Gut-associated Lymphoid Tissue Research Articles

HIV-1-Host Interaction in Gut-Associated Lymphoid Tissue (GALT): Effects on Local Environment and Comorbidities.

HIV-1 replication in the gastrointestinal (GI) tract causes severe CD4+ T-cell depletion and disruption of the protective epithelial barrier in the intestinal mucosa, causing microbial translocation, the main driver of inflammation and immune activation, even in people living with HIV (PLWH) taking antiretroviral drug therapy. The higher levels of HIV DNA in the gut compared to the blood highlight the importance of the gut as a viral reservoir. CD4+ T-cell subsets in the gut differ in phenotypic characteristics and differentiation status from the ones in other tissues or in peripheral blood, and little is still known about the mechanisms by which the persistence of HIV is maintained at this anatomical site. This review aims to describe the interaction with key subsets of CD4+ T cells in the intestinal mucosa targeted by HIV-1 and the role of gut microbiome and its metabolites in HIV-associated systemic inflammation and immune activation that are crucial in the pathogenesis of HIV infection and related comorbidities.

LncRNA activates immune response against Vibrio anguillarum in the intestine-liver axis of turbot (Scophthalmus maximus L.) by sponging miRNA in a ceRNA regulatory network

Vibriosis, most commonly caused by the bacterium Vibrio anguillarum, is one of the most important diseases affecting the marine aquaculture industry throughout the world. The intestine is the main entry portal of V. anguillarum into host fishes. Although there has been extensive research on the immunity of the gut-associated lymphoid tissue (GALT) in teleost, the mechanisms underlying the immunity of the intestine-liver during bacterial infections are still not well understood. This study conducted an integrative analysis of the transcriptome in turbot (Scopthalmus maximus L.) intestine and liver after V. anguillarum infection. To provide evidence of immunological collaboration in the turbot intestine-liver axis, we constructed the immune gene libraries, and conducted the functional annotation and enrichment analyses of immune genes that were jointly expressed in both turbot intestine and liver. Additionally, we administered the bioinformatic analyses of transcriptomic data to investigate regulatory relationships between non-coding RNAs (ncRNAs) and their target immune genes, based on the ceRNA theory. The recognition and binding abilities to bacteria were activated by the Toll-like receptor (TLR) signaling pathway. Subsequently, NF-κB was activated by the TLR/MyD88 signaling, and its target genes were induced to up-regulate in intestine and associated tissues to the digestive tract to enhance disease resistance through the production of inflammation. Histology of the intestine and liver of infected fish showed pathological changes consistent with inflammation. Bioinformatic analysis suggested that ceRNA regulatory networks play a pivotal role in the regulation of TLR genes, and RT-qPCR analyses and dual-luciferase reporter assays showed confirmed evidence to verify these hypothesized regulatory relationships. Overall, the results in this study demonstrated that a lncRNA (LNC_002468) activated the TLR signaling pathway by upregulating the TLR9 gene through sponging miRNA (novel_709). This study provides a strong indication that ncRNAs play regulatory roles in the antibacterial immune response of teleost fishes. However, further functional verification is required of the key immune genes and their regulatory relationship with miRNAs and lncRNAs.

Influenza A virus infection during pregnancy causes immunological changes in gut-associated lymphoid tissues of offspring mice.

Maternal influenza A virus (IAV) infection during pregnancy can affect offspring immune programming and development. Offspring born from influenza-infected mothers are at increased risk of neurodevelopmental disorders and have impaired respiratory mucosal immunity against pathogens. The gut-associated lymphoid tissue (GALT) represents a large proportion of the immune system in the body and plays an important role in gastrointestinal (GI) homeostasis. This includes immune modulation to antigens derived from food or microbes, gut microbiota composition, and gut-brain axis signaling. Therefore, in this study, we investigated the effect of maternal IAV infection on mucosal immunity of the GI tract in the offspring. There were no major anatomical changes to the gastrointestinal tract of offspring born to influenza-infected dams. In contrast, maternal IAV did affect the mucosal immunity of offspring, showing regional differences in immune cell profiles within distinct GALT. Neutrophils, monocytes/macrophages, CD4+ and CD8+ T cells infiltration was increased in the cecal patch offspring from IAV-infected dams. In the Peyer's patches, only activated CD4+ T cells were increased in IAV offspring. IL-6 gene expression was also elevated in the cecal patch but not in the Peyer's patches of IAV offspring. These findings suggest that maternal IAV infection perturbs homeostatic mucosal immunity in the offspring gastrointestinal tract. This could have profound ramifications on the gut-brain axis and mucosal immunity in the lungs leading to increased susceptibility to respiratory infections and neurological disorders in the offspring later in life.NEW & NOTEWORTHY Influenza A virus (IAV) infection during pregnancy is associated with changes in gut-associated lymphoid tissue (GALT) in the offspring in a region-dependent manner. Neutrophils and monocytes/macrophages were elevated in the cecal patch of offspring from infected dams. This increase in innate immune cell infiltration was not observed in the Peyer's patches. T cells were also elevated in the cecal patch but not in the Peyer's patches.

Pharmacological Modulation of Host Immunity with Hen Egg White Lysozyme (HEWL)-A Review.

In the 100 years since its discovery, lysozyme has become an important molecule, both as model for studies in different fields and as a candidate for the therapy of various pathological conditions. Of the dozens of known lysozymes, in this review we focus on one in particular, lysozyme extracted from hen egg white (HEWL), and its interaction with the immune system when it is administered orally. Experimental data show that there is an axis that directs immune system activation from GALT (gut-associated lymphoid tissue) and the intestinal lymphocyte clusters. Although a contribution of peptidoglycans from digestion of the bacterial cell wall in the intestinal lumen cannot be excluded, immune stimulation is not dependent on the enzymatic activity of HEWL. The immune responses suggest that HEWL is able to recover from immunodepression caused by tumor growth or immunosuppressants, and that it also improves the success of chemotherapy. The positive results obtained in a small Phase 2 study in patients, the ease of oral administration of this protein, and the absence of adverse effects suggest that HEWL may play an important role in all diseases where the immune system is weakened or where its enhancement plays a critical role in the resolution of the pathology.

The role of vitamin A in non-ruminant immunology

Vitamin A (retinol) is an essential micronutrient with a crucial role in the immune system of non-ruminant animals, such as swine and poultry. It includes three chemical compounds with distinct properties and functions in the body: retinol, retinal, and retinoic acid. In monogastric feed, vitamin A is primarily present in the form of retinyl esters. The metabolism of dietary vitamin A esters involves their conversion to retinol, which is then transported to different tissues and cells for further metabolism into active forms such as retinoic acid. These active forms of vitamin A have been found to play a crucial role in regulating both innate and adaptive immune responses. Specifically, they are involved in the differentiation, proliferation, and function of immune cells such as T and B lymphocytes, as well as dendritic cells. Vitamin A deficiency can lead to impaired cellular immunity, reduced antibody production, and consequently an increased susceptibility to infections. In swine and poultry, hypovitaminosis A can also affect gut-associated lymphoid tissues, leading to gut-related health problems and compromised growth performance. On the other hand, vitamin A supplementation has been shown to have immunomodulatory effects on non-ruminant immune responses. By administering or supplementing retinol, immune cell proliferation, antibody production, and cytokine secretion can be enhanced, which can ultimately result in improved immune function and disease resistance. Therefore, vitamin A has potential applications as an immuno-micronutrient for improving health and preventing diseases in swine and poultry. However, the optimal dosage and timing of vitamin A supplementation need to be carefully determined based on the specific requirements of different non-ruminant species and their production stages. Overall, a better understanding of the role of vitamin A in non-ruminant nutritional immunology could have significant implications for animal health and productivity and could inform the development of effective dietary strategies to optimize immune function and prevent diseases in swine and domestic fowl. This review paper aims to offer valuable insights into the role of vitamin A in the nutritional immunology of non-ruminants while also emphasizing the current gaps in knowledge and potential areas for further research.

Exploring the Potential of Plant-Based CTB-INS Oral Vaccines in Treating Type 1 Diabetes

The 19th century saw the development of vaccines, which were biological preparations designed to enhance immunity against specific diseases. Edible vaccines function by stimulating both systemic and mucosal immune responses against foreign pathogens, and they may potentially protect the host from autoimmunity. The mucosal surfaces provide a convenient and rapid route for delivering therapeutic small molecules. This is due to their large surface areas and easy administration. The effectiveness of mucosal immunization relies on the fact that mucous membranes represent the body’s largest immunogenic organ. Within this interface, there is a well-organized lymphatic structure known as MALT (mucosa-associated lymphoid tissue), which includes both T and B cells and encompasses the adaptive arms of the immune system. Oral vaccines specifically stimulate immune responses in the gut-associated lymphoid tissue (GALT), which consists of lymph nodes, Payer’s patches (where B cells make up about 75% of the population and T cells account for approximately 20%), and isolated lymphoid follicles within the gastrointestinal tract (GIT). However, a significant challenge in developing vaccines is the rapid degradation of antigens within the harsh environment of the digestive tract, which hampers effective protein delivery to the GIT. In light of recent proteomic analysis revealing strong up-regulation of the tryptophan catabolic enzyme indoleamine 2, 3-dioxygenase (IDO1) in DCs inoculated with the Cholera toxin B-subunit-Insulin fusion protein vaccine (CTB-INS), we are interested in investigating the effects of transgene integration into a selected plant cell as an edible vaccine.

Gut-Associated Lymphatic Tissue in Food-Restricted Rats: Influence of Refeeding and Probiotic Supplementation.

Anorexia nervosa (AN) is a severe and often chronic eating disorder that leads to alterations in the gut microbiome, which is known to influence several processes, such as appetite and body weight regulation, metabolism, gut permeability, inflammation, and gut-brain interactions. Using a translational activity-based anorexia (ABA) rat model, this study examined the effect of chronic food starvation, as well as multistrain probiotic supplementation and refeeding, on the structure of the gut and gut-associated lymphatic tissue (GALT). Our results indicated that ABA had an atrophic influence on intestinal morphology and increased the formation of GALT in the small bowel and colon. Higher formation of GALT in ABA rats appeared to be reversible upon application of a multistrain probiotic mixture and refeeding of the starved animals. This is the first time that increased GALT was found following starvation in the ABA model. Our results underscore a potential role of gut inflammatory alterations in the underlying pathophysiology of AN. Increased GALT could be linked to the gut microbiome, as probiotics were able to reverse this finding. These results emphasize the role of the microbiome-gut-brain axis in the pathomechanisms of AN and point to probiotics as potentially beneficial addendum in the treatment of AN.

Gut epithelial barrier dysfunction in lupus triggers a differential humoral response against gut commensals.

Systemic lupus erythematosus is an autoimmune disease with multisystemic involvement including intestinal inflammation. Lupus-associated intestinal inflammation may alter the mucosal barrier where millions of commensals have a dynamic and selective interaction with the host immune system. Here, we investigated the consequences of the intestinal inflammation in a TLR7-mediated lupus model. IgA humoral and cellular response in the gut was measured. The barrier function of the gut epithelial layer was characterised. Also, microbiota composition in the fecal matter was analysed as well as the systemic humoral response to differential commensals. The lupus-associated intestinal inflammation modifies the IgA+ B cell response in the gut-associated lymphoid tissue in association with dysbiosis. Intestinal inflammation alters the tight junction protein distribution in the epithelial barrier, which correlated with increased permeability of the intestinal barrier and changes in the microbiota composition. This permeability resulted in a differential humoral response against intestinal commensals. Lupus development can cause alterations in microbiota composition, allowing specific species to colonize only the lupus gut. Eventually, these alterations and the changes in gut permeability induced by intestinal inflammation could lead to bacterial translocation.

Zearalenone-14-glucoside specifically promotes dysplasia of Gut-Associated Lymphoid Tissue: A natural product for constructing intestinal nodular lymphatic hyperplasia model

IntroductionZearalenone-14-glucoside (Z14G) is a modified mycotoxin that widely contaminates food across the world. Our preliminary experiment showed that Z14G degrades to zearalenone (ZEN) in the intestine exerting toxicity. Notably, oral administration of Z14G in rats induces intestinal nodular lymphatic hyperplasia. ObjectivesTo investigate the mechanism of Z14G intestinal toxicity and how it differs from ZEN toxicity. We conducted a precise toxicology study on the intestine of rats exposed to Z14G and ZEN using multi-omics technology. MethodsRats were exposed to ZEN (5 mg/kg), Z14G-L (5 mg/kg), Z14G-H (10 mg/kg), and pseudo germ free (PGF)-Z14G-H (10 mg/kg) for 14 days. Histopathological studies were performed on intestines from each group and compared. Metagenomic, metabolomic, and proteomic analyses were performed on rat feces, serum, and intestines, respectively. ResultsHistopathological studies showed that Z14G exposure resulted in dysplasia of gut-associated lymphoid tissue (GALT) compared to ZEN exposure. The elimination of gut microbes in the PGF-Z14G-H group alleviated or eliminated Z14G-induced intestinal toxicity and GALT dysplasia. Metagenomic analysis revealed that Z14G exposure significantly promoted the proliferation of Bifidobacterium and Bacteroides compared to ZEN. Metabolomic analysis showed that Z14G exposure significantly reduced bile acid, while proteomic analysis found that Z14G exposure significantly reduced the expression of C-type lectins compared to ZEN. ConclusionsOur experimental results and previous research suggest that Z14G is hydrolyzed to ZEN by Bifidobacterium and Bacteroides promoting their co-trophic proliferation. This leads to inactivation of lectins by hyperproliferative Bacteroides when ZEN caused intestinal involvement, resulting in abnormal lymphocyte homing and ultimately GALT dysplasia. It is noteworthy that Z14G is a promising model drug to establish rat models of intestinal nodular lymphatic hyperplasia (INLH), which is of great significance for studying the pathogenesis, drug screening and clinical application of INLH.

HIV Tissue Reservoirs: Current Advances in Research.

Acquired immunodeficiency syndrome (AIDS), caused by the human immunodeficiency virus (HIV), has become a heavy burden of disease and an important public health problem in the world. Although current antiretroviral therapy (ART) is effective at suppressing the virus in the blood, HIV still remains in two different types of reservoirs-the latently infected cells (represented by CD4+ T cells) and the tissues containing those cells, which may block access to ART, HIV-neutralizing antibodies and latency-reversing agents. The latter is the focus of our review, as blood viral load drops below detectable levels after ART, a deeper and more systematic understanding of the HIV tissue reservoirs is imperative. In this review, we take the lymphoid system (including lymph nodes, gut-associated lymphoid tissue, spleen and bone marrow), nervous system, respiratory system, reproductive system (divided into male and female), urinary system as the order, focusing on the particularity and importance of each tissue in HIV infection, the infection target cell types of each tissue, the specific infection situation of each tissue quantified by HIV DNA or HIV RNA and the evidence of compartmentalization and pharmacokinetics. In summary, we found that the present state of HIV in different tissues has both similarities and differences. In the future, the therapeutic principle we need to follow is to respect the discrepancy on the basis of grasping the commonality. The measures taken to completely eliminate the virus in the whole body cannot be generalized. It is necessary to formulate personalized treatment strategies according to the different characteristics of the HIV in the various tissues, so as to realize the prospect of curing AIDS as soon as possible.

A Clinical and Pathophysiological Overview of Intestinal and Systemic Diseases Associated with Pancreatic Disorders: Causality or Casualty?

The relationship between chronic intestinal disease, including inflammatory bowel disease (IBD) and celiac disease (CelD), and pancreatic disorders has been little investigated. Although an increased risk of acute pancreatitis (AP), exocrine pancreatic insufficiency with or without chronic pancreatitis, and chronic asymptomatic pancreatic hyperenzymemia have been described in these patients, the pathogenetic link remains unclear. It may potentially involve drugs, altered microcirculation, gut permeability/motility with disruption of enteric-mediated hormone secretion, bacterial translocation, and activation of the gut-associated lymphoid tissue related to chronic inflammation. In addition, the risk of pancreatic cancer seems to be increased in both IBD and CelD patients with unknown pathogenesis. Finally, other systemic conditions (e.g., IgG4-related disease, sarcoidosis, vasculitides) might affect pancreatic gland and the intestinal tract with various clinical manifestations. This review includes the current understandings of this enigmatic association, reporting a clinical and pathophysiological overview about this topic.

Tunable dynamics of B cell selection in gut germinal centers.

Abstract B lymphocytes are central to maintaining balanced enteric responses through production of immunoglobulins (Igs). A large fraction of Igs are produced in germinal center (GC) responses, which form upon immunization or infection in the majority of secondary lymphoid organs, but are constitutively present in gut-associated lymphoid tissue. However, the ontogeny and antigenic drivers of constitutive gut-associated GCs were poorly understood. Using a multicolor fate-mapping approach with the Confetti fluorescent allele to visualize GC clonal expansions, we observed single-color GCs in the steady state intestine, suggestive of strong selection events. By coupling fate-mapping, gnotobiotics and Ig sequencing, we showed affinity-driven selection occurring in gut-associated GCs in response to members of the microbiome. We observed that these GCs persist even in the absence of microbiota, although their isotype distribution and clonal composition are altered. Furthermore, we identified several prominent public Ig clonotypes in intestinal GCs, whose presence were tuned by microbial diversity.

Paneth cells regulates innate lymphoid cells and B1 cells throughout the body

Abstract Paneth cells are a subset of small intestinal epithelial cells specialized to maintain gastrointestinal homeostasis through production of antimicrobial products and cytokines. The fact that dysbiosis has been associated with several noninfectious pathologies, has solidified the notion that Paneth cells contribute to the general health. However, little is known about Paneth cells beyond their role as regulator of the gut microbiota. Using mice lacking Paneth cells (Sox9 ΔIECmice), we now report that Paneth cells also regulate the composition of immune cell subsets in Gut-Associated Lymphoid Tissues (GALT) and but also in sites distant from the gut. Thus, loss of Paneth cells significantly decreased the number of ILC3s and increased the number of ILC2s in the intestinal lamina propria. Paneth cell deficiency also affected Peyer’s patches. In this regard, Paneth cell deficient mice displayed an increased numbers of Peyer’s patches which were of larger size than Peyer’s patches in control wild-type mice. Furthermore, Peyer’s patches of Paneth cell deficient mice contained increase numbers of IgA +CD19 +B cells and B1a (CD19 +CD5 +) cells. Interestingly, when compared to control wild-type mice, the numbers of B1a cells were found to be also increased in mesenteric lymph nodes of Paneth cell deficient mice, but also at sites distant from the gut including the lungs, and bone marrow. Also, in the lungs there was an increase in ILC2s. Taken together, these findings indicate that Paneth cells play a key role as regulators of innate immune responses throughout the body via regulation of ILC subsets and B1 cells. NIH Grants

Gut microbiome-derived isodeoxycholic acid promotes mucosal immune non-responsiveness

Abstract Perturbations to the commensal gut microbiota are associated with the increasing prevalence of food allergies. Our lab has reported that colonization of germ-free mice with feces from healthy, but not cow’s milk allergic, infants protects against anaphylaxis to a cow’s milk allergen. Protection was associated with higher levels of the secondary bile acid (SBA) isodeoxycholic acid (isoDCA) in the feces of healthy-colonized mice. IsoDCA has been reported to induce regulatory T cells (Tregs) which suppress inflammation. We hypothesize that isoDCA-driven induction of mucosal Tregs promotes non-responsiveness and protects against food allergy. To study this, we identified two Clostridiaspecies, Peptacetobacter hiranonisand Ruminococcus gnavus, that together produce isoDCA from taurocholic acid (TCA), an abundant host bile acid. Using a Group II intron-based system, we engineered R. gnavus Δrumgna_00694, a functional knock-out of a 3β-hydroxysteroid dehydrogenase required to produce isoDCA. In our system, P. hiranonisconverts TCA to deoxycholic acid (DCA) and R. gnavusWT, but not Δrumgna_00694, converts DCA to isoDCA. Ongoing experiments will compare isoDCA-dependent Treg induction in gut-associated lymphoid tissues of mice co-colonized with P. hiranonisand R. gnavusWT or Δrumgna_00694. Once optimized, this system can be used in our allergic sensitization model to investigate the role of SBA in protection against food allergy and maintenance of intestinal homeostasis.

The P2X7 receptor in mucosal adaptive immunity.

The P2X7 receptor (P2X7R) is a widely distributed cation channel activated by extracellular ATP (eATP) with exclusive peculiarities with respect to other P2XRs. In recent years, P2X7R has been shown to regulate the adaptive immune response by conditioning T cell signaling and activation as well as polarization, lineage stability, cell death, and function in tissues. Here we revise experimental observations in this field, with a focus on adaptive immunity at mucosal sites, particularly in the gut, where eATP is hypothesized to act in the reciprocal conditioning of the host immune system and commensal microbiota to promote mutualism. The importance of P2X7R activity in the intestine is consistent with the transcriptional upregulation of P2xr7 gene by retinoic acid, a metabolite playing a key role in mucosal immunity. We emphasize the function of the eATP/P2X7R axis in controlling T follicular helper (Tfh) cell in the gut-associated lymphoid tissue (GALT) and, consequently, T-dependent secretory IgA (SIgA), with a focus on high-affinity SIgA-mediated protection from enteropathogens and shaping of a beneficial microbiota for the host.

The shaping of gut immunity in cirrhosis.

Cirrhosis is the common end-stage of chronic liver diseases of different etiology. The altered bile acids metabolism in the cirrhotic liver and the increase in the blood-brain barrier permeability, along with the progressive dysbiosis of intestinal microbiota, contribute to gut immunity changes, from compromised antimicrobial host defense to pro-inflammatory adaptive responses. In turn, these changes elicit a disruption in the epithelial and gut vascular barriers, promoting the increased access of potential pathogenic microbial antigens to portal circulation, further aggravating liver disease. After summarizing the key aspects of gut immunity during homeostasis, this review is intended to update the contribution of liver and brain metabolites in shaping the intestinal immune status and, in turn, to understand how the loss of homeostasis in the gut-associated lymphoid tissue, as present in cirrhosis, cooperates in the advanced chronic liver disease progression. Finally, several therapeutic approaches targeting the intestinal homeostasis in cirrhosis are discussed.

Evaluating the Intestinal Immunity of Asian Seabass (Lates calcarifer, Bloch 1790) following Field Vaccination Using a Feed-Based Oral Vaccine.

This study describes the levels of gut lysozyme and IgM, the number, size and density of gut-associated lymphoid tissue (GALT) regions, and the lymphocyte population in Asian seabass following field oral administration of a feed-based vaccine. Fish in a grow-out farm were selected and divided into two groups; Group 1 was vaccinated at week 0, 2, and 6, while Group 2 was not vaccinated. Samplings were done at 2-week intervals when the fish were observed for clinical signs, and gross lesions were recorded. The intestinal tissue and gut lavage fluid were collected. GALT regions (numbers, size, density and population of lymphocytes) were analyzed. Clinical signs such as abnormal swimming pattern and death, and gross lesions including scale loss, ocular opacity, and skin ulceration were observed in both groups. At the end of the study, the incidence rate between both groups were significantly different (p < 0.05). The gut IgM level and lysozyme activity, lymphocyte population, number, size and density of GALT regions of Group 1 were significantly (p < 0.05) higher than Group 2. Therefore, this study concludes that the feed-based vaccine reduces the incidence of vibriosis by stimulating the gut immunity of the vaccinated fish with an enhanced GALT region, specific IgM production against Vibrio harveyi, and lysozyme responses.

Mouse mammary tumor virus is implicated in severity of colitis and dysbiosis in the IL-10−/− mouse model of inflammatory bowel disease

BackgroundFollowing viral infection, genetically manipulated mice lacking immunoregulatory function may develop colitis and dysbiosis in a strain-specific fashion that serves as a model for inflammatory bowel disease (IBD). We found that one such model of spontaneous colitis, the interleukin (IL)-10 knockout (IL-10−/−) model derived from the SvEv mouse, had evidence of increased Mouse mammary tumor virus (MMTV) viral RNA expression compared to the SvEv wild type. MMTV is endemic in several mouse strains as an endogenously encoded Betaretrovirus that is passaged as an exogenous agent in breast milk. As MMTV requires a viral superantigen to replicate in the gut-associated lymphoid tissue prior to the development of systemic infection, we evaluated whether MMTV may contribute to the development of colitis in the IL-10−/− model.ResultsViral preparations extracted from IL-10−/− weanling stomachs revealed augmented MMTV load compared to the SvEv wild type. Illumina sequencing of the viral genome revealed that the two largest contigs shared 96.4–97.3% identity with the mtv-1 endogenous loci and the MMTV(HeJ) exogenous virus from the C3H mouse. The MMTV sag gene cloned from IL-10−/− spleen encoded the MTV-9 superantigen that preferentially activates T-cell receptor Vβ-12 subsets, which were expanded in the IL-10−/− versus the SvEv colon. Evidence of MMTV cellular immune responses to MMTV Gag peptides was observed in the IL-10−/− splenocytes with amplified interferon-γ production versus the SvEv wild type. To address the hypothesis that MMTV may contribute to colitis, we used HIV reverse transcriptase inhibitors, tenofovir and emtricitabine, and the HIV protease inhibitor, lopinavir boosted with ritonavir, for 12-week treatment versus placebo. The combination antiretroviral therapy with known activity against MMTV was associated with reduced colonic MMTV RNA and improved histological score in IL-10−/− mice, as well as diminished secretion of pro-inflammatory cytokines and modulation of the microbiome associated with colitis.ConclusionsThis study suggests that immunogenetically manipulated mice with deletion of IL-10 may have reduced capacity to contain MMTV infection in a mouse-strain-specific manner, and the antiviral inflammatory responses may contribute to the complexity of IBD with the development of colitis and dysbiosis.8hbTGJzMzAHuPYE9uy6yoBVideo

Microbial profiles and immune responses in seahorse gut and brood pouch under chronic exposure to environmental antibiotics

Ocean antibiotics pose substantial risks to the adaptation and lifespan of marine organisms. Seahorses are unique owing to the occurrence of brood pouches, male pregnancy, and loss of gut-associated lymphatic tissues and spleen, which lead to increased sensitivity to environmental changes. This study evaluated the changes in microbial diversity and immune responses within the gut and brood pouch in the lined seahorse Hippocampus erectus under chronic exposure to environmental levels of triclosan (TCS) and sulfamethoxazole (SMX), which are common antibiotics in coastal regions. The results showed that microbial abundance and diversity within the gut and brood pouch of seahorses were significantly changed following antibiotics treatment, with the expression of core genes involved in immunity, metabolism, and circadian rhythm processes evidently regulated. Notably, the abundance of potential pathogens in brood pouches was considerably increased upon treatment with SMX. Transcriptome analysis revealed that the expression of toll-like receptors, c-type lectins, and inflammatory cytokine genes in brood pouches was significantly upregulated. Notably, some essential genes related to male pregnancy significantly varied after antibiotic treatment, implying potential effects on seahorse reproduction. This study provides insights into the physiological adaptation of marine animals to environmental changes resulting from human activity.

The Role of Dietary Fiber or Prebiotics in Atopic Dermatitis

Introduction: Atopic Dermatitis (AD) is a chronic inflammatory skin condition with itchy eczematous lesions, mostly found in children, and may affect a patient’s quality of life. Individuals with AD were found to have dysbiosis of gut microbial, which may alter the immunologic tolerance of mucosa, causing inflammation and affecting skin conditions. Dietary fiber or prebiotics consumption may have a role in reversing dysbiosis and may affect AD. In this literature review, the authors would like to further explore the role of dietary fiber or prebiotics in the prevention and severity of AD/&#x0D; Methods: Relevant literature research was conducted in several sources: Pubmed, EBSCOHOST, Proquest, and Google Scholar, using keywords “atopic dermatitis, atopic eczema, dietary fiber, prebiotic, nutrition.” Studies published within the last 10 years were included.&#x0D; Discussions: Dietary fiber, particularly soluble fibers and those which can be fermented by gut bacteria (including prebiotics), plays a role in maintaining homeostasis of normal gut flora by producing SCFA, which increases the gut barrier, has anti-inflammatory properties, balances Th1/Th2 ratio, increases lymphocytes in gut-associated lymphoid tissues (GALT) system, and increases secretion of intestinal IgA. The role of dietary fiber/prebiotics in the prevention or decreasing rate of AD is still a matter of debate. Several studies showed no effect or correlation of prebiotic supplementation in decreasing the AD rate in pregnant women or babies with a high risk of atopy. On the other hand, several studies on prebiotic supplementation for babies and children have shown the benefits of prebiotic supplementation in preventing allergies (AD, rhinoconjunctivitis, and urticaria).&#x0D; Conclusion: The role of dietary fiber/prebiotics in preventing or treating AD is still a matter of debate. Different study results make it difficult to conclude the clinical effect of prebiotics in allergy prevention, particularly AD. This may be caused by the heterogeneous studies and the limited number of studies on humans. Further studies (RCT) involving large-scale respondents are needed to define the effects of prebiotic supplementation in the prevention or alternative therapy for AD.