Tissue Barriers最新文献

Ulcerative colitis (UC) is a chronic and debilitating disorder that falls under the broad category of inflammatory bowel disease (IBD). Therefore, affects the colon and rectum, resulting in inflammation and ulcers in the lining of these organs. Over the years, there has been a significant shift in the management of UC. The focus has moved from achieving symptom-free daily living to attaining mucosal healing. Mucosal healing means completely restoring the colon and rectum's lining, significantly reducing the risk of complications and relapse. Macrophages are a crucial component of the immune system that play a vital role in the regeneration and repair of colonic ulcers. These immune cells are responsible for production of a variety of cytokines and growth factors that facilitate tissue repair. Macrophages are responsible for maintaining a balance between inflammation and healing. When this balance is disrupted, it can lead to chronic inflammation and tissue damage, exacerbating UC symptoms. Thus, this review aims to investigate the contribution of macrophages to mucosal repair and remission maintenance in UC patients.

Tight junctions (TJs) are an important component of cellular connectivity. Claudin family proteins, as a constituent of TJs, determine their barrier properties, cell polarity and paracellular permeability. Claudin-12 is an atypical member of the claudin family, as it belongs to the group of non-classical claudins that lack a PDZ-binding domain. It has been shown that claudin-12 is involved in paracellular Ca²⁺ transients and it is present in normal and hyperplastic tissues in addition to neoplastic tissues. Dysregulation of claudin-12 expression has been reported in various cancers, suggesting that this protein may play an important role in cancer cell migration, invasion, and metastasis. Some studies have shown that claudin-12 gene functions as a tumor suppressor, but others have reported that overexpression of claudin-12 significantly increases the metastatic properties of various tumor cells. Investigating this dual role of claudin-12 is of utmost importance and should therefore be studied in detail. The aim of this review is to provide an overview of the information available to date on claudin-12, including its structure, expression in various tissues and substances that may affect it, with a final focus on its role in cancer.

Diabetes Mellitus presents a formidable challenge as one of the most prevalent and complex chronic diseases, exerting significant strain on both patients and the world economy. It is recognized as a common comorbidity among severely ill individuals, often leading to a myriad of micro- and macro-vascular complications. Despite extensive research dissecting the pathophysiology and molecular mechanisms underlying vascular complications of diabetes, relatively little attention has been paid to potential lung-related complications. This review aims to illuminate the impact of diabetes on prevalent respiratory diseases, including chronic obstructive pulmonary disease (COPD), acute respiratory distress syndrome (ARDS), idiopathic pulmonary fibrosis (IPF), tuberculosis (TB), pneumonia infections, and asthma, and compare the vascular complications with other vascular beds. Additionally, we explore the primary mechanistic pathways contributing to these complications, such as the expression modulation of blood-tissue-barrier proteins, resulting in increased paracellular and transcellular permeability, and compromised immune responses rendering diabetes patients more susceptible to infections. The activation of inflammatory pathways leading to cellular injury and hastening the onset of these respiratory complications is also discussed.

Although the majority of the population will be protected due to the advent and widespread use of the HPV vaccine, the treatment of cervical cancer for all causes, including HPV-negative cervical cancer, is still worthy of further research. The focal point of this study was Canadine's inhibition of epithelial-mesenchymal transformation (EMT) in cervical cancer. Immunoblotting, wound healing and tumor invasion experiments showed that low concentration of Canadine could inhibit the EMT process, proliferation and migration of HT-3 cells (HPV-negative cell line). Combined with GEO database, it was found that the expression levels of several genes highly expressed in cervical tumor tissues could be inhibited by Canadine, especially MAGEA3. Further experiments confirmed that the inhibition of Canadine on MAGEA3 protein increased with time. The small interference and overexpression plasmid of MAGEA3 were designed and verified. In HT-3 cells, when MAGEA3 levels were directly decreased, mesenchymal phenotypic markers were decreased and epithelial phenotypic markers were increased. The opposite result was obtained by overexpression of MAGEA3. In addition, the inhibition of EMT due to the reduction of endogenous MAGEA3 by Canadine was also offset by the overexpression of exogenous MAGEA3. The study concludes that Canadine inhibits EMT of cervical cancer by inhibiting MAGEA3.

NAFLD is a condition that develops when the liver accumulates excess fat without alcohol consumption. This chronic liver ailment progresses along with insulin resistant and is typically not diagnosed until the patients have cirrhosis. Nuclear hormone receptor superfamily PPARs are essential for metabolism of fatty acids and glucose. In liver, lipid metabolism is regulated by nuclear receptors and PPARα, and PPARβ/δ encourages fatty acid β-oxidation. PPAR-γ, an energy-balanced receptor is a crucial regulator in NAFLD. The partial activation of PPAR-γ could lead to increased level of adiponectin and insulin sensitivity, thus improved NAFLD. Because of less side effects, natural compounds are emerged as potential therapeutic agents for NAFLD by PPARγ agonists. Although the results from preclinical studies are promising, further research is needed to determine the potential dosing and efficacy of mentioned compounds in human subjects. In this review, we summarize the effect of natural PPARγ agonist in the NAFLD.

The rising prevalence of fungal infections is a significant and growing public health threat, and this risk is further underscored by our incomplete understanding of why organs like the kidney are so susceptible to systemic candidiasis. To combat the high mortality of such infections, we urgently need to advance our understanding of fungal pathogenesis and how it articulates with human immune response. Now, a recent landmark study has illuminated a crucial role of the complement system in the response to candidiasis and determined the stepwise local response of phagocytes within the kidney during infection. These fundamental discoveries provide crucial insights that can be leveraged to improve the care and outcome for patients with fungal infections.

The epidermis of the skin provides a barrier between the organism and the external environment. It is constantly subjected to physical and chemical insults, and thus susceptible to wounding and to neoplastic transformation. Long-lasting epigenetic modifications in epidermal stem cells are now shown to link responses to skin injuries with cell priming for carcinoma development, through regulation of histone H2A ubiquitylation.

Sertoli cells are a crucial component of the blood-testis barrier (BTB), which isolates the adluminal compartment of the seminiferous tubules from the rest of the testis thus forming an environment to immunely protect the developing germ cells. The mechanisms of regulating immune responses within this environment are currently under investigation. Here, we focused on Sertoli cell regulation of the complement system.

Sertoli cells are unique cells that contribute to the formation of the blood-testis barrier, which is important in sustaining the environment to promote spermatogenesis and to protect immunogenic germ cells from autoimmune destruction. This is achieved through tight junctions and production of regulatory immune factors. These Sertoli cell attributes make them a relevant model for various studies involving male reproduction, autoimmune protection, and even transplantation. RNA sequencing analyses were performed on baseline neonatal porcine Sertoli cells (NPSC) and NPSC after incubation in normal human serum for 90 minutes. We previously analyzed this data for immune-related factors, such as complement components, and for differentially expressed genes related to immune function. Still, these data sets provide insight into understanding how Sertoli cells create an immunoregulatory environment, which has applications in reproduction, transplantation, and autoimmunity.

The microbiome is a keystone of adult gastrointestinal (GI) tract health, where it facilitates digestion, wards off pathogen colonization, and exerts a powerful influence on the physiological health of organs ranging from the brain to the kidneys. From its establishment at birth and through the initial years of childhood, the human microbiome is particularly dynamic, shifting in its composition and alpha (species) diversity to an adult profile as dietary sustenance transitions from milk-based sources to others such as solid food. An innovative study has now demonstrated how microbiome maturation is requisite both for the progression of immune system development and for long-term gut barrier function. These insights have significant ramifications for designing pediatric approaches to cultivate immune cell ontogeny in the formative stages of human infancy.