, weak-, and non-allergenic proteins based on the experiments reported here.

A water-soluble polysaccharide (LJP-1), with a molecular weight of 1.8×10(5) Da, was isolated from the flower buds of Lonicera japonica. Gas chromatography (GC) analysis showed that the LJP-1 was mainly composed of d-glucose and a small amount of d-arabinose. On the basis of methylation analysis, LJP-1 had the backbone chain mainly consisting of 1,6-linked Glc and 1,3,6-linked Glc, which was terminated with 1-linked Ara residues at the O-3 position of 1,3,6-linked Glc in a relative molar ratio of 2.9:1:0.9. The anti-allergic effect of LJP-1 was evaluated on allergic contact dermatitis (ACD) induced by picryl chloride (PC) in mouse ear. Similar to prednisolone, orally administrated LJP-1 (20, 40 and 80 mg/kg) potently inhibited the PC-induced ACD, leading to substantial reductions in ear thickness, serum level of IgE and histamine, as well as tissue TNF-α. These results demonstrate that treatment with LJP-1 may be effective for preventing the development of PC-induced ACD.

Background It is a widespread belief in Asian countries that mung bean soup (MBS) may afford a protective effect against heat stress. Lack of evidence supports MBS conferring a benefit in addition to water. Results Here we show that vitexin and isovitexin are the major antioxidant components in mungbean (more than 96% of them existing in the bean seed coat), and both of them could be absorbed via gavage into rat plasma. In the plasma of rats fed with mungbean coat extract before or after exposure to heat stress, the levels of malonaldehyde and activities of lactate dehydrogenase and nitric oxide synthase were remarkably reduced; the levels of total antioxidant capacity and glutathione (a quantitative assessment of oxidative stress) were significantly enhanced. Conclusions Our results demonstrate that MBS can play additional roles to prevent heat stress injury. Characterization of the mechanisms underlying mungbean beneficial effects should help in the design of diet therapy strategies to alleviate heat stress, as well as provide reference for searching natural medicines against oxidative stress induced diseases.