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PubMed2006

Gene expression changes in thalamus and inferior colliculus associated with inflammation, cellular stress, metabolism and structural damage in thiamine deficiency.

Identification of gene expression changes that promote focal neuronal death and neurological dysfunction can further our understanding of the pathophysiology of these disease states and could lead to new pharmacological and molecular therapies. Impairment of oxidative metabolism is a pathogenetic mechanism underlying neuronal death in many chronic neurodegenerative diseases as well as in Wernicke's encephalopathy (WE), a disorder induced by thiamine deficiency (TD). To identify functional pathways that lead to neuronal damage in this disorder, we have examined gene expression changes in the vulnerable thalamus and inferior colliculus of TD rats using Affymetrix Rat Genome GeneChip analysis in combination with gene ontology and functional categorization assessment utilizing the NetAffx GO Mining Tool. Of the 15 927 transcripts analysed, 125 in thalamus and 141 in inferior colliculus were more abundantly expressed in TD rats compared with control animals. In both regions, the major functional categories of transcripts that were increased in abundance after TD were those associated with inflammation (approximately 33%), stress (approximately 20%), cell death and repair ( approximately 26%), and metabolic perturbation (approximately 19%), together constituting approximately 98% of all transcripts up-regulated. These changes occurred against a background of neuronal cell loss and reactive astro- and microgliosis in both structures. Our results indicate that (i) TD produces changes in gene expression that are consistent with the observed dysfunction and pathology, and (ii) similar alterations in expression occur in thalamus and inferior colliculus, brain regions previously considered to differ in pathology. These findings provide important new insight into processes responsible for lesion development in TD, and possibly WE.

Animals↗
PubMed2006

Ischemic acute tubular necrosis models and drug discovery: a focus on cellular inflammation.

Acute renal failure (ARF) is a common cause of mortality and morbidity in hospitalized patients. Ischemia is an important cause of ARF, and ARF caused by ischemic injury is referred to as ischemic acute tubular necrosis (ATN). There is growing evidence from models that ischemic ATN is associated with intrarenal inflammation. Consequently, intrarenal inflammation is an attractive target for the development of novel drug therapies for ARF. This review outlines ischemic ATN models, the pathophysiological roles of inflammatory cells such as T and B cells in ischemic ATN models, and effective T and B cell therapeutic reagents.

Animals↗
PubMed1991

Substance P: a neurogenic mediator of acute cellular inflammation in the dog?

Substance P (SP) is a neuropeptide that has recently been implicated in the pathogenesis of neurogenic inflammation. SP has been shown to activate polymorphonuclear leukocytes (PMN) as well as other inflammatory cells. The present study investigated the direct stimulatory and priming effects of SP on canine PMN aggregation and migration. Direct stimulation of cell migration by SP was present at an unphysiologically high concentration of the mediator. However, when micromolar concentrations of SP were added to PMN prior to stimulation with sub-optimal concentrations of leukotriene B4 (LTB4), the cells exhibited enhanced aggregation and migration, i.e. priming, when stimulated with the latter. Since SP has been reported to act via the formyl-Met-Leu-Phe (fMLP) chemotaxin receptor, this mediator was also studied and found not to possess any effects similar to SP. Thus, the results indicate that SP acts as a primer of canine PMN functions in vitro via a receptor different from that for fMLP. Before ascribing SP a mediator role in canine neurogenic inflammation, in vivo studies determining the concentrations of, and responses to SP in inflamed tissue should be performed.

Animals↗
PubMedDate not supplied

Chronic sinusitis with nasal polyps: staphylococcal exotoxin immunoglobulin E and cellular inflammation.

BACKGROUND: The etiology of chronic sinusitis with nasal polyposis (CS/NP) remains enigmatic. Frequently, Staphylococcus aureus is present in the nose of CS/NP patients, although the significance is unclear. Recent reports have suggested the hypothesis that these bacteria may secrete exotoxins triggering the inflammatory mucosal changes seen in CS/NP. This mechanism of immunopathology has been established in other diseases associated with Staphylococcus colonization and exotoxin secretion such as atopic dermatitis. In atopic dermatitis, the exotoxins incite a local superantigen response in which clonal T-cell activation and massive cytokine release occur in the affected skin. Second, these exotoxins can act as traditional allergens, stimulating a typical immunoglobulin E (IgE) response in the serum, which has been correlated with disease severity. This study is designed to begin the assessment of the hypothesis that a similar mechanism takes place in CS/NP. METHODS: Serum was drawn from patients with CS/NP undergoing endoscopic sinus surgery as well as 13 atopic and nonatopic control subjects without sinusitis. IgE levels to S. aureus exotoxins A (SEA), SE exotoxins B (SEB), and toxic shock syndrome toxin 1 were measured using enzyme-linked immunosorbent assay. Tissue eosinophilia and the presence of lymphocytes on hemotoxylin and eosin-stained sections of polyps were scored by a blinded pathologist and correlated to presence of toxin IgE in the serum. RESULTS: Staphylococcal exotoxin (SE)-specific IgE was found in the serum of 5/10 (50%) of the patients with CS/NP. In contrast, 0/13 control patients had IgE to the exotoxins (p = 0.031). Polyp eosinophil, lymphocyte, and mononuclear cell counts were compared in IgE exotoxin-positive and -negative subjects. A trend toward increased eosinophil counts in patients with SE IgE (SE IgE+) was present, but not statistically significant. CONCLUSION: These results indicate that a high percentage of CS/NP patients show a systemic IgE response to S. aureus exotoxins in comparison with controls without CS/NP. Although these results are consistent with the actions of Staphylococcus toxins in other diseases, additional work is necessary to establish a local superantigen response in the nasal mucosa of CS/NP patients.

Adult↗
PubMed1990

[Cytological diagnosis of intrathoracic epithelioid-cellular inflammations].

In the period between 1987 and 1989, 441 epitheliodcell granulomas were diagnosed on the basis of cytological investigations, and confirmed histologically. The material involved was obtained via perbronchial puncture, imprint preparations from bronchial biopsies, transbronchial biopsies and thoracoscopic biopsies. The sensitivity of the cytological investigations of imprint preparations in the case of small biopsies is some 7-12.5% better than that of the histological examination. Thus, the histological diagnosis is supplemented by cytology. In 92.9% of the cases, granulomatous disease was diagnosed on the basis of the evaluation of the perbronchial puncture material alone, so that in these cases, mediastinoscopy could have been avoided.

Biopsy, Needle↗
PubMed1982

Effect of pregnancy of cellular inflammation.

Pregnancy inhibits macrophage accumulation within the peritoneal cavity of Wistar rats when inflammation is induced by phytohaemagglutinin (PHA). The inhibition of macrophages was considerably greater than that of polymorphonuclear leucocytes (PMNs) induced by sodium caseinate. Pregnancy did not significantly alter macrophage accumulation to PHA injected into the pleural space or to nitrocellulose filters placed s.c. Cell-free homogenates prepared from the products of conception, but not normal liver, contained an anti-flammatory factor which, when injected i.v., inhibited macrophage accumulation to peritoneal but not to pleural or s.c. irritants. The responsible anti-inflammatory factor was identified as a peptide of mol. wt less than 1000.

Animals↗
PubMed1997

[Clinical value of evaluating "markers" of cellular inflammation in monitoring bronchial asthma].

In the base of bronchial asthma is a chronic inflammatory process which takes place in bronchial mucous membrane. The main cells of allergic reaction are: mastocytes., basophils, eosinophiles and others. There are many factors released from them in various periods of allergic inflammation. Evaluation of a concentration of these factors may be very usefull in diagnostic and treatment of bronchial asthma.

Asthma↗
PubMed1989

Cellular and molecular aspects of inflammation.

Cellular host reaction to noxious agents and damaging events consists of inflammatory, immune and repair responses. These are usually involved in different phases of the host reaction in a well co-ordinated manner, contributing to the well-being of the host. However, when they are excessive, uncontrolled or occur in a vulnerable anatomic location, they can contribute greatly to injury. In general, the effects of the initiating stimulus are much enhanced by secondary involvement of amplification loops, leading to recruitment of nonspecific cells. The number of initially stimulated and/or actively involved cell is, therefore, usually low but of crucial importance for the outcome of the process. As important as understanding of the mechanisms responsible for initiation and amplification of the host response is knowledge of the negative feedback loops responsible for down-regulation of the whole process.

Cell Line↗
PubMed2003

Nicotinamide: necessary nutrient emerges as a novel cytoprotectant for the brain.

Although usually identified as an essential cellular nutrient for cellular growth and maintenance, nicotinamide is under development as a novel cytoprotectant for acute and chronic neurodegenerative disorders. Here, we outline support for the premise that nicotinamide both prevents and reverses neuronal and vascular cell injury. Nicotinamide fosters DNA integrity and maintains phosphatidylserine membrane asymmetry to prevent cellular inflammation, cellular phagocytosis and vascular thrombosis. The downstream cellular and molecular cascades are considered vital for the cytoprotection offered by nicotinamide. These pathways encompass the modulation of Akt, the forkhead transcription factor FKHRL1, mitochondrial membrane potential, caspase activities and cellular energy metabolism, but remain independent of intracellular pH and mitogen-activated protein kinases. As both a therapeutic agent and an investigational tool, nicotinamide offers new therapeutic strategies for degenerative disorders of the CNS.

Animals↗
PubMed1999

Cytokine regulation of cellular adhesion molecule expression in inflammation.

Cellular adhesion molecules (CAMs) play an essential role in tethering circulating leukocytes to the vascular endothelium at sites of inflammation. They are also instrumental in enabling leukocytes to transmigrate from blood vessels into adjacent inflamed tissues. In the absence of signals to stimulate expression of CAMs, the adhesive forces between leukocytes and the vascular endothelium are below the threshold level required to tether leukocytes. Research in the last decade has shown that several cytokines, including tumour necrosis factor alpha (TNF alpha) and interleukin-1 beta (IL-1beta), potently increase the expression of many CAMs and thus increase the adhesiveness between leukocytes and the endothelium. The CAM-inducing activity of these cytokines is therefore crucial to the regulation of inflammatory processes. Overactivation of CAM expression is linked to a number of acute and chronic inflammatory conditions, and has led to the rationale of antagonising cytokine activity and or CAM expression in order to treat these conditions. The potential application of 'adhesion' antagonists for the therapy of acute chronic inflammatory conditions is briefly discussed.

Animals↗