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The increase of amyloid beta (Aβ) release and hyperphosphorylation of Tau protein represents the main events related to Alzheimer's disease (AD). Furthermore, the sporadic type represents the most common form of AD. Therefore, the establishment of a non-transgenic animal model that resembles the characteristics of the disease is of particular importance. Scopolamine has been linked to increases in both Aβ production and oxidative stress in rat and mice brains. Thus, the purpose of the present work was to identify changes in biomarkers that are related to AD after chronic administration of scopolamine (2 mg/kg i.p., during 6 and 12 weeks) to male Wistar rats. The results showed increased Aβ deposition at rat hippocampus which could be due to an increase of β-site amyloid-β-protein precursor cleaving enzyme 1 (BACE1) expression and activity. These findings could be related to the increase of glycogen synthase kinase 3 phosphorylated (GSK3βP9) expression. Finally, the establishment of a state of oxidative stress in groups treated with scopolamine was demonstrated by an increase in free radical content and MDA levels. The present study facilitates our understanding of the changes that occur in biomolecules related to AD in Wistar rats after the chronic administration of scopolamine.

Bovine lactoferrin (bLf), a component of milk and a dietary supplement, modulates intestinal immunity at effector and inductor sites. Considering the regional difference in intestinal compartments and the dynamics of local cytokine-producing cells in the gut across time, the aim of this work was to characterize the effects of bLf on the proximal small intestine in a BALB/c murine model of oral administration. Male BALB/c mice were treated with oral bLf vs. saline control as mock by buccal deposition for 28 days. Intestinal secretions were obtained at different time points and cells were isolated from Peyer’s patches (PP) and lamina propria (LP) of the proximal small intestine as representative inductor and effector sites, respectively. Total and specific anti-bLF IgA and IgM were determined by enzyme-immuno assay, the percentages of IgA+ and IgM+ plasma cells (PC) and cytokine-producing CD4+ T cells of PP and LP were analyzed by flow cytometry. We found that total and bLf-specific IgA and IgM levels were increased in the intestinal secretions of the bLf group in comparison to mock group and day 0. LP IgA+ PC and IgM+ PC presented an initial elevation on day 7 and day 21, respectively, followed by a decrease on day 28 in comparison to mock. Higher percentages of CD4+ T cells in LP were found in the bLf group. Cytokines-producing CD4+ T cells populations presented a pattern of increases and decreases in the bLf group in both LP and PP. Transforming growth factor beta (TGF-β)+ CD4+ T cells showed higher percentages after bLf administration with a marked peak at day 21 in both LP and PP in comparison to mock-treated mice. Oral bLf exhibits complex immune properties in the proximal small intestine, where temporal monitoring of the inductor and effector compartments reveals patterns of rises and falls of different cell populations. Exceptionally, TGF-β+ CD4+ T cells show consistent higher numbers after bLf intervention across time. Our work suggests that isolated measurements do not show the complete picture of the modulatory effects of oral bLf in immunological sites as dynamic as the proximal small intestine.

Muscarinic-acetylcholine-receptors (mAChRs) modulate intestinal homeostasis, but their role in inflammation is unclear; thus, this issue was the focus of this study. BALB/c mice were treated for 7 days with muscarine (mAChR/agonist), atropine (mAChR/antagonist) or saline. Small-intestine samples were collected for histology and cytofluorometric assays in Peyer's patches (PP) and lamina propria (LP) cell-suspensions. In LP, goblet-cells/leukocytes/neutrophils/MPO+ cells and MPO/activity were increased in the muscarine group. In PP, IFN-γ+/CD4+ T or IL-6+/CD4+ T cell numbers were higher in the muscarine or atropine groups, respectively. In LP, TNF-α+/CD4+ T cell number was higher in the muscarine group and lower in the atropine.

BACKGROUND It has been reported that boron induces changes in the immune response, including in inflammatory processes. Recently, the effect of boric acid has been documented on the differentiation of lymphocyte clusters in mice and rats. However, the differences among boron-containing compounds (BCC) have been poorly explored. METHODS In this study, we analyzed the effects after oral administration of boric acid (BOR), methylboronic (MET), 3-thyenylboronic (3TB), 4-hydroxymethyl-phenylboronic (4 M P) and 4-methanesulfonyl-phenylboronic (4SP) acids on the populations of lymphocytes from spleen and Peyer’s patch (PP) as well as on antibodies. Groups of six male BALB/C were orally treated with 4.6 mg/kg of body weight with BOR, MET, 3TB, 4 M P, and 4SP/daily for 10 days) or vehicle (VEH) as a control group. After euthanasia, the spleen and small intestine were dissected. We conducted flow cytometry assays to assess B, CD3+ T, CD4+ T, and CD8+ T cells. Levels of IgG and IgM in serum, and IgA in intestinal fluid samples were analyzed by enzyme immunoassay. RESULTS In particular, we observed the effects of the administration of boronic acids on the number of lymphocytes; these changes were more notable in spleen than in PP. We found different profiles for each boron-containing compound, that is BOR induced an increase in the percentage of CD8+ T and CD19+/IgA+ cells in spleen, but a decrease in CD8+ T and B220+/CD19+ cells in PP. Meanwhile MET induced a decrease of CD4+ T in spleen, but induced an increase of CD4+ T cells and a decrease in the number of CD8+ T cells in PP. Boronic acids with an aromatic ring moiety induced changes in serum immunoglobulins levels, while 3TB acid induced a notable increase in S-IgA. CONCLUSIONS Effects in lymphocyte populations and antibodies are different for each tested compound. These results highlight the establishment of the necessary structure-activity relationship for BCC as immunomodulatory drugs. This is relevant in the biomedical field due to their attractiveness for selecting compounds to develop therapeutic tools.

Objective: The posterior vagus nerve trunk innervates the entire small intestine, and elucidating its modulatory role in the IgA response was the aim of this study. Methods: Two groups of six male BALB/c mice underwent sham or posterior subdiaphragmatic vagotomy and were euthanized on the 14th postoperative day; then, the small intestines were dissected. The intestinal fluid was harvested for antibody analysis by ELISA, and cell suspensions from Peyer’s patches and lamina propria were prepared for cytofluorometric analysis of plasma cells and T lymphocytes. The CD4+ T cells were labeled for the intracellular IgA-producing interleukins (ILs)-4, -5, -6, and -10; transforming growth factor (TGF)-β; and the inflammatory cytokines tumor necrosis factor (TNF)-α, interferon (IFN)-γ, and IL-12. In the intestinal tissue samples, myeloperoxidase (MPO) visualization and the enzymatic activity were assessed by immunohistochemistry and ELISA, respectively. The data were analyzed by Student’s t test, and the differences were considered significant at p < 0.05. Results: In the vagotomy group, the IgA levels and the CD4+ T cells labeled with mediators that promote IgA secretion, including IL-4 (only at lamina propria), TNF-α, and IFN-γ, were decreased, whereas the lamina propria IgA+ plasma cells and MPO presence/activity were increased; changes in the IgM levels, IgM+ plasma cells, and CD4+ T cells labeled with TGF-β, which have a role in class switch recombination, were not observed. Conclusion: The downmodulating impact of vagotomy on IgA levels may result from defective IgA secretion without affecting class switch recombination, whereas vagotomy evoked a proinflammatory response regarding MPO. These findings may reflect the role of the vagus nerve on the control of the IgA response in the small intestine.

Boron-containing compounds induce effects on immune responses. Such effects are interesting to the biomedical field for the development of therapeutic tools to modulate the immune system.The scope of BCC use to modify immune responses is expanding, mainly with regard to inflammatory diseases. The information was organized to demonstrate the breadth of reported effects. BCCs act as modulators of innate and adaptive immunity, with the former including regulation of cluster differentiation and cytokine production. In addition, BCCs exert effects on inflammation induced by infectious and noninfectious agents, and there are also reports regarding their effects on mechanisms involving hypersensitivity and transplants. Finally, the authors discuss the beneficial effects of BCCs on pathologies involving various targets and mechanisms.Some BCCs are currently used as drugs in humans. The mechanisms by which these BCCs modulate immune responses, as well as the required structure-activity relationship for each observed mechanism of action, should be clarified. The former will allow for the development of improved immunomodulatory drugs with extensive applications in medicine. Patenting trends involve claims concerning the synthesis and actions of identified molecules with a defined profile regarding cytokines, cell differentiation, proliferation, and antibody production.

Alzheimer&rsquo, s disease (AD) is a neurodegenerative disease with no cure nowadays, there is no treatment either to prevent or to stop its progression. In vitro studies suggested that tert-butyl-(4-hydroxy-3-((3-(2-methylpiperidin-yl)propyl)carbamoyl)phenyl) carbamate named the M4 compound can act as both &beta, secretase and an acetylcholinesterase inhibitor, preventing the amyloid beta peptide (A&beta, ) aggregation and the formation of fibrils (fA&beta, ) from A&beta, 1-42. This work first aimed to assess in in vitro studies to see whether the death of astrocyte cells promoted by A&beta, 1-42 could be prevented. Second, our work investigated the ability of the M4 compound to inhibit amyloidogenesis using an in vivo model after scopolamine administration. The results showed that M4 possesses a moderate protective effect in astrocytes against A&beta, 1-42 due to a reduction in the TNF-&alpha, and free radicals observed in cell cultures. In the in vivo studies, however, no significant effect of M4 was observed in comparison with a galantamine model employed in rats, in which case this outcome was attributed to the bioavailability of M4 in the brain of the rats.

Background. Diabetes mellitus is considered a chronic noncommunicable disease in which inflammation plays a main role in the progression of the disease and it is known that n-3 fatty acids have anti-inflammatory properties. One of the most recent approaches is the study of the fatty acids of microalgae as a substitute for fish oil and a source rich in fatty acids EPA and DHA. Objective. To analyze the effect of supplementation with n-3 fatty acids extracted from microalgae on the inflammatory markers from two different strains of mice. Methods. Mice of two strains, db/db and CD1, were supplemented with n-3 fatty acids extracted from microalgae in lyophilized form and added to food; the experiment was carried out from week 8 to 16 of life. Flow cytometry was performed to determine the percentage of TCD4+ cells producing Th1 and Th2 cytokines. Results. Supplementation with microalgae fatty acids decreased the percentage of TCD4+ cells producing IFN-γ and TNF-α and increased the ones producing IL-17A and IL-12 in both strains; on the other hand, supplementation decreased percentage of TCD4+ cells producing IL-4 and increased the ones producing TGF-β. Conclusions. Microalgae n-3 fatty acids could be a useful tool in the treatment of diabetes as well as in the prevention of the appearance of health complications caused by inflammatory states.

Bovine lactoferrin (bLf) up-modulates intestinal IgA that is essential for homeostasis and which might confer protection to the distal small intestine that is vulnerable to inflammation. This study analyzed the effects of bLf administered orally on the IgA response at inductive (Peyer's patches) and effector (lamina propria) sites of the distal small intestine in mice. Groups of five healthy male BALB/c mice were orally treated with 5 mg of bLf for 7, 14, 21, or 28 days. Then, mice were killed and the distal small intestine was dissected. Intestinal fluid samples were analyzed to determine IgA and IgM levels by enzyme-immuno assay. Peyer's patches and lamina propria were analyzed for IgA(+) or IgM(+) plasma cells, B, CD4(+) T and CD8(+) T cells as well as CD4(+) T cells positive for either pro-inflammatory cytokines [tumor necrosis factor (TNF)-α, interferon-γ and interleukin (IL)-12] or for IgA-producing ILs (IL-4, -5, -10 and -6) by cytofluorometry. Antibodies, antibody-secreting cells, and B and T responses in both Peyer's patches and lamina propria were higher in bLf-treated than bLf-untreated mice. The generation of IL-10 and IL-6 CD4(+) T cells in Peyer's patches or TNF-α and IL-12 CD4(+) T cells in lamina propria showed similar response patterns. On days 14 and 28, cytokine/IL CD4(+) T cell responses were increased in Peyer's patches or decreased in lamina propria. The effect of bLf on the elicitation of IgA indicates a potential application of bLf as a nutraceutical to control inflammation in the distal small intestine.

GPR41 and GPR43 receptors are located at the level of the ileum and colon in the enteroendocrine cells, being activated by short-chain bacterial fatty acids, products of fermentation, these become a key to activate the mechanisms involved in this intestinal homeostasis. GPR43 and GPR41 mediate inflammatory processes such as colitis, but it has not been demonstrated their participation in vivo models of stress. In a model of acute and chronic restraint stress BALB/c mice we evaluated their expression. The measurement of serum corticosterone was performed to validate our model. Gene expression of Gpr41/Gpr43 through qPCR and protein expression of GPR41/GPR43 by Western Blot in both Large Intestine (IG) and Small Intestine (ID). Our results show that stress increases corticosterone levels being higher in chronic stress. Gene expression may show an increase for both receptors in chronic stress. Protein expression, unlike gene, has a greater increase in acute stress, except for GPR41 in ID where its increase is not significant. This suggests that an acute stimulation increases the expression of this receptor to conserve intestinal homeostasis, which initially deplete the gene machinery and then increase it by the constant appearance of the stressor stimulus although there seem to be post-translational mechanisms that do not allow. This shows us that the gradual increase of corticosterone apparently affects the expression of the protein of both receptors.

Intermittent fasting (IF) reportedly increases resistance and intestinal IgA response to Salmonella typhimurium infection in mature mice. The aim of this study was to explore the effect of aging on the aforementioned improved immune response found with IF. Middle-aged male BALB/c mice were submitted to IF or ad libitum (AL) feeding for 40 weeks and then orally infected with S. typhimurium. Thereafter, infected animals were all fed AL (to maximize their viability) until sacrifice on day 7 or 14 post-infection. We evaluated body weight, bacterial load (in feces, Peyer's patches, spleen and liver), total and specific intestinal IgA, lamina propria IgA+ plasma cells, plasma corticosterone, and messenger RNA (mRNA) expression of α-chain, J-chain, and the polymeric immunoglobulin receptor (pIgR) in liver and intestinal mucosa. In comparison with the infected AL counterpart, the infected IF group (long-term IF followed by post-infection AL feeding) generally had lower intestinal and systemic bacterial loads as well as higher total IgA on both post-infection days. Both infected groups showed no differences in corticosterone levels, body weight, or food and caloric intake. The increase in intestinal IgA was associated with enhanced pIgR mRNA expression in the intestine (day 7) and liver. Thus, to maintain body weight and caloric intake, IF elicited metabolic signals that possibly induced the increased hepatic and intestinal pIgR mRNA expression found. The increase in IgA probably resulted from intestinal IgA transcytosis via pIgR. This IgA response along with phagocyte-induced killing of bacteria in systemic organs (not measured) may explain the resolution of the S. typhimurium infection.

The immune-suppression caused by acute stress can be reduced by a regular practice of moderate exercise which is known to modulate the expression of secretory-IgA. This antibody is essential for protection against infections and maintenance of homeostasis at the mucosal level. In order to explore the effects of moderate exercise on secretory-IgA production in ileum of the small intestine, 2 groups of mice were submitted to this protocol for 6 months, an exercise group and a sedentary group. After sacrifice, levels of secretory-IgA in intestinal fluid and levels of adrenal hormones in serum were determined by enzyme immunoenzymatic assay. IgA-plasma cells in lamina propria were evaluated by flow cytometry. Transcriptional mRNA expression in mucosa of alpha-chain, J-chain, pIgR and cytokines (Interleukin-2, -4, -6, -10, transforming growth factor-beta, interferon-gamma and tumor necrosis factor) were determined by RT-PCR. In comparison with sedentary mice, moderate exercised mice displayed an up-regulating effect on the production of secretory-IgA and IgA-plasma cells, on the expression of all mRNA transcripts from secretory-IgA associated proteins, and on all cytokines tested. However, serum levels of adrenal hormones were not altered. Future studies on secretory-IgA production are necessary to support the substantive effect of moderate exercise on protection and homeostasis at the intestinal level.

Moderate exercise enhances resistance to pathogen-associated infections. However, its influence on intestinal IgA levels and resistance to Salmonella typhimurium in mice has not been reported. The aim of this study was to assess the impact of moderate exercise on bacterial resistance and the intestinal-IgA response in a murine typhoid model. Sedentary and exercised (under a protocol of moderate swimming) BALB/c mice were orally infected with Salmonella typhimurium and sacrificed on days 7 or 14 post-infection (n=5 per group). Compared with infected sedentary mice, infected exercised animals had i) lower intestinal and systemic bacterial loads; ii) higher total and specific intestinal-IgA levels, iii) a higher percentage of IgA plasma cells in lamina propria; iv) a higher level on day 7 and lower level on day 14 of intestinal α- and J-chain mRNA and plasma corticosterone, v) unchanged mRNA expression of intestinal pIgR, and vi) a higher mRNA expression of liver pIgR, α-chain and J-chain on day 7. Hence, it is likely that an increase in corticosterone levels (stress response) induced by moderate exercise increased intestinal IgA levels by enabling greater liver expression of pIgR mRNA, leading to a rise in IgA transcytosis from the liver to intestine. The overall effect of these changes is an enhanced resistance to infection.

We investigated whether intranasal immunization with amoebic lysates plus cholera toxin modified the populations of T and B lymphocytes, macrophages and dendritic cells by flow cytometry from nose-associated lymphoid tissue (NALT), cervical lymph nodes (CN), nasal passages (NP) and spleen (SP). In all immunized groups, the percentage of CD4 was higher than CD8 cells. CD45 was increased in B cells from mice immunized. We observed IgA antibody-forming cell (IgA-AFC) response, mainly in NALT and NP. Macrophages from NP and CN expressed the highest levels of CD80 and CD86 in N. fowleri lysates with either CT or CT alone immunized mice, whereas dendritic cells expressed high levels of CD80 and CD86 in all compartment from immunized mice. These were lower than those expressed by macrophages. Only in SP from CT-immunized mice, these costimulatory molecules were increased. These results suggest that N. fowleri and CT antigens are taking by APCs, and therefore, protective immunity depends on interactions between APCs and T cells from NP and CN. Consequently, CD4 cells stimulate the differentiation from B lymphocytes to AFC IgA-positive; antibody that we previously found interacting with trophozoites in the nasal lumen avoiding the N. fowleri attachment to nasal epithelium.

Intermittent fasting prolongs the lifespan and unlike intense stress provides health benefits. Given the role of the immunoglobulin A (IgA) in the intestinal homeostasis, the aim of this study was to assess the impact of intermittent fasting plus intense stress on secretory IgA (SIgA) production and other mucosal parameters in the duodenum and ileum. Two groups of six mice, with intermittent fasting or fed ad libitum for 12weeks, were submitted to a session of intense stress by a bout of forced swimming. Unstressed ad libitum fed or intermittently fasted groups were included as controls. After sacrifice, we evaluated intestinal SIgA and plasma adrenal hormones, lamina propria IgA+ plasma-cells, mRNA expression of polymeric immunoglobulin receptor, α- and J-chains in the liver and intestinal mucosa, as well as pro- (tumor necrosis factor-α, interleukin-6 and Interferon-γ) and anti- (interleukin-2, -4, -10 and transforming growth factor-β) inflammatory cytokines in mucosal samples. Under intense stress, intermittent fasting down- or up-modulated the levels of most parameters in the duodenum and ileum, respectively while up-regulated corticosterone levels without affecting epinephrine. Our data suggest intermittent fasting plus intense stress elicited neuroendocrine pathways that differentially controlled IgA and pIgR expression in duodenum and ileum. These findings provide experimental foundations for a presumable impact of intermittent fasting under intense stress on the intestinal homeostasis or inflammation by triggering or reducing the IgA production in ileum or duodenum respectively.

Nervous System in coordination with an other systems as endocrine and immune. Several studies have shown that conditions of stress modify the expression and concentration of SIgA, which has been attributed to factors as glucocorticoids and catecholamines produced in the adrenal gland. The objective of this study was determined the effect of adrenalectomy on secretion of IgA in the large intestine of BALB/c mice under acute stress by immobilization. We determined the concentration of serum corticosterone by RIA, the concentration of SIgA in intestinal fluid by ELISA and the percentage of T CD4+, T CD8+, B lymphocytes and plasma cells IgA+ in lamina propria by flow cytometry. The results showed that the serum corticosterone in the group SHAM+stress increased due to the effect of the activation of the hypothalamic-pituitary-adrenal axis and the concentration of SIgA. Regarding the cellular percentage, we founded an increased percentage of lymphocytes B and plasma cells positives to IgA; due to the effect of glucocorticoids and catecholamines over the cells of the immune system. The concentration of SIgA in intestinal fluid decreased compared to the SHAM group. Stress showed an important decreased on SIgA levels in comparison with SHAM+E group. We can conclude that the suppression of cortisol and catecholamines with acute exposure to stress directly affects the immune status in the large intestine. This work was supported by SIP-COFAA-IPN .

To maintain internal balance is a complex process that requires the activation of neuroendocrine mechanisms that allows organisms to conserve the systemic, tissular and cellular homeostasis. One of the most important pathways of the immune regulation in gut is through the Acetylcholine (ACh) release, which not only modules inflammation by suppressing the release of pro-inflammatory cytokines (cholinergic anti-inflammatory pathway); but also modulates IgA secretion by muscarinic receptors, in accordance with studies made in small and large intestine. As the last response has been poorly studied in animal models, we made a truncal vagotomy in BALB/c mice in order to know if vagus nerve module the IgA secretion. Twenty male mice underwent sham or sub-diaphragmatic truncal vagotomy, on 14th postoperative day were collected plasma, lymphocytes of Peyer’s patches and lamina propria and intestinal fluid in order to determine total secretory IgA by ELISA, plasmatic cells IgA+ and intracellular cytokines (TGF-b, IL-4, IL-5, IL-6, IL-10) by flow cytometry. The vagotomy group showed a decrease in levels of SIgA in intestinal fluid and TGF-b, IL-4, IL-5, IL-6 and IL-10 compared with SHAM group. Moreover, further studies are needed to clarify whether the changes in small intestine IgA and cytokine levels are induced by vagotomy directly or produced by some other indirect effects. This work was supported by SIP-COFAA-IPN .

Stress, which has become a public health problem, is an emotional and physical–chemical process inducing a tension that favors the release of cytokines, hormones, neurotransmitters and cortisol. The effects of acute stress on the cellular composition and secretion of IgA in large intestine has not yet been described. The secretory IgA plays an important role in host immune response as a first line of defense, including biochemical and cellular defense mechanisms capable of responding rapidly to pathogens. In the present study, acute stress was induced by restriction of movement, and its effect was evaluated in relation to the levels of IgA in intestinal fluid by ELISA and the percentage of T CD4+, T CD8+, B lymphocytes and plasma cells IgA+ in lamina propria by flow cytometry. Serum corticosterone levels were determined to confirm that stress was induced with the model of restraint used and to demonstrate the association of stress with immune system. Corticosterone levels increased in acute stress compared to healthy mice. Significative increase was found in the levels of IgA intestinal fluids. In the large intestine, a increase was observed in CD4+ T cells, CD19+ B cells, and the B220+/CD19+ relation, demonstrating the important role that stress plays in the integrity of the mucosal immune system, as well as its relationship to an increased prevalence of infectious diseases. This work was supported by SIP-COFAA-IPN .

Stress causes an increase in the secretion of glucocorticoid and catecholamine hormones by activation of the hypothalamic-pituitary–adrenal axis. These hormones interact with receptors on immune cells, causing changes in their response. Currently, several illness have been associated with repeated and chronic exposure to stress. Examples are neurodegenerative, cardiovascular, allergic, infectious and inflammatory diseases. However, the mechanisms through which stress can modulate the immune system and cause these pathologies are still completey unknown. The aim of this study was to determine the effect of the acute stress induced by restraint on the immune system associated with the mucosa of the small intestinal of BALB/c mice. Accordingly, a determination was made of the levels of IgA in serum and intestinal fluid of healthy mice and mice subjected to stress by ELISA, the percentage of T helper cells, cytotoxic T and B lymphocytes by flow cytometry, and the concentration of serum corticosterone by the EIA technique. Finally, it was examined whether there is any difference in IgA levels and the percentage of lymphocytes in the small intestine in both study groups. Flow cytometry showed that CD4 + T and B cells increased in the stressed animals in small intestine. Therefore, acute stress induced by restraint increased the secretion of IgA. This work was supported by SIP-COFAA-IPN.

It is known that stress causes significant changes on the immune system through the production of glucocorticoids and catecholamines. The objective of this study was to determined the effect of adrenalectomy on production and secretion of IgA pIgR in the small intestine of BALB/c under acute stress by immobilization 1 h. We considered 5 study groups: (1) control, (2) SHAM (surgery without adrenalectomy) (3) SHAM + E (with stress), (4) Adrenalectomized (ADX), and (5) Stressed Adrenalectomized (ADX + E). In all groups were determined the serum corticosterone levels by EIA, SIgA in intestinal fluid by ELISA and pIgR, IgA and J chain in epithelial cells by Western Blot. The results showed in group SHAM + E an increase in serum corticosterone levels, SIgA in intestinal fluid, IgA, J-chain and pIgR in epithelial cells; The corticosterone ADX levels were near zero; pIgR showed no difference from the control and can be directly related their production to hormonal stimulation. The changes in the morphology and physiology of intestinal epithelium in adrenalectomized mice without stress, favored the increase in the transport of IgA and J chain in epithelial cells, in stress conditions adrenalectomy undergoes further changes in the intestine, explaining why ADX + E group shows no change in the expression of IgA in epithelial cells compared to control groups. This work was supported by SIP-COFAA-IPN.

Stress is considered a disease of our time, affecting a number of people every day, people usually do not understand the stress as something that affects your health. Studies on the effect of stress on the immune system specifically in animal models have shown that the effect varies depending on the type of stress, its duration and if applied acutely or chronically. Changes in cell percentages of different cell populations produced by the application of restraint stress protocol for acute motion has been studied as a reference and in parallel to other parameters such as the effect of hormones, but has not paid sufficient attention to these changes. The aim of this work is to establish changes in the percentages of the populations of LB (B220/CD19), T CD4+ and TCD8+ in Peyer’s patches proximal and distal both during the state of acute stress-induced restriction of movement and during the subsequent recovery status of 2 h. Populations were studied by flow cytometry and corticosterone was measured by enzyme immunoassay (EIA). Flow cytometry showed that CD4+ T, B cells and plasmatic cells IgA+ increased in the stressed animal in Peyer’s patches. Actual changes were observed in lymphocyte populations, but to know the nature of these is necessary for future work studying the degree of apoptosis and the expression of integrins. This work was supported by SIP-COFAA-IPN.

The nose-associated lymphoid tissue (NALT), a compartment located at the base of the nose of some rodents, induces an immune response. Stress causes an increase in the secretion of glucocorticoid and catecholamine hormones by activation of the hypothalamic–pituitary–adrenal axis. The aim of this study was to determine the effects of stress by forced swimming on cell populations of B and T lymphocytes, the secretion of IgA, and the production of corticosterone. We used 10-week-old male BALB/c mice divided into a control group and an experimental group. The secretion of IgA in the nasal wash was determined by ELISA, the cell populations of B and T lymphocytes were quantified by flow cytometry, and the corticosterone levels were measured by an enzyme immunoassay. A significant difference of the secretion of IgA in nasal wash was found in stressed mice. Flow cytometry showed that CD4+ T cells increased in the stressed animals in both the NALT and the spleen, the latter organ representing the control system. We conclude that in response to the acute stressor applied in this study, the NALT showed itself to be sensitive, both in its cellular immune response represented by T lymphocytes as well as its humoral immune response represented by IgA, possibly as a result of the influence of hormones secreted during stress. This work was supported by SIP-COFAA-IPN.

A caloric restriction dietary regimen has been shown to downregulate secretory IgA (SIgA) levels in the proximal and distal segments of the small intestine. Contrarily, both moderate exercise and strenuous exercise upregulate this same parameter, although by distinct mechanisms. The aim of the present study was to assess the effect on SIgA and other mucosal parameters on a mouse model with a protocol of caloric restriction or ad libitum feeding followed by strenuous exercise. After sacrifice an evaluation was made of intestinal SIgA and plasma adrenal hormones (by immunoenzymatic assay), lamina propria IgA plasma-cells (by cytofluorometry), mRNA expression for polymeric immunoglobulin receptor (pIgR), alpha- and J-chains in liver and intestinal mucosa, and pro- and anti-inflammatory cytokines in mucosa samples (by real-time PCR). Caloric restriction showed a net suppressive effect in the proximal small intestine on SIgA production, pIgR transcription and mRNA levels of most IgA producing cytokines, without affecting the mRNA expression of pIgR producing cytokines. Contrarily, caloric restriction had a net stimulatory effect on these same parameters in the distal segment. Compared to the ad libitum group, animals under caloric restriction had lower levels of epinephrine and similar levels of corticosterone. It would thus be interesting to explore the clinical implications of caloric restriction on intestinal homeostasis in a future study, taking into account the distinct response in the proximal and distal segments of the small intestine. This work was supported by SIP and COFAA-IPN.

Diverse studies have shown the effect of acute stress on the immune system. For example, an increase has been observed in IgA levels in the lumen of the small intestine. However, it is not known whether this effect of stress is caused by an increase in the secretion and transport of IgA in the small intestine (SI). The aim of the current study was to determine if stress modifies the secretion and transport of IgA in the duodenum and ileum of the SI in Balb/c mice. Serum samples were obtained for the determination of corticosterone by RIA. Duodenum and ileum were extracted and lymphocytes were obtained from the lamina propia and Peyer’s patches to evaluate the percentage of IgA-producing plasmatic cells by flow cytometry, and epithelial cells were analyzed to measure the expression of pIgR and IgA by Western Blot. The results show that stress increased the levels of serum corticosterone. Additionally an increase in the expression of pIgR was observed in epithelial cells, as well as the percentage of IgA+-producing plasmatic cells in duodenum and ileum. Therefore, acute stress induced by immobilization increased the synthesis, transport and secretion of IgA in both intestinal segments tested, being significantly greater in the ileum. This work was supported by SIP and COFAA-IPN.