Severe Histopathological Changes Research Articles

Tamm-Horsfall protein augments neutrophil NETosis during urinary tract infection.

Urinary neutrophils are a hallmark of urinary tract infection (UTI), yet the mechanisms governing their activation, function, and efficacy in controlling infection remain incompletely understood. Tamm-Horsfall glycoprotein (THP), the most abundant protein in urine, uses terminal sialic acids to bind an inhibitory receptor and dampen neutrophil inflammatory responses. We hypothesized that neutrophil modulation is an integral part of THP-mediated host protection. In a UTI model, THP-deficient mice showed elevated urinary tract bacterial burdens, increased neutrophil recruitment, and more severe tissue histopathological changes compared to WT mice. Furthermore, THP-deficient mice displayed impaired urinary NETosis during UTI. To investigate the impact of THP on NETosis, we coupled in vitro fluorescence-based NET assays, proteomic analyses, and standard and imaging flow cytometry with peripheral human neutrophils. We found that THP increases proteins involved in respiratory chain, neutrophil granules, and chromatin remodeling pathways, enhances NETosis in an ROS-dependent manner, and drives NET-associated morphologic features including nuclear decondensation. These effects were observed only in the presence of a NETosis stimulus and could not be solely replicated with equivalent levels of sialic acid alone. We conclude that THP is a critical regulator of NETosis in the urinary tract, playing a key role in host defense against UTI.

Histopathological changes in the human tissues in various types of poisoning: A cross-sectional autopsy study

BackgroundPoisoning is a critical health issue caused by exposure to harmful substances, leading to a range of biological effects from mild irritation to severe organ damage and death. Acute poisoning is particularly prevalent in developing countries reliant on agriculture, where agricultural poisons such as organophosphates, carbamates, pyrethroids, and aluminum/zinc phosphide are common. This study aims to analyze the histopathological changes in various organs in autopsy of poisoning cases to understand the extent and nature of organ damage. MethodsAutopsies were performed on cases with an established or suspected history of poison ingestion. Tissue samples from the stomach, intestine, liver, spleen, kidneys, brain, and lungs were examined for histopathological changes. ResultsOut of 52 cases analyzed, aluminum phosphide was the predominant poison, accounting for 76.92 % of cases. Histopathological findings in poisoning cases included significant pulmonary edema (55.77 %), intra-alveolar hemorrhage (48.08 %), liver ballooning degeneration (48.08 %), acute tubular necrosis (51.92 %) in kidney, and universal brain and spleen congestion (100 %). Stomach findings showed partial loss of rugosity (80.77 %), congestion (51.92 %), necrosis of the mucosa (30.77 %), congestion (71.15 %), denudation of the epithelium (48.08 %), and mucosal inflammation (48.08 %) as predominant findings. Aluminum phosphide caused severe histopathological changes across all examined organs. ConclusionThe study highlights the critical role of histopathological examination in diagnosing and understanding organ damage in poisoning cases. Forensic pathologists can use these histopathological patterns as reference points to differentiate poisoning from other causes of death, aiding in accurate diagnosis and targeted treatment.

Comparative pathogenicity of duck hepatitis A virus genotype 3 in different duck breeds: Implications of the diagnosis and prevention of duck viral hepatitis

Duck hepatitis A virus (DHAV) infection in ducklings causes acute hepatitis with considerable economic losses. In this study, Pekin and Muscovy duckling flocks (n=9) suffering from high mortality and hepatic lesions were examined by RT-PCR for DVHA. 44.4 % (4/9) of samples were positive for DHAV (5′ UTR region), of which 100 % (4/4) were DVHA-3 (VP1 gene). VP1 sequencing and phylogenetic analysis of an isolate originated from Muscovy ducklings showed that it shared 96.8 % −100 %, 88.5–89.2 %, and 86.5–88.2 % nucleotide similarity (ns) with the Egyptian, Korean-Vietnamese, and Chinese DVHA-3 strains, respectively. It was distinguished from the DHAV-1 vaccine (67.6 % ns). The sequenced DVHA-3 isolate was used to experimentally infect 5-day-old Pekin and Muscovy ducklings vs. control groups. No apparent clinical signs or deaths were reported in the experimentally-infected groups. Pekin ducklings showed greater cloacal viral shedding than Muscovy until the 6th dpi (P<0.05). DVHA-3 induced a significant rise in IFN-β and IL-1β serum levels, where Muscovy ducklings' levels were higher than Pekin ducklings. Among the biochemical parameters, AST was only increased on the 4th dpi in both breeds vs. control (P<0.05). Compared to Muscovy ducklings at 2, 4, and 6 day post infection (dpi), the infected Pekin group had lower lipase levels (P≥0.05, p<0.05, and p<0.05, respectively), while ALT was higher at 4 and 6 dpi (P<0.05). The histopathological lesions supported the gross lesions, and their scores were dominant at 2 and 4 dpi in both breeds. At 6 and 8 dpi, Pekin showed more severe histopathological changes compared to Muscovy for the liver, heart, brain, and intestines; the pancreas, kidney, and lung showed the opposite pattern. In conclusion, Pekin ducklings displayed distinct DHAV-3 infection results from Muscovy ducklings, and more research utilizing a variety of DHAV-3 strains has to be carried out.

Protective Role of Melatonin Against Abamectin-Induced Biochemical, Immunohistochemical, and Ultrastructural Alterations in the Testicular Tissues of Rats.

Abamectin is one of the most widely used pesticides due to its strong insecticidal and anthelmintic activities. Melatonin is a neurohormone with potent antioxidant, anti-apoptotic, and anti-inflammatory effects. This study aimed to investigate the potential ameliorative effects of melatonin against abamectin-induced testicular toxicity in rats. Twenty-four rats were divided into four groups: control group (1 mL/kg/day corn oil), melatonin-treated group (10 mg/kg/day), abamectin-treated group (0.5 mg/kg/day), and melatonin plus abamectin-treated group. Test substances were administered via oral gavage once daily for 28 days. While MDA and 8-OHdG levels increased in the testicular tissue of rats treated with abamectin, SOD, CAT, GPx, and GST enzyme activities decreased significantly. While interleukin-17 levels, TNF-α, and caspase3 expression increased in the testicular tissue, acetylcholinesterase activity decreased. At the same time, serum gonadotropins (luteinizing and follicle-stimulating hormones) and testosterone levels decreased. Light microscope examinations of testicular tissues revealed severe histopathological changes, such as atrophic hyalinized seminiferous tubules, basement membrane irregularity, degeneration, spermatogenic cell loss, and necrosis. Electron microscopy examinations revealed large vacuoles in Sertoli and spermatogenic cells, swelling and vacuolization in mitochondria, lysosomal structures, and increased pyknotic nuclei. In contrast, melatonin supplementation significantly ameliorated abamectin-induced testicular toxicity in rats through antioxidant, antiapoptotic, and anti-inflammatory mechanisms.

Fifteen day repeat air: liquid Interface air-only exposures can cause respiratory epithelium injury in MucilAir™ nasal respiratory epithelial cells that parallels chemically induced cytotoxicity

New Approach Methodologies (NAMs) are being widely used to reduce, refine, and replace, animal use in studying toxicology. For respiratory toxicology, this includes in silico and in vitro alternatives using air:liquid interface (ALI) exposures to replace traditional in vivo inhalation studies. In previous studies using 1,3-dichloropropene (1,3-DCP), a 5-day 4 h repeat exposures of MucilAir™ nasal cell culture models caused, dose-dependent cytotoxicity, depletion of GSH, changes in differential gene expression and histopathological transitions in cellular morphology from pseudostratified columnar epithelium to squamous epithelium. In this report we attempted to extend these studies using 15-day 1,3-DCP 4 h exposures to using MucilAir™ nasal cultures as outlined by an US EPA recent task order (US EPA 2023). For the 15-day repeat exposure, there were severe histopathologic changes in the MucilAir™ nasal mock-treatment (air-only) VITROCELL® chamber controls compared to incubator controls preventing any further analysis. The histopathological transitions in cellular morphology from pseudostratified columnar epithelium to squamous epithelium observed in the air only control in this study and previously with 1,3-DCP in MucilAir™ nasal cultures is also a hallmark of chemically induced cytotoxic responses in vivo in the respiratory tract. Histopathology assessments of 3D respiratory tract models used in ALI exposures can provide the linkage between in vitro to in vivo outcomes as part of the validation efforts of ALI use in regulatory toxicology. This report indicates that importance of histopathological assessments of incubator and mock-treatment (air-only) controls from each ALI exposure experiment along with exposed cell based model.

Effect of recurrent severe insulin-induced hypoglycemia on the cognitive function and brain oxidative status in the rats

BackgroundEpisodes of recurrent or severe hypoglycemia can occur in patients with diabetes mellitus, insulinoma, neonatal hypoglycemia, and medication errors. However, little is known about the short-term and long-term effects of repeated episodes of acute severe hypoglycemia on the brain, particularly in relation to hippocampal damage and cognitive dysfunction.MethodsThirty-six wistar rats were randomly assigned to either the experimental or control group. The rats were exposed to severe hypoglycemia, and assessments were conducted to evaluate oxidative stress in brain tissue, cognitive function using the Morris water maze test, as well as histopathology and immunohistochemistry studies. The clinical and histopathological evaluations were conducted in the short-term and long-term.ResultsThe mortality rate attributed to hypoglycemia was 34%, occurring either during hypoglycemia or within 24 h after induction. Out of the 14 rats monitored for 7 to 90 days following severe/recurrent hypoglycemia, all exhibited clinical symptoms, which mostly resolved within three days after the last hypoglycemic episode, except for three rats. Despite the decrease in catalase activity in the brain, the total antioxidant capacity following severe insulin-induced hypoglycemia increased. The histopathology findings revealed that the severity of the hippocampal damage was higher compared to the brain cortex 90 days after hypoglycemia. Memory impairments with neuron loss particularly pronounced in the dentate gyrus region of the hippocampus were observed in the rats with severe hypoglycemia. Additionally, there was an increase in reactive astrocytes indicated by GFAP immunoreactivity in the brain cortex and hippocampus.ConclusionRecurrent episodes of severe hypoglycemia can lead to high mortality rates, memory impairments, and severe histopathological changes in the brain. While many histopathological and clinical changes improved after three months, it seems that the vulnerability of the hippocampus and the development of sustained changes in the hippocampus were greater and more severe compared to the brain cortex following severe and recurrent hypoglycemia. Furthermore, it does not appear that oxidative stress plays a central role in neuronal damage following severe insulin-induced hypoglycemia. Further research is necessary to assess the consequences of repeated hypoglycemic episodes on sustained damage across various brain regions.

Combined effect and mechanism of microplastic with different particle sizes and levofloxacin on developing Rana nigromaculata: Insights from thyroid axis regulation and immune system

Microplastics (MPs) usually appear in the aquatic environment as complex pollutants with other environmental pollutants, such as levofloxacin (LVFX). After 45-day exposure to LVFX and MPs with different particle sizes at environmental levels, we measured the weight, snout-to-vent length (SVL), and development stages of Rana nigromaculata. Furthermore, we analyzed proteins and genes related to immune system and thyroid axis regulation, intestinal histological, and bioaccumulation of LVFX and MPs in the intestine and brain to further explore the toxic mechanism of co-exposure. We found MPs exacerbated the effect of LVFX on growth and development, and the order of inhibitory effects is as follows: LVFX-MP3>LVFX-MP1>LVFX-MP2. 0.1 and 1 μm MP could penetrate the blood–brain barrier, interact with LVFX in the brain, and affect growth and development by regulating thyroid axis. Besides, LVFX with MPs caused severer interference on thyroid axis compared with LVFX alone. However, 10 μm MP was prone to accumulating in the intestine, causing severe histopathological changes, interfering with the intestinal immune system and influencing growth and development through immune enzyme activity. Thus, we concluded that MPs could regulate the thyroid axis by interfering with the intestinal immune system.

Histopathological Study of Kidney and Liver of Rats after Induction of Poisoning by Nitrate

The purpose of this research is to investigate the effects of nitrate as a calcium appearance on the hepatic and renal histology. Iraqi fertilizer firm in supplied the calcium nitrate tetrahydrate was used in this study. Twenty-four male albino wistar rats weighing 220 ± 25 g were kept under conditions of natural photoperiod, humidity 50±10%, and temperature 25±2° C. These were divided into 3 groups: G1 control group, G2 received 200 mg/kg, G3 received 400 mg/kg. Rats were administered calcium nitrates orally for thirty days after the salts were dissolved in mineral water. Animals were then sacrificed by being beheaded in the neck region. Organs such as the kidneys and liver were taken for histological analysis. Liver and kidney samples were taken from rats that were given varying amounts of calcium nitrate for a duration of 30 days. The liver sections showed regular histological architecture with hexagonal lobules and visible capillary sinusoids. The livers of the 200 mg/kg group showed mild histological damage, while the 400 mg/kg doses showed significant vascular dilatation, congestion, hepatocyte degeneration, bleeding, and lipid vacuolation. The kidneys showed severe histopathological changes, including glomerular atrophy, intra-glomerular hemorrhage, and vascular congestion, compared to the G2 which showed mild renal lesions. In conclusion, nitrate induced significant alterations in the kidneys and liver architecture that were dose-dependent. Finally, greater dosages of calcium nitrate used excessively might be harmful to humans and other mammals.

Stressing out-carp edema virus induces stress and modulates immune response in common carp.

Carp edema virus (CEV) is a fish poxvirus that primarily infects the gills of common carp. CEV causes koi sleepy disease (KSD), which is highly contagious and can result in mortality of up to 100%. In the present study, we analyzed the stress and immune responses during KSD in two strains of common carp with different resistance to CEV: susceptible koi and resistant Amur sazan. Experiments were performed at two temperatures: 12°C and 18°C. In the case of koi carp, we also analyzed the effect of supplementation of 0.6% NaCl into tank water, which prevents mortality of the CEV-infected fish (salt rescue model). We found that CEV-infected koi kept at 18°C had the highest viral load, which correlated with the most severe histopathological changes in the gills. CEV infection resulted in the activation of stress response reflected by the upregulated expression of genes involved in stress response in the stress axis organs and increased levels of cortisol and glucose in the blood plasma. These changes were the most pronounced in CEV-infected koi kept at 18°C. At both temperatures, the activation of antiviral immune response was observed in koi kept under freshwater and NaCl conditions upon CEV infection. Interestingly, a clear downregulation of the expression of adaptive immune genes was observed in CEV-infected koi kept under freshwater at 18°C. CEV induces a stress response and modulates adaptive immune response in koi, and this is correlated with the level of viral load and disease development.

Red ginseng ameliorates lipotoxicity-induced renal fibrosis in hyperuricemia mice

Ethnopharmacological relevanceChronic kidney disease can be caused by numerous diseases including obesity and hyperuricemia (HUA). Obesity may exacerbate the renal injury caused by HUA. Red ginseng, a steamed products of Panax ginseng Meyer root, is known for its remarkable efficacy in improving metabolic syndrome, such as maintaining lipid metabolic balance. However, the role of red ginseng on hyperuricemia-induced renal injury in obese cases remains unclear. Aim of the studyThis study aimed to investigate the action of red ginseng extract (RGE) on lipotoxicity-induced renal injury in HUA mice. Materials and methodsA high-fat diet (HFD)-induced obesity model was employed to initially investigate the effects of RGE on body weight, TC, OGTT, renal lipid droplets, and renal function indices such as uric acid, creatinine, and urea nitrogen. Renal structural improvement was demonstrated by H&E staining. Subsequently, an animal model combining obesity and HUA was established to further study the impact of RGE on OAT1 and ACC1 expression levels. The mechanisms underlying renal injury regulation by RGE were postulated on the basis of RNA sequencing, which was verified by immunohistochemical (including F4/80, Ki67, TGF-β1, α-SMA, and E-cadherin), Masson, and Sirius red staining. ResultsRGE modulated HFD-induced weight gain, glucose metabolism, and abnormalities of uric acid, urea nitrogen, and creatinine. RGE alleviated the more severe renal histopathological changes induced by obesity combined with HUA, with down-regulated the protein levels of ACC1, F4/80, Ki67, TGF-β1, and α-SMA, and up-regulated OAT1 and E-cadherin. ConclusionsRGE has ameliorative effects on chronic kidney disease caused by obesity combined with HUA by maintaining lipid balance and reducing renal inflammation and fibrosis.

Tilapia lake virus infection disrupts the gut microbiota of red hybrid tilapia (Oreochromis spp.)

Viral infections have the potential to damage fish intestines and disrupt the composition and diversity of the bacterial populations. In this study, we investigated the gut microbiota profiles of 23 red hybrid tilapia (10 ± 3 g) infected with Tilapia lake virus (TiLV) via two different methods. For the intraperitoneal (IP)-injection, 50 μl of TiLV at a concentration of 105 TCID50/ml was administered into the fish's coelomic cavity. In the cohabitation challenge method, infection was achieved by injecting the virus into the coelomic cavity of the inducer fish and allow them to cohabited with cohabitation fish at a ratio of 1:3. The cohabitation infected fish had a cumulative mortality rate of 49%, while the IP-injection group had 81.5%, which was accompanied by clinical signs, severe histopathological changes in the intestines and high viral loads in the intestines over the infection period at 6, 12 and 21 days post challenge (dpc). Most importantly, an analysis of the bacterial populations based on the alpha and beta diversity patterns revealed distinct alterations in the intestines of the fish infected via IP injection and cohabitation and the control fish. Specifically, our findings highlighted a reduction in Cetobacterium (phylum Fusobacterium) and an increase in Brevinema (phylum Spirochaetes) in the infected fish at 6 and 12 dpc. Indeed, the elevation of Brevinema population is associated with a higher mortality rate within the IP-injection compared to the cohabitation group. Remarkably, the fish that survived TiLV infection at 21 dpc showed a higher abundance of Bacillus (phylum Firmicutes), which was in contrast to that at earlier time points (6 and 12 dpc). While Brevinema has been recognised as a potentially opportunistic pathogen in fish, different strains of Bacillus are commonly used as probiotics to promote fish health and enhance disease resistance. Our findings thus provide valuable insights into the distinct shifts occurring within fish gut microbiota during TiLV infection and suggest potential implications for improving gut health and resistance to viral infections in tilapia. Taken together, our study establishes that TiLV infection triggers significant changes in the diversity and composition of the intestinal microbiota in red hybrid tilapia.

Investigating the Protective Effect of Ellagic Acid on Cholemic Nephropathy in Cholestatic Rats

Background: Cholemic nephropathy (CN), a renal dysfunction caused by bile acids, is a severe complication of chronic liver damage and bile duct ligation (BDL), which may lead to complete kidney failure. Objectives: This study investigated the protective effect of ellagic acid on CN in cholestatic rats. Methods: Sixty male Wistar rats weighing about 180 - 200 g were randomly divided into 6 groups for in vivo investigation. The rats were randomly divided into 5 groups of 10. Cholestasis was induced in rats by closing the bile ducts; then, the animals were treated with different doses of ellagic acid (10, 25, and 50 mg/kg). Then, the induction effect of cholestasis and the protective effects of ellagic acid on serum and urinary factors, oxidative stress indices, and histopathological changes in liver and kidney tissue were investigated. Results: Bile duct ligation in rats led to an increase in serum and urinary factors. It was also associated with increased reactive oxygen species (ROS), lipid peroxidation, glutathione (GSH) oxide form, decrease in antioxidant systems, GSH and severe histopathological changes, and fibrosis of the liver and kidney tissues. Another finding of this research was the beneficial effect of ellagic acid in improving serum and urinary factors, oxidative stress indices, and histopathological changes. Conclusions: Due to its antioxidant properties, ellagic acid can potentially serve as a novel therapeutic approach for treating kidney damage caused by increased serum levels of bile acids.

Therapeutic benefit of melatonin in 5-fluorouracil-induced renal and hepatic injury.

Nephrotoxicity and hepatotoxicity include increased oxidative stress and apoptosis; as a result, liver and kidney damage are related to its pathogenesis. These are significant side effects caused in cancer patients treated with 5-FU. In the research, 25 rats were divided into five groups, including control, 5-FU and 5-FU + 2.5, 5 and 10 mg/kg melatonin (MEL), and the protective impact of MEL against 5-FU-induced hepatorenal damage in rats was investigated. 5-FU caused significant harm, resulting in severe renal failure and histopathological changes. It also increased BUN, creatinine and hepatic function markers levels while decreasing superoxide dismutase and glutathione peroxidase activity. Additionally, 5-FU led to a notable increase in malondialdehyde content. However, MEL co-administration to rats reversed most biochemical and histologic effects. In the control and MEL + 5-FU groups, the values were comparable. The doses of MEL treatment had a significant positive impact on 5-FU-induced oxidative stress, apoptosis, lipid peroxidation and kidney damage. Our data concluded that MEL has an ameliorative effect on hepatorenal damage caused by 5-FU.

Investigation of the effect of thymoquinone on kidney damage in isoproterenol-induced myocardial infarction in rats and cardiorenal interactions

This study aimed to determine whether thymoquinone has any protective effects on renal tissue after an isoproterenol-induced myocardial infarction (MI). Experimental groups were formed as 4 groups (n=8). Control group (C). Thymoquinone group (THQ), 20 mg/kg single dose intragastric (i.g.) daily for seven days. Isoproterenol group (ISO) was administered 100 mg/kg intraperitoneally in two doses on days 7 and 8 of the experiment. Thymoquinone+Isoproterenol group (THQ+ISO), THQ 20 mg/kg i.g. was administered once a day for seven days. In addition, two doses of ISO 100 mg/kg i.p. were administered on the seventh and eighth days. Kidney tissues were evaluated histopathologically. Kidney tissues were evaluated histopathologically. Tumour necrosis factor alpha(TNF-α) and alpha Smooth Muscle Actin(α-SMA) immunoreactivity density changes were determined by immunohistochemistry. Glutathione(GST), Glutathione S-transferases(GSTs) and Interleukin-6(IL-6) levels were evaluated by ELISA method. Isoproterenol injection caused severe histopathological changes on kidney tissue. Also TNF-α and α-SMA levels were found to be higher in groups where ISO was administered. THQ could be effective on kidney tissue to partially correct these histopathological damages, by decreasing fibrosis and inflammation. This study shows that treatment with THQ is effective in preventing kidney damage caused by ISO-induced MI. We think that THQ as a supplementary food will be effective to prevent kidney damage.

Testicular Toxicity following Subacute Exposure of Arsenic and Mancozeb alone and in Combination: Ameliorative Efficacy of Quercetin and Catechin

Mancozeb (MZ) is a contact fungicide having low toxicity in non-target species, but its continuous exposure can be harmful. The aim of the present study was to determine the impact of the toxic interaction between MZ and arsenic on the testicular tissue of rats and to compare the amelioration potential of quercetin and catechin against the induced toxicity. Sixty adult rats were randomly allocated into 10 groups with 6 animals in each. A significant (p&lt;0.05) decline in TAS, TTH, SOD, CAT, GPx, GR and TTH and a rise (p&lt;0.05) in MDA and AOPP-were recorded in testicular tissue of MZ-treated rats in comparison to control. Exposure to different doses of arsenic (10, 50, 100 ppb) also produced a dose-dependent effect on these oxidative biomarkers. Arsenic exposure produces potentiating MZ-induced testicular toxicity in Wistar rats. Testicular damage was further corroborated by extremely severe histopathological changes viz., interstitial as well as sub-capsular congestion, oedema aside from degeneration, necrosis and loss of seminiferous tubules and a drastic deterioration in sperm motility in this group. In contrast, administration of toxicants along with quercetin or catechin markedly attenuated the alterations in oxidative as well as cellular damage biomarkers and testicular histopathological alterations. Our results suggested that simultaneous low dose exposure to arsenic potentiated testicular toxicity induced by MZ. Furthermore, catechin was more potent as compared to quercetin in ameliorating testicular changes induced by concurrent arsenic and MZ exposure.

The protective role of chicken cathelicidin-1 against Streptococcus suis serotype 2 in vitro and in vivo

Streptococcus suis serotype 2 (SS2) is an important zoonotic pathogen with the characteristics of high mortality and morbidity, which brings great challenges to prevent and control epidemic disease in the swine industry. Cathelicidins (CATH) are antimicrobial peptides with antimicrobial and immunomodulatory activities. In this study, bactericidal and anti-inflammatory effects of chicken cathelicidin-1 (CATH-1) were investigated in vitro and in vivo against SS2 infection. The results show that CATH-1 exhibited a better bactericidal effect compared to other species’ cathelicidins including chickens (CATH-2, -3, and -B1), mice (CRAMP) and pigs (PMAP-36 and PR-39), which rapidly killed bacteria in 20 min by a time-killing curve assay. Furthermore, CATH-1 destroyed the bacterial morphology and affected bacterial ultrastructure as observed under electron microscopy. Moreover, CATH-1 antibacterial activity in vivo shows that CATH-1 increased survival rate of SS2-infected mice by 60% and significantly reduced the bacterial load in the lungs, liver, spleen, blood, and peritoneal lavage as well as the release of SS2-induced inflammatory cytokines including IL-1α, IL-1β, IL-12, and IL-18. Importantly, CATH-1 did not show severe histopathological changes in mice. Further studies on the mechanism of anti-inflammatory activity show that CATH-1 not only reduced the inflammatory response through direct neutralization, but also by regulating the TLR2/4/NF-κB/ERK pathway. This study provides a scientific basis for the research and development of antimicrobial peptides as new antimicrobial agents.

The impact of non-caloric artificial sweetener aspartame on female reproductive system in mice model

BackgroundArtificial sweeteners, used as sugar substitutes have found their ways into almost all the food items due to the notion that they are non-caloric. Aspartame is used in numerous food products throughout the world. The primary users of aspartame include diabetics and calorie conscious people who intend to limit their calorie intake.MethodsFemale Swiss albino mice were divided into three groups (12 mice each) for the duration of 30 and 60 days consecutively. The treatment groups received 40 mg/kg b. w. aspartame orally. Hormone assays using ELISA and tissue histopathology have been performed along with the fertility assay to access the treatment outcomeon the fertility of treated mice in comparison to controls.ResultsPresent study reports that female mice treated with aspartame for 30 and 60 days showed significant reduction in body weight, relative organ weight of (liver and kidney) and gonadosomatic index. These changes were more significantly recorded in 60 days treatment group. Aspartame treated animals for 30 and 60 days showed duration-dependent decrease gonandotropins (follicle stimulating hormone and luteinizing hormone), and steroids (estradiol and progesterone). Moreover, severe histopathological changes, reduction in number of growing follicles, degenerative changes in follicular structure, corona radiata and zonagranulosa were also observed. Besides, histomorphological changes were also observed in the uterine structure including atrophic uterine endometrial glands, contracted endometrial lining, disruption of the endometrial structure and the shapes of blood vessels were also altered.ConclusionNon-nutritive artificial sweeteners including aspartame negatively impact the function of ovaries and feedback mechanism of reproductive hormones by affecting the hypothalamic–pituitary–gonadal axis. In light of present findings the aspartame negatively impacted the reproductive system of female mice. More studies are required to identify the molecular mechanism and the pathways involved.

Isolation, identification of an Aeromonas veronii strain, and the immune response of hybrid sturgeon (Acipenser baerii ♀ × Acipenser schrenckii ♂) to the bacteria

Hybrid sturgeon (Acipenser baerii ♀ × Acipenser schrenckii ♂) holds significant importance in the aquaculture industry in China. However, the recurring disease outbreaks caused by Aeromonas veronii have led to substantial economic losses in hybrid sturgeon culture. Further, the immune response of hybrid sturgeon to A. veronii infection remains poorly understood. Therefore, this study isolated and characterized a bacterial strain from affected fish, which was subsequently identified as A. veronii based on various characteristics. Moreover, severe histopathological changes, including degeneration and necrosis of the gill cells and intestinal villi, were observed in the diseased fish. Transcriptome data analysis using GO and KEGG enrichment revealed dynamic changes and enrichment of classical immune-and hematopoietic-related pathways following A. veronii infection. Additionally, significant changes were observed in the proportion of blood lymphocytes and antioxidative enzyme levels during A. veronii infection. Further investigations showed that the infected fish serum inhibited A. veronii replication. These findings provide valuable insights into the immune response of hybrid sturgeon against A. veronii infection.

Histopathological evaluation of hepatic tissue of yellow Rasbora (Rasbora lateristriata) exposed to paracetamol

Excessive consumption of paracetamol may lead to hepatic necrosis, nephrotoxicity, extra-hepatic lesions, and even fatality in both humans and animals. The objective of this study was to examine the histological changes in the hepatocytes of yellow rasbora (Rasbora lateristriata) exposed to paracetamol. The fish were subjected to varying concentrations of paracetamol over a period of four days. Group I served as the control group without any paracetamol exposure. Groups II, III, and IV were exposed to 2, 3, and 4 mg/L of paracetamol, respectively. A total of six individuals were allocated to each of the four experimental groups. The histological analysis of the hepatic tissue following paracetamol exposure at concentrations of 2, 3, and 4 mg/L revealed hepatic damage characterized by picnosis, necrosis, and vacuolization. In summary, higher concentrations of paracetamol were associated with an increase in the severity of histopathological changes in the hepatic tissues of yellow rasbora.

Higher-temperature-adapted dengue virus serotype 2 strain exhibits enhanced virulence in AG129 mouse model.

The factors that drive dengue virus (DENV) evolution, and selection of virulent variants are yet not clear. Higher environmental temperature shortens DENV extrinsic incubation period in mosquitoes, increases human transmission, and plays a critical role in outbreak dynamics. In the present study, we looked at the effect of temperature in altering the virus virulence. We found that DENV cultured at a higher temperature in C6/36 mosquito cells was significantly more virulent than the virus grown at a lower temperature. In a mouse model, the virulent strain induced enhanced viremia and aggressive disease with a short course, hemorrhage, severe vascular permeability, and death. Higher inflammatory cytokine response, thrombocytopenia, and severe histopathological changes in vital organs such as heart, liver, and kidney were hallmarks of the disease. Importantly, it required only a few passages for the virus to acquire a quasi-species population harboring virulence-imparting mutations. Whole genome comparison with a lower temperature passaged strain identified key genomic changes in the structural protein-coding regions as well as in the 3'UTR of the viral genome. Our results point out that virulence-enhancing genetic changes could occur in the dengue virus genome under enhanced growth temperature conditions in mosquito cells.