Luteolin is a flavonoid that has been shown to reduce proinflammatory molecule expression in vitro. In the present study, we have tested the ability of luteolin to inhibit lipopolysaccharide (LPS)- induced lethal toxicity and proinflammatory molecule expression in vivo. Mice receiving LPS (Salmonella enteriditis LPS, 32 mg/kg, intraperitoneally) exhibited high mortality with only 4.1% of the animals surviving seven days after the LPS challenge. On the contrary, mice that had received luteolin (0.2 mg/kg, intraperitoneally) before LPS showed an increased survival rate with 48% remaining alive on Day 7. To investigate the mechanism by which luteolin affords protection against LPS toxicity we measured intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor-alpha (TNF-alpha) production in response to LPS in the presence or absence of luteolin pretreatment. Treatment of animals with LPS increased serum TNF-alpha levels in a time-dependent manner. The increase in peak serum TNF-alpha levels was sensitive to luteolin pretreatment. Luteolin pretreatment also reduced LPS-stimulated ICAM-1 expression in the liver and abolished leukocyte infiltration in the liver and lung. We conclude that luteolin protects against LPS-induced lethal toxicity, possibly by inhibiting proinflammatory molecule (TNF-alpha, ICAM-1) expression in vivo and reducing leukocyte infiltration in tissues.
NASH improved significantly with massive weight loss in non-diabetic, non-alcoholic, morbidly obese subjects, while fibrosis improved in nearly half of the patients.
Background: Several studies have implicated a role of inflammation in the pathogenesis of lung damage in idiopathic pulmonary fibrosis (IPF). Parenchymal lung damage leads to defects in mechanics and gas exchange and clinically manifests with exertional dyspnea. Investigations of inflammatory cells in IPF have shown that eosinophils, neutrophils and CD 8+ TLs may be associated with worse prognosis. We wished to investigate by quantitative immunohistochemistry infiltrating macrophages, neutrophils and T lymphocytes (TLs) subpopulations (CD 3+ , CD 4+ and CD 8+ ) in lung tissue of patients with IPF and their correlation with lung function indices and grade of dyspnoea.
The aims of the study were (a) to investigate the prevalence of Sjögren's-like syndrome (SLS) in an unselected population of HIV-1-positive patients and (b) to describe the pathology and immunopathology of the labial minor salivary gland biopsy. Seventy-seven HIV-1-positive patients were asked to answer the validated questionnaire of the European preliminary criteria for the classification of Sjögren's syndrome on oral and ocular sicca symptoms. Twenty-six patients gave one positive answer to both ocular and oral symptoms, and of these 14 (hepatitis C virus negative) consented to participate in the study (patients group). Ten age- and sex-matched HIV-1-positive patients with a negative questionnaire constituted the control group. Patients and controls had: (a) Schirmer's test and slit-lamp examination after Rose Bengal staining; (b) parotid gland scanning with technetium; (c) detection of autoantibodies in sera to Ro/SSA and La/SSB; (d) labial salivary gland biopsy (patients group only). The control group gave negative parotid gland scanning and only one gave a positive Rose Bengal staining test. In the patients group, parotid gland enlargement was manifested by three patients and only one gave positive Rose Bengal staining test. Six out of the 14 patients had biopsies identical with Sjögren's syndrome and five of these gave positive parotid gland scanning. In the biopsies of four other patients, mucoid degeneration of the stroma was found. Immunopathology revealed that the predominant cells were T cells with the CD8 phenotype. None of the patient and control sera had autoantibodies to Ro/SSA and La/SSB, whereas all patients had hypergammaglobulinaemia. The overall prevalence of possible SLS in a mixed population of HIV(+) patients (88.3% men and 11.7% women) was 7.79% which is >2.5 times higher than that observed in normal Greek adult females.
BackgroundAdvanced age is associated with a reduction in clinical visceral pain perception. However, the underlying mechanisms remain largely unknown. Previous studies have suggested that an abnormal interplay between mast cells, enterochromaffin (EC) cells, and afferent nerves contribute to nociception in gastrointestinal disorders. The aim of this study was to investigate how aging affects afferent sensitivity and neuro‐immune association in the human bowel.MethodsMechanical and chemical sensitivity of human bowel afferents were examined by ex vivo afferent nerve recordings. Age‐related changes in the density of mast cells, EC cells, sensory nerve terminals, and mast cell‐nerve micro‐anatomical association were investigated by histological and immune staining.Key ResultsHuman afferents could be broadly classified into subpopulations displaying mechanical and chemical sensitivity, adaptation, chemo‐sensitization, and recruitment. Interestingly human bowel afferent nerve sensitivity was attenuated with age. The density of substance P‐immunoreactive (SP‐IR) nerve varicosities was also reduced with age. In contrast, the density of ileal and colonic mucosal mast cells was increased with age, as was ileal EC cell number. An increased proportion of mast cells was found in close apposition to SP‐IR nerves.Conclusions & InferencesAfferent sensitivity in human bowel was reduced with advancing age. Augmentation of mast cells and EC cell numbers and the mast cell‐nerve association suggest a compensatory mechanism for sensory neurodegeneration.
In this study both polypectomy techniques were found to be safe and highly effective, but further large multicenter trials are required.Clinical trial registration at www.clinicaltrials.gov: NCT02208401.
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