Splenic Tissue Research Articles

Yogurt Alleviates Cyclophosphamide-Induced Immunosuppression in Mice through D-Lactate.

Numerous studies have investigated the immunomodulatory effects of yogurt, but the underlying mechanism remained elusive. This study aimed to elucidate the alleviating properties of yogurt on immunosuppression and proposed the underlying mechanism was related to the metabolite D-lactate. In the healthy mice, we validated the safety of daily yogurt consumption (600 μL) or D-lactate (300 mg/kg). In immunosuppressed mice induced by cyclophosphamide (CTX), we evaluated the immune regulation of yogurt and D-lactate. The result showed that yogurt restored body weight, boosted immune organ index, repaired splenic tissue, recovered the severity of delayed-type hypersensitivity reactions and increased serum cytokines (IgA, IgG, IL-6, IFN-γ). Additionally, yogurt enhanced intestinal immune function by restoring the intestinal barrier and upregulating the abundance of Bifidobacterium and Lactobacillus. Further studies showed that D-lactate alleviated immunosuppression in mice mainly by promoting cellular immunity. D-lactate recovered body weight and organ development, elevated serum cytokines (IgA, IgG, IL-6, IFN-γ), enhanced splenic lymphocyte proliferation and increased the mRNA level of T-bet in splenic lymphocyte to bolster Th1 differentiation. Finally, CTX is a chemotherapeutic drug, thus, the application of yogurt and D-lactate in the tumor-bearing mouse model was initially explored. The results showed that both yogurt (600 μL) and D-lactate (300 mg/kg) reduced cyclophosphamide-induced immunosuppression without promoting tumor growth. Overall, this study evaluated the safety, immune efficacy and applicability of yogurt and D-lactate in regulating immunosuppression. It emphasized the potential of yogurt as a functional food for immune regulation, with D-lactate playing a crucial role in its immunomodulatory effects.

Laparoscopic excision of accessory spleen for recurrent autoimmune hemolytic anemia after splenectomy: a case report

BackgroundSplenectomy is indicated in cases of autoimmune hemolytic anemia (AIHA), which are refractory to medical management. In post-splenectomy, there exists a theoretical risk of AIHA recurrence, especially if an accessory spleen undergoes compensatory hypertrophy. In this context, we present a unique case of recurrent AIHA managed through laparoscopic excision of the accessory spleen (LEAS).Case presentationA 60-year-old male underwent laparoscopic splenectomy (LS) for AIHA refractory to standard medical therapies. Following the surgery, there was a marked improvement in hemolytic anemia symptoms, and oral steroid therapy was terminated 7 months post-LS. Nonetheless, a year after the LS, the patient exhibited a marked decline in hemoglobin levels, dropping to a concerning 5.8 g/dl, necessitating the reintroduction of oral steroids. A subsequent contrast-enhanced computed tomography (CT) scan unveiled an enlarged accessory spleen. The patient then underwent LEAS, during which the accessory spleen, obscured within adipose tissue, proved challenging to visualize laparoscopically. This obstacle was surmounted utilizing intraoperative ultrasonography (US), enabling successful excision of the accessory spleen. The post-surgical period progressed without complications, and the steroid dosage was reduced to one-twelfth of its initial preoperative quantity.ConclusionsRecurrent AIHA can be instigated by post-splenectomy compensatory hypertrophy of the accessory spleen. Ensuring comprehensive splenic tissue excision is crucial in AIHA management to obviate recurrent stemming from hypertrophic remnants. In scenarios of AIHA recurrence tied to an enlarged accessory spleen, LEAS stands as a viable and effective therapeutic modality.

Physiologically based pharmacokinetic model for predicting the biodistribution of albumin nanoparticles after induction and recovery from acute lung injury

The application of nanomedicine in the treatment of acute lung injury (ALI) has great potential for the development of new therapeutic strategies. To gain insight into the kinetics of nanocarrier distribution upon time-dependent changes in tissue permeability after ALI induction in mice, we developed a physiologically based pharmacokinetic model for albumin nanoparticles (ANP). The model was calibrated using data from mice treated with intraperitoneal LPS (6 mg/kg), followed by intravenous ANP (0.5 mg/mouse or about 20.8 mg/kg) at 0.5, 6, and 24 h. The simulation results reproduced the experimental observations and indicated that the accumulation of ANP in the lungs increased, reaching a peak 6 h after LPS injury, whereas it decreased in the liver, kidney, and spleen. The model predicted that LPS caused an immediate (within the first 30 min) dramatic increase in lung and kidney tissue permeability, whereas splenic tissue permeability gradually increased over 24 h after LPS injection. This information can be used to design new therapies targeting specific organs affected by bacterial infections and potentially by other inflammatory insults.

Potential Protective Role of Radicut in Valproic Acid-Induced Oxidative Stress in Rat Spleen

Aim: The study aims to evaluate the potential protective role of Radicut (RAD) in Valproic acid (VPA)-induced oxidative stress in splenic tissues of rats. Method: Rats were divided into groups as follows: Group 1: Controls (n=8), Group II: R: RAD-given group (30 mg/kg/day, n=8), Group III: V: VPA-given group (0.5 g/kg/day, n=10), Group IV: V+R: VPA+RAD-given group (30 mg/kg/day, n=11). VPA, RAD, and VPA+RAD were given to the animals for 7 days (i.p). Biochemical parameters related to oxidative stress were determined in spleen homogenates. Results: VPA elevated oxidative stress by increasing lipid peroxidation and sialic acid levels, increasing alkaline phosphatase activity, and decreasing superoxide dismutase, glutathione-S- transferase, and glutathione peroxidase activities. Administration of RAD to VPA-given group decreased LPO, SA levels, and acid phosphatase levels, and increased tissue factor, SOD, GST, and GPx activities. Conclusion: RAD reversed the biochemical results in the V group, by clarifying its protective effect. RAD has the potential to prevent oxidative stress during VPA treatment, which could be beneficial.

Dietary garden cress (Lepidium sativum) seeds mitigate the effect of aflatoxin B1 contamination on growth, antioxidant status, AFB1 residues, immune response, and tissue architecture of Oreochromis niloticus

The contamination of fish diets with aflatoxin B1 (AFB1) poses a significant hazard to the aquaculture sector. This study investigates the efficacy of supplementing Nile tilapia (Oreochromis niloticus) diets with garden cress (Lepidium sativum) seeds (GCS) to mitigate the adverse effects of AFB1. For this purpose, a factorial design was utilized, consisting of a 2×3 arrangement of treatments. This included two contamination levels of AFB1: (0 and 2 mg kg−1 diet). Within each contamination level, three dietary levels of GCS were used (0 %, 1 %, and 2 %). The study involved 270 healthy O. niloticus with an average weight of 25.14 ± 0.39 g (45 fish/group and 15 fish/replicate). The duration of the trial was 60 days. The study evaluated growth performance, hematological indices, hepatorenal function, immune and antioxidant indicators, histomorphology of organs, AFB1 residues in muscles, and fish resistance to Aeromonas hydrophila. The results indicated that GCS dietary supplementation significantly counteracted AFB1-induced growth retardation and reduced fish survival. Additionally, GCS effectively reversed the anemia, leukopenia, hypoproteinemia, hypoalbuminemia, and hypoglobulinemia that were produced by AFB1. Moreover, GCS dietary supplementation significantly suppressed the AFB1-induced increase in serum bilirubin, hepatic enzymes, kidney damage products, cortisol, and glucose. Additionally, the inclusion of GCS in the fish's diet effectively eliminated the accumulation of AFB1 in their muscles. Moreover, GCS supplementation demonstrated significant restoration of depleted antioxidant and innate immune components induced by AFB1. Furthermore, GCS significantly reduced the degenerative changes in renal, hepatic, splenic, and small intestine tissues caused by AFB1. Fish fed a GCS-fortified diet and exposed to AFB1 displayed restored disease resistance when challenged with A. hydrophila. In conclusion, supplementing Nile tilapia diets with GCS at 2 %, even in the presence the AFB1 contamination, significantly enhanced the fish growth, improved health, and increased disease resistance while reducing AFB1 residues, thereby benefiting consumer health.

Littoral cell angioma: An incidental finding in a traumatic spleen

Littoral cell angioma (LCA) of the spleen, a rare vascular tumor, is usually asymptomatic, often discovered incidentally and a majority of them are benign in nature. A 20-year-old boy with a history of blunt abdominal trauma, who underwent splenectomy showed the presence of a capsular tear and variegated outer surface on gross examination of the spleen. On the cut section, multiple nodular areas with areas of hemorrhage were noted. Microscopical examination revealed the proliferation of anastomosing, irregular, tortuous blood-filled channels with plenty of histiocytes in the splenic tissue and extensive areas of hemorrhage, inflammatory cell infiltration, and fibrinoid deposits. Immunohistochemistry revealed positivity for CD31 (endothelial differentiation), CD68, and lysozyme (histiocytic differentiation) but was negative for CD34. The final diagnosis was LCA in a case of ruptured spleen after ruling out angiosarcoma. The possibility of this benign entity to have contributed to the potentially fatal splenic injury cannot be overlooked.

Role of the CXCR4-Gnαq-Plcβ signaling pathway in the pathogenesis of collagen-induced arthritis in rats

Rheumatoid arthritis (RA) is a chronic autoimmune disease in which immune cells and inflammatory cytokines are abnormally activated, leading to immunoregulatory dysfunction in the body and triggering systemic inflammatory responses. The interaction between CXC chemokine receptor 4 (CXCR4) and heterotrimeric G-protein α-subunit Gαq (Gnαq) activates phospholipase Cβ (PLCβ), which influences the expression of downstream effectors and participates widely in the onset and development of various diseases, thus suggesting the potential involvement of these molecules in RA pathogenesis. Therefore, the present study aimed to determine whether the CXCR4-Gnαq-PLCβ signaling pathway participates in the onset and development of RA. Using a collagen-induced arthritis (CIA) rat model, we found that compared with the control (healthy) rat group, CIA rats exhibited highly time-dependent arthritis, with the maximum arthritis score occurring in week 3. In contrast to the splenic and joint tissue of control rats, CIA rats showed obvious hyperplasia in the lymphoid white pulp and main germination centers of the spleen, narrowing of joint cavities, and inflammatory cellular infiltration on articular surfaces. The serum levels of expression of IL-1β, IL-4, IL-6, and TNF-α were significantly elevated (P < 0.05, P < 0.01). Core genes of the CXCR4-Gnαq-PLCβ pathway, namely CXCR4, Gnαq, PLCβ1, MMP1, and MMP3, also showed a significant increase in mRNA and protein expression levels (P < 0.05, P < 0.01). Proteins related to the CXCR4-Gnαq-PLCβ pathway were mainly localized to the red and white pulp regions in the spleen as well as in stromal, endothelial, and subdifferentiated synovial cells in the joints. These results indicated that CXCR4 is dependent on Gnαq for inducing the expression of PLCβ1 and stimulation of secretion of inflammatory cytokines by inflammatory cells. This consequently affects the expression of matrix metalloproteinases (MMPs), which serve as downstream effectors, thereby promoting RA pathogenesis. Our findings play an important role in elucidating the mechanisms of the onset and development of RA.

PJ‑001, a small‑molecule proteolysis‑targeting chimera, ameliorates atopic dermatitis‑like inflammation in mice by inhibiting the JAK2/STAT3 pathway and repairing the skin barrier.

Atopic dermatitis (AD) is a common allergic skin disease, and its pathogenesis involves genetic and environmental factors, as well as the immune response and skin barrier. PJ-001 is a small-molecule proteolysis-targeting chimera, which can degrade proteins related to the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway. In the present study, 0.5% 2,4-dinitrofluorobenzene was used to induce a mouse model of AD. Following treatment with PJ-001, the number of scratches and the severity of skin damage in the AD mice were recorded. Pathological changes in skin lesions were observed with hematoxylin and eosin staining. The expression levels of JAK2/STAT3, Toll-like receptor 4/nuclear factor-κB (TLR4/NF-κB), Beclin 1 and microtubule-associated protein 1 light chain 3 (LC3) were detected using western blotting. Furthermore, reverse transcription-PCR was used to detect the mRNA expression levels of filaggrin (FLG) and keratin 17, and the change in interleukin-10 levels in the splenic tissue of the mice. Compared with in the control group, the model group exhibited severe skin lesions. Following treatment with PJ-001, the AD-like inflammation in mice decreased. The expression levels of LC3 II/LC3 I and Beclin 1 were significantly reduced (P<0.01), and the expression levels of JAK2, STAT3, TLR4 and NF-κB were significantly downregulated (P<0.001). Additionally, the mRNA expression levels of FLG were significantly upregulated (P<0.001). These results indicated that PJ-001 may alleviate the skin condition in a mouse model of AD. The underlying mechanism may involve inhibition of the JAK/STAT signaling pathway, thereby suppressing the release of inflammatory factors, reducing excessive autophagy at the site of skin lesions, and enhancing the skin barrier function. In conclusion, PJ-001 could be considered a potential therapeutic option for AD.

Novel insights into heat tolerance: the impact of dwarf and frizzled feather traits on crossbreed chicken performance under thermal stress

Heat stress (HS) poses significant challenges to broiler production, negatively influencing growth performance and meat quality. This study explores the resilience and the meat quality of hybrid chickens with dwarf size and frizzled feather traits to HS. We investigated F1 progeny derived from a crossbreed of dwarf yellow chickens (DYCs) with Yuexi frizzled feather chickens. Following a rearing period of 12 weeks, we randomly assigned 72 chickens into two distinct environmental conditions: a HS group subjected to 35 ± 1 °C for 8 h per day, and a control group (CN) maintained at 26 ± 1 °C. Seven days post-HS, multiple tissue samples were collected to assess meat quality attributes and measure expression levels of heat shock proteins (HSPs), muscle growth-related genes and cytokines. The results demonstrated a substantial reduction in weight gain of the F1 chickens exposed to HS, along with decreased expression of insulin-like growth factor-1 (IGF-1) and its receptor (IGF-1R) in the liver. Furthermore, HS exposure significantly increased muscle shear force and the expression of HSP70 in both liver and pectoral muscle tissues (p < .05). Despite these changes, there were no significant alterations in the other meat quality indices, or indicators of splenic and hepatic tissue injury. Likewise, expression levels of growth hormone receptor (GHR) and cytokines remained stable, implying a lack of heightened inflammation. These observations suggest an inherent thermotolerance in the chickens possessing dwarf size and frizzled feather traits, warranting further exploration for their potential in heat-stress-prone poultry production environments. Highlights Dwarf and frizzled feather traits in crossbreed chickens show potential for improved heat tolerance in poultry production. Heat stress had limited impact on meat quality parameters, suggesting resilience of these local chicken traits. Understanding the genetic basis of thermotolerance can inform breeding strategies for climate-resilient chickens.

Changes in splenic tissue and immune response profile of Schistosoma mansoni infected mice submitted to chronic ethanol intake.

In Schistosoma mansoni infection, the spleen is one of the organs affected, causing its enlargement (splenomegaly). Intake of ethanol through alcoholic beverages can cause spleen atrophy and interfere with immune activity. To gain knowledge of this association on the spleen and on the immune response profile, male mice were used as an experimental model. These animals were divided into four groups: C. control; EC. uninfected/ethanol gavage; I. infected; and IE. infected/ethanol gavage. Groups I and IE were infected with about 100 cercariae (BH strain) of S. mansoni and in the fifth week of infection, gavage 200 μL/day/animal of 18 % ethanol was started for 28 consecutive days. At the end of the gavage (9th week of infection) all animals were euthanized. The spleen was removed and longitudinally divided in two parts. After histological processing, the sections were stained with H&E and Gomori's Reticulin for histopathological and stereological analyses, white pulp morphometry and quantification of megakaryocytes. The other fragment was macerated (in laminar flow) and the cell suspension, after adjusting the concentration (2 × 106), was plated to obtain cytokines produced by spleen cells that were measured by flow cytometry (Citometric Bead Array). Histopathological and quantitative analyzes in the spleen of the IE group showed an increase in the number of trabeculae and megakaryocytes, a decrease in reticular fibers, as well as important organizational changes in the white pulp and red pulp. Due to the decrease in the levels of cytokines measured and the result of the calculation of the ratio between the IFN-y and IL-10 cytokines (p = 0.0079) of the infected groups, we suggest that ethanol decreased the inflammatory and anti-inflammatory response generated by the infection (group IE, the production of cytokines was significantly decreased (p < 0.01). These changes demonstrate that ethanol ingestion interferes with some parameters of experimental S. mansoni infection, such as changes in splenic tissue and in the pattern of cytokine production.

Calcitriol restrains microglial M1 polarization and alleviates dopaminergic degeneration in hemiparkinsonian mice by boosting regulatory T-cell expansion.

Vitamin D deficiency is a risk factor for Parkinson's disease (PD) and vitamin D supplementation robustly alleviates neurodegeneration in PD models. However, the mechanisms underlying this effect require further clarification. Current evidence suggests that harnessing regulatory T cells (Treg) may mitigate neuronal degeneration. In this study, we investigated the therapeutic effects of vitamin D receptor activation by calcitriol on PD, specifically focusing on its role in Treg. Hemiparkinsonian mice model was established through the injection of 6-OHDA into the striatum. Mice were pretreated with calcitriol before 6-OHDA injection. The motor performance, dopaminergic neuronal survival, contents of dopamine, and dopamine metabolites were evaluated. The pro-inflammatory cytokines levels, T-cell infiltration, mRNA expression of indicated microglial M1/M2 phenotypic markers, and microglial marker in the midbrain were detected. Populations of Treg in the splenic tissues were assessed using a flow cytometry assay. PC61 monoclonal antibody was applied to deplete Treg in vivo. We show that calcitriol supplementation notably improved motor performance and reduced dopaminergic degeneration in the 6-OHDA-induced PD model. Mechanistically, calcitriol promoted anti-inflammatory/neuroprotective Treg and inhibited pro-inflammatory/neurodestructive effector T-cell generation in this model. This process significantly inhibited T-cell infiltration in the midbrain, restrained microglial activation, microglial M1 polarization, and decreased pro-inflammatory cytokines release. This more favorable inflammatory microenvironment rescued dopaminergic degeneration. To further verify that the anti-inflammatory effects of calcitriol are associated with Treg expansion, we applied an antibody-mediated Treg depletion assay. As predicted, the anti-inflammatory effects of calcitriol in the PD model were diminished following Treg depletion. These findings suggest that calcitriol's anti-inflammatory and neuroprotective effects in PD are associated with its potential to boost Treg expansion.

Subchronic exposure to fenpyroximate causes multiorgan toxicity in Wistar rats by disrupting lipid profile, inducing oxidative stress and DNA damage

Background Fenpyroximate (FEN) is an acaricide that inhibits the complex I of the mitochondrial respiratory chain in mites. Data concerning mammalian toxicity of this acaricide are limited; thus the aim of this work was to explore FEN toxicity on Wistar rats, particularly on cardiac, pulmonary, and splenic tissues and in bone marrow cells. Methods rats were treated orally with FEN at 1, 2, 4, and 8 mg/Kg bw for 28 days. After treatment, we analyzed lipid profile, oxidative stress and DNA damage in rat tissues. Results FEN exposure increased creatinine phosphokinase (CPK) and lactate dehydrogenase (LDH) activities, elevated total cholesterol (T-CHOL), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C) concentrations, while decreasing high-density lipoprotein cholesterol (HDL-C). It inhibited acetylcholinesterase (AChE) activity, enhanced lipid peroxidation, protein oxidation, and modulated antioxidant enzymes activities (superoxide dismutase, catalase, glutathione peroxidase, and glutathione S-transferase). Comet assay indicated that FEN induced a dose-dependent DNA damage, contrasting with the micronucleus test showing no micronuclei formation. Nonetheless, FEN exhibited cytotoxicity to bone marrow cells, as evidenced by a reduction in the number of immature erythrocytes among total cells. Conclusion FEN appears to carry out its genotoxic and cytotoxic activities most likely through an indirect pathway that involves oxidative stress.

Alterations in Blaood Profiles and Spleen Tissue Following Purple Sweet Pota-to Anthocyanin Extract Treatment in Restraint-Stressed Mice

Stress is associated with broad changes in blood and immune cell dysfunction, which are correlated with the spleen as a secondary lymphoid organ. Anthocyanin, a plant bioactive compound from purple sweet potatoes, has previously been reported to have a beneficial effect on stress response behavior. However, the limited studies evaluated anthocyanin's effect on blood profiles and spleen tissue under stress. Therefore, this study aimed to explore the effect of total anthocyanin extract (ANC) from purple sweet potatoes (PSP) on the blood profiles and spleen tissue of restraint stressed mice. A total of 20 male adult BALB/c mice were divided into control (CTRL), stress (STR), stress + ANC 10 mg/kgBW (STR+ANC10), stress + ANC 20 mg/kgBW (STR+ANC20), and stress + ANC 40 mg/kgBW (STR+ANC10). Restraint stress was applied two hours/day for 14 days. An automatic blood analyzer was used for blood profiling. Immunoblotting of caspase-3 and hematoxylin-eosin-stained histological slides were observed for spleen tissue analysis. Combination of STR and ANC treatment reduced the erythrocyte count, hemoglobin level, and leucocyte count. The ANC-treated groups had a higher percentage of lymphocytes and a lower percentage of granulocytes. The expression of caspase-3 declined among ANC-treated groups. Spleen extramedullary erythropoiesis, vacuolization, and white pulp involution were demonstrated in stress and ANC-treated animals. In summary, restraint stress modified the blood cell profiles and spleen tissue in the mice model. Further research is necessary to evaluate the mechanism of ANC during stress on blood cells and splenic tissue repair enhancement

Anti-radiation effect of MRN-100: a hydro-ferrate fluid, in vivo.

Ionizing radiation (IR) severely harms many organs, especially the hematopoietic tissue, mandating the development of protective nutraceuticals. MRN-100, a hydro-ferrate fluid, has been shown to protect γ-radiated fish against hematopoietic tissue damage and lethality. The current study aimed to examine MRN-100's protective effect against irradiated mice and explore the mechanisms underlying its effect. Mice received a single acute, sub-lethal, 5Gy, whole body dose of X-ray IR. MRN-100 treatment was administered daily for 2-weeks pre-irradiation until 1-week post-irradiation. Spleen and blood were analysed for oxidative stress, hematological, histological and biochemical parameters. Radiation exposure markedly decreased complete blood count (CBC) parameters including hemoglobin, hematocrit, red blood cells, platelets, white blood cells and lymphocytes, and significantly increased neutrophils. In contrast, MRN-100 supplementation to irradiated mice ameliorated all CBC parameters and protected against DNA damage in both splenic cells and serum. It also had an antioxidant effect, increasing the levels of glutathione, superoxide dismutase, catalase and total antioxidant capacity, which were otherwise decreased by irradiation. MRN-100 intake reduced the oxidative stress biomarker levels of nitric oxide, protein carbonyl, malondialdehyde, reactive oxygen species and 8-hydroxydeoxyguanosine, a marker specific to DNA damage. Furthermore, MRN-100 enhanced serum iron and reversed the radiation-induced elevations of liver enzymes. Finally, MRN-100 protected splenic tissue from irradiation as observed by histology. We conclude that MRN-100 consumption may protect against oxidative stress generated by radiation exposure, suggesting that it may be employed as an adjuvant treatment to prevent radiation's severe damage to important organs.

Molecular force-induced liberation of transforming growth factor-beta remodels the spleen for ectopic liver regeneration

Ectopic liver regeneration in the spleen is a promising alternative to organ transplantation for treating liver failure. To accommodate transplanted liver cells, the splenic tissue must undergo structural changes to increase extracellular matrix content, demanding a safe and efficient approach for tissue remodelling. We synthesised sulphated hyaluronic acid (sHA) with an affinity for the latent complex of transforming growth factor-β (TGF-β) and cross-linked it into a gel network (sHA-X) via click chemistry. We injected this glycan into the spleens of mice to induce splenic tissue remodelling via supraphysiological activation of endogenous TGF-β. sHA-X efficiently bound to the abundant latent TGF-β in the spleen. It provided the molecular force to liberate the active TGF-β dimers from their latent complex, mimicking the 'bind-and-pull' mechanism required for physiological activation of TGF-β and reshaping the splenic tissue to support liver cell growth. Hepatocytes transplanted into the remodelled spleen developed into liver tissue with sufficient volume to rescue animals with a metabolic liver disorder (Fah-/- transgenic model) or following 90% hepatectomy, with no adverse effects observed and no additional drugs required. Our findings highlight the efficacy and translational potential of using sHA-X to remodel a specific organ by mechanically activating one single cytokine, representing a novel strategy for the design of biomaterials-based therapies for organ regeneration. Cell transplantation may provide a lifeline to millions of patients with end-stage liver diseases, but their severely damaged livers being unable to accommodate the transplanted cells is a crucial hurdle. Herein, we report an approach to restore liver functions in another organ - the spleen - by activating one single growth factor in situ. This approach, based on a chemically designed polysaccharide that can mechanically liberate the active transforming growth factor-β to an unusually high level, promotes the function of abundant allogenic liver cells in the spleen, rescuing animals from lethal models of liver diseases and showing a high potential for clinical translation.

Endogenous blocking of TLR2 along with TNF-α and IL-1β ameliorates the severity of the S. aureus arthritis via modulating STAT3/SOCS3 expressions in tissue resident macrophages

In vivo studies identifying a role of TLR2 in septic arthritis models are lacking. TNF-α played as the most important proinflammatory cytokine, and connected directly to the pathogenesis of bacterial arthritis. IL-1β is another central mediator cytokine in arthritis. It is therefore reasonable to question the role of neutralization of endogenous TNF-α and IL-1β along with TLR2 and associated downstream signaling as crucial mediators in the S. aureus -induced inflammatory arthritis. In reaction to an injury or a pathogen encounter, innate immune cells serve as the initial line of defense. TLR2 mediated entry of S. aureus into macrophage cells initiates an array of inflammatory cascades. After macrophage cell gets activated at the site inflammation, they generate elevated number of cytokines which includes TNF-α, IL-1β. This cytokines signals through STAT1/STAT3 mediated pathways. Thus, aim of this study was to discover how This bone damage could be altered by altering the STAT/STAT3/SOCS3 ratio by blocking TLR2, a particular S. aureus binding site, in conjunction with the use of IL-1 and TNF- antibodies for neutralizing endogenous IL-1β and TNF-α. Additionally, the role of local macrophages in therapy of arthritis was investigated in synovial and Splenic tissue. To comprehend the inflammatory milieu within the system, ROS and other antioxidant enzymes, along with the expression of mTOR in macrophage cells, were also taken into consideration. The detrimental impact of bacterial burden on synovial joints was reduced by simultaneously inhibiting TLR2, TNF-α, and IL-1β. Lowered IFN-γ decreases its sensitivity to STAT1 and lowered IL-6 reduces STAT3 expressions. Whereas, elevated IL-10 enhances SOSC3 expression, which thereby able to limits STAT1/STAT3 inter-conversion. As a result, NF-κB activity was downregulated.

Splenogonadal fusion: a case report

BackgroundAccessory splenic tissue is a commonly encountered phenomenon in medical literature. Typically, these accessory spleens are found in close proximity to the main spleen, either in the hilum or within the surrounding ligaments. Nevertheless, it is noteworthy that they can also be located in unusual sites such as the jejunum wall, mesentery, pelvis, and, exceptionally rarely, the scrotum. The first documented case of accessory splenic tissue in the scrotum was reported by Sneath in 1913 and is associated with a rare congenital anomaly called splenogonadal fusion. This report describes an infant who presented with a scrotal mass noted by his mother and after examination, investigations, and surgical exploration, it was revealed to be splenogonadal fusion.Case descriptionAn 8-month-old Caucasian male patient presented with a mass in the left testicle and bluish discoloration of the scrotum, which had been incidentally noticed in the previous 2 months. The general physical examination was unremarkable. Other than a palpable scrotal mass that was related to the upper pole of the testis, the rest of examination was unremarkable. Imaging revealed that this mass originated from the tail of the epididymis without infiltrating the testis and tumor markers were normal. On inguinal exploration, a reddish brown 2 × 2 cm mass was found attached to the upper pole and was completely excised without causing any harm to the testis, vessels, or epididymis. Histopathological evaluation confirmed the presence of intratesticular ectopic splenic tissue.ConclusionAlthough uncommon, splenogonadal fusion can be included in the differential diagnosis of a testicular swelling. Accurate diagnosis allows for appropriate treatment planning which helps to avoid unnecessary radical orchiectomy, which can have a significant impact on the patient’s reproductive and psychological wellbeing.

The fish spleen

In the present study, we review the structure and function of fish spleen with special emphasis on its condition in Elasmobranchs, Teleosts and Lungfish. Apart from the amount of splenic lymphoid tissue, the histological organization of the organ ensures the existence of areas involved in antigen trapping, the ellipsoids, and exhibit numerous melano-macrophages which appear isolated or forming the so-called melano-macrophage centres. An extensive discussion on the functional significance of these centres conclude that they are mere accumulations of macrophages consequence of tissue homeostasis rather than primitive germinal centres, as proposed by some authors.

Assessment of environmental safety and protective efficacy of O-antigen deficient DIVA capable Salmonella Enteritidis against chicken salmonellosis

In this study, we incorporated deletion of the O-antigen ligase gene to an attenuated Salmonella Enteritidis (SE) strain, JOL919 (SE PS; Δlon ΔcpxR), using the Lambda-Red recombination method and evaluated the safety and immunological aspects of the novel genotype, JOL2381 (SE VS: Δlon, ΔcpxR, ΔrfaL). Assessment of fecal shedding and organ persistence following administration via oral and IM routes revealed that the SE VS was safer than its parent strain, SE PS. Immunological assays confirmed that immunization via the oral route with SE PS was superior to the SE VS. However, chickens immunized with SE PS and SE VS strains via the IM route showed higher humoral and cell-mediated immune responses. Compared to PBS control, the IM route of immunization with SE VS resulted in a higher IgY antibody titer and expansion of CD4+ and CD8+ T-cell populations, which resulted in the clearance of Salmonella from the liver and splenic tissues. Furthermore, deletion of the O-antigen ligase gene caused lower production of LPS-specific antibodies in the host, promoting DIVA functionality and making it a plausible candidate for field utilization. Due to significant protection, high attenuation, and environmental safety concerns, the present SE VS strain is an ideal choice to prevent chicken salmonellosis and ensure public health.

Regeneration of Thyroid Glands in the Spleen Restores Homeostasis in Thyroidectomy Mice.

Surgical removal of the thyroid gland (TG) for treating thyroid disorders leaves the patients on lifelong hormone replacement that partially compensates the physiological needs, but regenerating TG is challenging. Here, an approach is reported to regenerate TG within the spleen for fully restoring the thyroid's functions in mice, by transplanting thyroid tissue blocks to the spleen. Within 48 h, the transplanted tissue efficiently revascularizes, forming thyroid follicles similar to the native gland after 4 weeks. Structurally, the ectopically generated thyroid integrates with the surrounding splenic tissue while maintaining its integrity, separate from the lymphatic tissue. Functionally, it fully restores the native functions of the TG in hormone regulation in response to physiological stimuli, outperforming the established method of oral levothyroxine therapy in maintaining systemic homeostasis. The study demonstrates the full restoration of thyroid functions post-thyroidectomy by intrasplenic TG regeneration, providing fresh insights for designing novel therapies for thyroid-related disorders.