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Results for “Epithelial inflammation”

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At least 19 recordsLinked to original sources
PubMed2025

Altered ruminal microbiome tryptophan metabolism and their derived 3-indoleacetic acid inhibit ruminal inflammation in subacute ruminal acidosis goats.

BACKGROUND: Subacute ruminal acidosis (SARA) is a digestive disorder that often severely jeopardizes the health and lactation performance of ruminants fed a high-energy diet. Different dairy ruminants exhibit varying degrees of inflammation accompanied by variations in the rumen microbiota when SARA occurs. Our understanding of the occurrence of SARA and varying degrees of rumen epithelial inflammation is lacking. Hence, we performed rumen metagenomic, metagenome-assembled genome and metabolomic analyses, with transcriptome and single-nucleus RNA sequence analyses, to explore the microbial mechanism of SARA occurrence and different degrees of inflammation. RESULTS: A total of 36 goats fed two diets with gradually increasing levels of rumen-degradable starch (RDS) were included in this study, and SARA goats fed 70% concentrate diets supplemented with whole corn (HGW-SARA) and SARA goats fed 70% concentrate diets supplemented with crushed corn (HGC-SARA) were identified. Moreover, 11 goats fed a control basal diet, named LGW-CON, were also included. Compared with those in the LGW-CON group, the rumen fermentation capacity was enhanced, accompanied by ruminal epithelial and systemic inflammation, in goats from HGW-SARA and HGC-SARA. Between them, HGC-SARA goats presented less inflammation. Notably, the ruminal inflammation-related pathways were increased only in the HGW-SARA group but not in the HGC-SARA group. Metagenomic analysis revealed that the β diversity of SARA goats was significantly different from that of LGW-CON goats. Ruminococcus significantly increased in both SARA groups, whereas Prevotella and Bacteroidales significantly decreased, which was accompanied by a decrease in cellulose and hemicellulose enzymes and an increase in lysozymes and lipopolysaccharide synthesis enzymes. Multi-omics analysis of the ruminal contents and tissues suggested that epithelial inflammation was caused by disturbed ruminal microbiome-induced Th17 cell differentiation and IL-17 signalling pathway activation. Comparative analyses between the HGW-SARA and HGC-SARA groups highlighted the importance of Selenomonas and Bifidobacterium, as well as bacterial tryptophan metabolism, in the production of 3-indoleacetic acid, which mitigated ruminal epithelial inflammation by modulating Th17 cells and inhibiting IL-17 signalling. Ruminal microbiota transplantation from HGW-SARA goats to healthy dairy goats and mice revealed the role of microbes in epithelial inflammation. Additionally, 3-indoleacetic acid supplementation reduced rumen inflammation and the IL-17 concentration in the serum, improved VFAs absorption, and enhanced milk production. CONCLUSIONS: This study unveiled that after SARA was induced by high-concentrate feeding, the rumen homeostasis was disrupted, and rumen fiber degradation capacity of dairy goats decreased, but the LPS synthesis capacity increased, and inflammation of the rumen epithelium was observed. However, the ruminal microbial species from the Bifidobacterium and Selenomonas genera and bacterial 3-indole acetic acid are pivotal in mitigating ruminal epithelial inflammation during SARA in dairy goats. This could potentially be attributed to the modulation of ruminal Th17 cell proportions and the inhibition of IL-17 signalling pathways. Video Abstract.

Rumen↗
PubMedDate not supplied

A review of modern concepts of healing of cutaneous wounds.

Basic-science aspects of wound healing are discussed in the light of recent developments in wound-healing research. The author discusses wound healing in six, arbitrarily chosen phases, namely, inflammation, epithelialization, vascularization, contraction, collagen synthesis and late remodeling of scars that occur simultaneously in concert, but in such a manner that enables one to distinguish clinically between healing by primary intention and healing by secondary intention.

Aged↗
PubMed1976

Morphological features and healing of stress ulcers induced by alcohol and restraint.

Gastric mucosal damage was produced in 130 mice by forced ingestion of alcohol, followed by restraint in the cold. Animals were killed at intervals from six hours to 27 days following the stress. Linear hemorrhagic erosions and diffuse hemorrhagic patches were found grossly, predominantly in the glandular portion of the stomach, in about 75% of the animals 6 to 24 hours after stress. At later time intervals, the linear mucosal depressions persisted; these became progressively less prominent with time but substantial numbers were still readily discernible three weeks after injury. Microscopical examination of the fresh lesions showed a variable amount of mucosal necrosis and acute inflammation. Epithelial regeneration became prominent after three days and persisted for several weeks. The first regenerating epithelial cells were primitive, cuboidal elements followed by mucous cells, parietal cells, and zymogen cells, in that order. The morphological features and evolution of the lesions were similar to that described in human stress ulcers.

Animals↗
PubMed1977

[Behavior of the middle ear mucosa in cholesteatoma and following tympanoplasty. An experimental histological study in rabbits].

After operation three consecutive phases can be observed: 1. thickening of epithelial cell layer with development of edema in the submucosa, 2. metaplasia of epithelium with formation of ciliated and goblet cells, concomitantly round cells are found in the submucous tissue, 3. regression of inflammation and epithelial metaplasia. After 6 months goblet and ciliated cells disappear and eventually a slightly irregular monolayer epithelium is seen. If cholesteatoma is present the second phase persists. Remarkably epithelial and subepithelial changes are not concentrated in the vicinity of cholesteatoma but are seen in the whole middle ear. By autoradiography it was demonstrated, that the subepithelial tissue of cholesteatoma has a normal metabolic rate. It can be concluded that high metabolic activity postulated by other authors cannot be responsible for inflammation.

Animals↗
PubMed2026

Prophylactic Inhaled Pattern Recognition Receptor Agonists Reprogram Lung Epithelial Response and Prevent Type 2 Allergic Inflammation.

Prophylactic inhalation of the synergistic agents ODN M362 and Pam2CSK4 ("Pam2ODN") protects mice against allergic lung disease, including allergic inflammation caused by house dust mite (HDM). By preventing sensitization, Pam2ODN reduces HDM-induced eosinophilic and lymphocytic inflammation. How Pam2ODN affects interactions among lung epithelial cells, dendritic cells, and T cells to prevent eosinophilic lung inflammation remains unclear. In the present study, we show that a single inhaled dose of Pam2ODN before HDM sensitization reduces airway Th2 polarization without affecting Th1 or Treg responses. Furthermore, Pam2ODN pretreatment inhibits the recruitment of lung monocyte-derived dendritic cells (moDCs) and conventional Type 2 dendritic cells (DC2s), while preventing the HDM-induced decrease in conventional Type 1 dendritic cells (DC1s). Bulk RNA-seq of the whole lung reveals that Pam2ODN pretreatment restricts the expression of proinflammatory transcripts induced by HDM sensitization. This tolerogenic effect is also reflected at the single-cell level in lung epithelial cells, where proinflammatory transcripts, pathways, and chromatin accessibility are inhibited. These results indicate that Pam2ODN reprograms lung epithelial cells to attenuate allergen-induced Th2-promoting cytokines and DCs while maintaining the population of protective DC1s. These findings suggest a strategy to mitigate chronic allergic lung diseases.

Animals↗
PubMed2026

IL-13 and calpain-14 suppress the expression of SPINK7 by regulating OVOL1 in eosinophilic esophagitis.

Eosinophilic esophagitis (EoE) is a type 2 allergic disease characterized by esophageal inflammation and epithelial cell dysfunction. The acquired loss of the anti-serine protease of kazal type 7 (anti-SPINK7) in the squamous epithelium of the esophagus has a causal role in EoE pathogenesis. However, there is a limited understanding of the factors that regulate its expression and responsiveness to inflammatory stimuli. Herein, we have identified the transcription factor, ovo like transcriptional repressor 1 (OVOL1), as an esophageal selective gene product that regulates SPINK7 promoter activity. Overexpression of OVOL1 increased SPINK7 expression, whereas its depletion decreased SPINK7 expression, impaired epithelial barrier, and increased production of the proatopy cytokine thymic stromal lymphopoietin (TSLP). Stimulation with IL-13 abrogated the nuclear translocation of OVOL1 and promoted enhanced degradation of OVOL1 protein. This effect of IL-13 was dependent on the esophageal specific cysteine protease calpain-14 at least in part. Analysis of human esophageal biopsies demonstrated that the expression of esophageal OVOL1 correlated with SPINK7 transcript expression and was lost as a function of EoE disease activity. In summary, our study identifies key regulatory mechanisms in EoE pathogenesis, demonstrating that OVOL1 promotes SPINK7 transcription, whereas IL-13 suppresses this pathway in EoE.

Humans↗
PubMedDate not supplied

Significance of Schistosomiasis japonica in the development of cancer of the large intestine: report of a case and review of the literature.

A 68-year-old man had a tumor in the ascending colon, following schistosomiasis 58 years earlier. Right hemicolectomy was performed. Examination of the specimen showed adenocarcinoma with schistosomiasis japonica. A total of 276 such cases in medical literature were reviewed. There were significant differences between carcinoma with schistosomiasis and ordinary carcinoma in symptoms, age range, sec ratio, and histopathologic findings. These suggest that schistosomiasis induces carcinoma. Chronic inflammation and epithelial proliferation due to intestinal schistosomiasis may be a promoting factor rather than a direct carcinogenic factor in the development of adenocarcinoma of the large intestine.

Adenocarcinoma↗
PubMed1977

Incidence of epithelial atypia in radicular cysts: a preliminary investigation.

Histologic sections of 100 radicular cysts were scored for epithelial atypia, inflammation, and presence of other histologic features. No atypia was found in 32 cases. In 34 cases, atypia occurred in epithelium that was heavily infiltrated with chronic inflammatory cells. There were 26 cases of slight atypia, six cases of moderate atypia, one case of severe atypia, and one case that appeared to be carcinoma arising in a cyst wall. There was no evidence that inflammation in the connective tissues occurred more frequently or was more severe in cases that exhibited greater degrees of atypia.

Aged↗
PubMed1978

Soft tissue responses to high frequency use of experimental and commercial mouthwashes.

A recent study reported that regular use of commercial mouthwashes produced a significant incidence of oral reactions, including epithelial peeling, inflammation, ulceration and geographic tongue-like lesions. In view of the widespread use of these preparations, without apparent deleterious effects, an investigation of two commercial preparations (Scope, Listerine) and an experimental mouthwash containing cetyl pyridinium chloride was undertaken to assess the possible irritant effects on the oral soft tissue under stringent test conditions. A double blind design was used and soft tissue effects were measured over a two week period. Rinses were used full strength, 20 cc 3 times daily. Examinations were conducted by an oral pathologist at the start and conclusion of the test period, and a record was made of the occurrence of erythema, hyperemia/prominent vasculature, inflammation, petechia, keratosis, tongue coating, and ulceration. These observations did not reveal any soft tissue conditions beyond those which would be expected in the normal population.

Adolescent↗
PubMed2025

Single-dose cathepsin L CRISPR nanotherapy mitigates PASC-like lung damage in hamsters.

Respiratory post-acute sequelae of COVID-19 (PASC) persists in many SARS-CoV-2 survivors, yet no therapies specifically address its long-term pulmonary damage. We demonstrate that a single-dose CRISPR-CasRx nanotherapy targeting the host enzyme cathepsin L (SCNC) effectively reduces acute SARS-CoV-2 infection in Syrian hamsters, with antiviral efficacy comparable to Paxlovid. Importantly, SCNC outperforms Paxlovid in alleviating alveolar epithelial hyperplasia and lung inflammation at 31 days post-infection, a recognized PASC time point. Single-cell RNA sequencing reveals that SCNC enhances alveolar repair by promoting the differentiation of alveolar type 2 cells into alveolar type 1 cells and by reducing inflammatory infiltration through multiple signaling pathways. Thus, SCNC exerts a dual mechanism: host-directed viral inhibition and promotion of epithelial repair with reduced inflammation. This distinguishes it from therapies focused solely on viral suppression or symptom relief. These findings support SCNC as a promising therapeutic candidate for acute infection and, particularly, for PASC-related lung injury, where options remain limited.

alveolar epithelial regeneration↗
PubMed2026

Generation of a novel Slc7a9G105R mutant mouse identifies new biomarkers for cystinuria.

INTRODUCTION: Cystinuria is a rare inherited disease characterized by increased urinary cystine levels resulting in the formation of cystine stones in the urinary tract. Mutations in the genes encoding the cystine transporter complex, SLC3A1 and SLC7A9, are the primary drivers of the disease. Current mouse models used to study cystinuria rely on gene deficiency or spontaneous mutations in mice that do not accurately reflect the pathogenic mutations found in humans. METHODS: We generated a novel Slc7a9G105R knock-in mouse model in which glycine at position 105 is replaced by arginine, recapitulating the most common pathogenic mutation in human SLC7A9. Disease onset and progression were assessed using micro-CT imaging, fecal metagenomics, and urine and serum metabolomics and proteomics. RESULTS: Both male and female Slc7a9G105R mice developed a cystinuria phenotype by nine weeks of age, characterized by substantial cystine stone formation and increased urinary cystine, lysine, arginine, and ornithine. Slc7a9G105R mice displayed distinct serum and urinary metabolite profiles, mapped to dibasic amino acid pathways, and serum protein profiles, mapped to disease progression. Fecal metagenomics revealed that Slc7a9G105R mice had a heterogeneous microbiota with altered functional pathways, including increased L-cysteine biosynthesis. Antibiotic-induced depletion of the microbiota did not affect cystine stone burden but reduced urinary tract inflammation. Prophylactic or therapeutic dietary supplementation with alpha-lipoic acid reduced stone burden and inflammation, but it also caused urothelial damage. Untargeted metabolomics analysis following alpha-lipoic acid supplementation identified metabolites that can increase cystine solubility, reduce inflammation, and damage epithelial cells. Correlation analysis revealed novel serum metabolite biomarkers of stone burden, including 2-hydroxybutyric acid and 2-amino-2-thiazoline-4-carboxylic acid, which were also detected in human serum. CONCLUSIONS: Collectively, the Slc7a9G105R mutant mouse model offers a precise, rapid-onset, and translational platform for investigating cystinuria pathogenesis and evaluating potential therapeutic strategies.

SLC7A9↗
PubMed2026

Enteral Nutrition Is Associated with a Distinct Gut Microbiome Composition and Fermentation Capacity Profile After Acute Colonic Injury in Rats.

Enteral nutrition (EN) is known to promote mucosal healing in inflammatory bowel disease, and multi-omics data suggest that the gut microbiome mediates its therapeutic effects. However, the impact of EN and its components on the gut community during recovery from acute epithelial injury remains incompletely understood. We used whole-genome metagenomic sequencing to investigate the effect of an EN formula based on extruded amaranth flour and pea protein on the gut microbiome in a dextran sulfate sodium (DSS) rat model of acute colonic injury. Three groups were compared, as follows: an unchallenged control (n = 9) with standard chow, a colonic injury (5% DSS; n = 9) group with standard chow, and a colonic injury (5% DSS; n = 9) group with EN. Injury was confirmed histologically (median MCHI score was 2, indicating epithelial damage without inflammation). DSS caused significant weight loss. Animals receiving EN regained baseline weight faster, by day 14, whereas animals on standard chow achieved recovery only by day 21. Differences in energy intake should be further investigated to validate the effect of EN on body weight recovery. At day 21, both injury groups demonstrated higher relative abundances of Bacteroidaceae and Erysipelotrichaceae, including the mucin-degrader Allobaculum mucilyticum, compared with the control group. Conversely, Lactobacillus abundance, notably Lactobacillus acidophilus, was higher in the EN group than in both other groups, as was the inferred capacity for lactate-producing fermentation. These findings suggest that EN is associated with a distinct microbial composition and inferred metabolic profile during the post-injury period, with lactobacilli as one of the potential mediators of its effects.

Animals↗
PubMed1978

Aphakic glaucoma.

The cause of aphakic glaucoma should always be determined because treatment must be directed towards the aetiological mechanism. We have defined early aphakic glaucoma as that occurring within the first 6 postoperative weeks and late aphakic glaucoma as occurring at any later time. Of the various causes of glaucoma in each category, among the most serious and challenging to treat are pupillary block and angle closure. These emanate from postoperative shallow or empty anterior chambers which are associated with wound fistula, choroidal detachment, or a combination of both. Other mechanisms producing aphakic glaucoma are inflammation, alpha chymotrypsin, epithelial downgrowth, and iris cysts. Pressure elevation unrelated to aphakic glaucoma may also result from intraocular tumours, recurrence of glaucoma secondary to uveitis, and undiagnosed preexisting primary glaucoma.

Aphakia, Postcataract↗
PubMed1976

[Subepithelial changes in simple leukoplakic hyperplasia of the laryngeal mucosa (author's transl)].

Subepithelial changes in hyperplasia of the laryngeal mucosa consist in edema and cellular inflammatory reaction. 150 cases of epithelial hyperplasia without atypia have been investigated histologically in regard to these subepithelial changes. The cases were subdivided into 3 categories, according to the degree of hyperplasia. The degree of inflammatory reaction in the subepithelial compartment also was classfied into 3 groups. A, B and C. There was evidence of a positive correlation between the increase in the epithelial hyperplasia and the increase of a positive correlation between the increase in the inflammatory process in the subepithelial layer. It could not be decided, which one of these two pathological changes was primary and which secondary. The therapy, however, should aim at both, epithelial proliferation, as well as, subepithelial inflammation.

Epithelial Cells↗
PubMed1979

A histologic study of ovarian endometriosis with emphasis on hyperplastic and atypical changes.

One hundred ninety-four cases of ovarian endometriosis, encountered during a 3-year period, were studied. In addition to endometrial-type epithelium and stroma that were present in each of these cases, oviduct-type epithelium was demonstrated in 26, papillary epithelial-lined projections in 7, and hobnail cells in 36 patients. Forty-three cases showed reactive epithelial changes, probably due to inflammation and regeneration. There were 4 cases of adenomatous hyperplasia. Severe epithelial atypism was seen in 7 patients (3.6%), 1 in conjunction with adenomatous hyperplasia. Although the areas of severe epithelial atypism in ovarian endometriosis may be of reactive origin, one must also consider the possibility that in some instances these atypical changes may constitute a neoplastic potential.

Adult↗