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2.
Eur Ann Allergy Clin Immunol ; 48(5): 182-7, 2016 Sep.
Article in English | MEDLINE | ID: mdl-27608474

ABSTRACT

Background. In chronic spontaneous urticaria (CSU) first-line therapy with an antihistamine-based regimen may not achieve satisfactory control in patients. Thus, a continuing need exists for effective and safe treatments for refractory CSU. Aim. To evaluate the clinical efficacy and safety of an intake of a combination of 2 probiotics (Lactobacillus salivarius LS01 and Bifidobacterium breve BR03) in patients with CSU who remain symptomatic despite concomitant H1-antihistamine therapy. Methods. This report analyzes the effects of therapy with two probiotic strains on the clinical progress of 52 unselected patients with difficulty to treat CSU underwent to medical examination in two Italian specialist urticaria Clinics between September 2013 and September 2014. A mixture of Lactobacillus LS01 and Bifidobacterium BR03 were administered in each patient twice daily for 8 weeks. To evaluate patients' improvement with probiotics, urticaria activity score over 7 days (UAS7) was used at baseline and at week 8 in addition to a 5-question urticaria quality of life questionnaire. Results. Fifty-two patients with CSU were included in this study (10 male and 42 female, age range 19-72 years). Mean disease duration was 1.5 years. Fourteen patients discontinued treatment, so evaluable population consisted of 38 patients. Nine of the 38 patients experienced mild clinical improvement during probiotic treatment (23.7%); one patient reported significant clinical improvement (2.6%) and one patient had complete remission of urticaria (2.6%). Twenty-seven patients did not have improvement in symptoms (71.1%). No side effects during the course of therapy were reported. Conclusions. A combination of Lactobacillus salivarius LS01 and Bifidobacterium breve BR03 administered twice daily for 8 weeks might reduce the symptoms scores and improve quality of life scores in a part of patients with CSU who remained symptomatic despite treatment with H1 antihistamine mostly in subjects with allergic rhinitis.


Subject(s)
Bifidobacterium breve/physiology , Histamine H1 Antagonists, Non-Sedating/therapeutic use , Hypersensitivity/therapy , Ligilactobacillus salivarius/physiology , Probiotics , Urticaria/therapy , Adult , Aged , Chronic Disease , Combined Modality Therapy , Female , Histamine H1 Antagonists, Non-Sedating/adverse effects , Humans , Hypersensitivity/diagnosis , Hypersensitivity/immunology , Hypersensitivity/microbiology , Italy , Male , Middle Aged , Probiotics/adverse effects , Quality of Life , Remission Induction , Surveys and Questionnaires , Time Factors , Treatment Outcome , Urticaria/diagnosis , Urticaria/immunology , Urticaria/microbiology , Young Adult
3.
FASEB J ; 21(7): 1422-32, 2007 May.
Article in English | MEDLINE | ID: mdl-17264168

ABSTRACT

Prolonged exposure to hyperoxia results in hyperoxic acute lung injury (HALI). Vascular endothelial growth factor (VEGF) has been shown to have cytoprotective effects and prolong survival in an in vivo model of HALI. Heme oxygenase-1 (HO-1) has protective effects in hyperoxia; therefore, we hypothesized that induction of HO-1 would be an important contributor to VEGF-induced cytoprotection. Using inducible, lung-specific VEGF overexpressing transgenic mice, we demonstrated that VEGF is a potent inducer of HO-1 mRNA and protein in mouse lung. To evaluate the effect of inhibition of HO-1 on injury, VEGF transgenic mice were treated with HO-1 short interfering RNA (HO-1 siRNA) and exposed to hyperoxia. Total lung lavage protein concentration, TUNEL staining, lipid peroxidation, and wet-to-dry ratio were all increased, consistent with increased injury. These findings were corroborated by survival studies in which inhibition of HO-1 function using tin-protoporphryin or silencing of HO-1 with lentiviral HO-1 short hairpin RNA (ShRNA) significantly decreased survival in hyperoxia. We conclude from these data that VEGF-induced HO-1 is an important contributor to cytoprotection in this in vivo model of acute lung injury and that alterations in VEGF function in the lung are likely to be important determinants of the outcome of acute lung injury.


Subject(s)
Cytoprotection , Heme Oxygenase (Decyclizing)/biosynthesis , Hyperoxia/prevention & control , Vascular Endothelial Growth Factor A/physiology , Animals , Base Sequence , Bronchoalveolar Lavage Fluid , DNA Primers , Disease Models, Animal , Enzyme Induction , Heme Oxygenase (Decyclizing)/genetics , Humans , Hyperoxia/enzymology , In Situ Nick-End Labeling , Lipid Peroxidation , Lung/enzymology , Mice , Mice, Transgenic , RNA, Small Interfering , Respiratory Distress Syndrome/enzymology , Reverse Transcriptase Polymerase Chain Reaction
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