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Urothelial Functional Protein and Sensory Receptors in Patients with Interstitial Cystitis/Bladder Pain Syndrome with and Without Hunner’s Lesion


Urology, Available online 26 August 2016

Jia-Fong Jhang, Yung-Hsiang Hsu, Hann-Chorng Kuo (Buddhist Tzu Chi General Hospital and Tzu Chi University, Hualien, Taiwan)



To investigate the urothelium function and sensory receptors difference between interstitial cystitis/bladder pain syndrome (IC/BPS) patients with or without Hunner lesion.


Fourteen female IC/BPS patients with Hunner’s lesion (Hunner IC) and 14 age-matched IC/BPS patients without Hunner’s lesions (non-Hunner IC) were enrolled. Bladder mucosa biopsies were obtained. Bladder inflammation, eosinophil infiltration, and urothelial denudation were graded on a 4-point scale after staining with hematoxylin and eosin stain. Adhesive protein E-cadherin, tryptase, and zonula occuldens-1 in the bladder tissues were assessed with immunofluorescence staining. Urothelial muscarinic receptors M2, M3, endothelial nitric oxide synthase (e-NOS) and purinergic receptor P2X3 were evaluated by western blotting.


Hunner IC patients had a significantly higher mean visual analog scale pain score and smaller cystometric bladder capacity than non-Hunner IC patients. The Hunner IC bladder specimens showed more severe or moderate eosinophilic infiltration and urothelial denudation than the non-Hunner IC bladder specimens did. The E-cadherin expression was significantly lower, and e-NOS expression was significantly higher in the Hunner IC bladder samples than in non-Hunner IC samples. The other functional proteins or sensory receptors did not differ between groups.


Bladder inflammation and urothelial cell adhesion defects were more severe in the Hunner IC than that in non-Hunner IC patients. ENOS was significantly higher in the Hunner IC than non-Hunner IC bladder samples, suggesting that eNOS expression difference may implicate different pathogenesis in two types of IC.

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Effects of LED Irradiation on the Proinflammatory Cytokines Production


International Journal of Health Care and Information Technology, Vol 1(1), January 2016

Jeong-Sook Park (Department of Nursing, Nambu University, Gwangju, Republic of Korea)


Although the anti-inflammatory effects have been reported in clinical fields for specific wavelength irradiation during wound healing, the physiological mechanism has not been clarified yet. The aim of the present study is to investigate the anti-inflammatory effect of Light-Emitting-Diode (LED) irradiation. The present study was designed to determine the effect of LED irradiation onTNF-α, IL-1β and IL-6 Detection and NOproduction in Lipopolysaccharide (LPS) – stimulated RAW264.7 macrophages. Cell toxicity was determined by MTS assay. The amount of NO was measured using the NO Detection Kit and the ELISA was performed by coating 96-well plates of monoclonal antibody with specificity for TNF-α and IL-6 respectively. 440nm LED irradiation reduced TNF-α and IL-6 Detection and NO production without cytotoxity. Our results suggest that 440nm LED irradiation may have an anti-inflammatory property through suppressing inflammatory mediator productions and appears to be useful as an anti-inflammatory tool.

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Mast Cell – Presentation given by Dr. Anne Maitland on April 2, 2013


http://www.ustream.tv/channel/eds-nyc (stream)

Noted Allergist/Immunologist Dr. Anne Maitland spoke for almost 2 hours about mast cells, EDS, allergies versus hypersensitivity, and much, much more April 2, 2013.

So far the Ustream link is ready to go:


You need to create a Ustream account, but that’s easy or you can log in with Facebook.

The 24 minute segment, which currently is the bottom of the three segments on the list, is the first one. That starts with the introduction.

We are all extremely grateful to Dr. Maitland, who took so much of her time and was so generous with information. She mentioned that two years ago there really was no research on this mast cell activity, which makes this pretty cutting edge.

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Mast cell degranulation and de novo histamine formation contribute to sustained post-exercise vasodilation in humans


Journal of Applied Physiology Published 25 August 2016 Vol. no. , DOI: 10.1152/japplphysiol.00633.2016

Steven A. Romero, Jennifer L. McCord, Matthew R. Ely, Dylan C. Sieck, Tahisha M. Buck, Meredith J. Luttrell, David A. MacLean, John R. Halliwill


In humans, acute aerobic exercise elicits a sustained post-exercise vasodilation within previously active skeletal muscle. This response is dependent on activation of histamine H1 and H2 receptors, but the source of intramuscular histamine remains unclear. We tested the hypothesis that interstitial histamine in skeletal muscle would be increased with exercise and would be dependent on de novo formation via the inducible enzyme histidine decarboxylase and/or mast cell degranulation. Subjects performed 1 h of unilateral dynamic knee-extension exercise or sham (seated rest). We measured the interstitial histamine concentration and local blood flow (ethanol washout) via skeletal muscle microdialysis of the vastus lateralis. In some probes, we infused either α-fluoromethylhistidine hydrochloride (α-FMH), a potent inhibitor of histidine decarboxylase, or histamine H1/H2 receptor blockers. We also measured interstitial tryptase concentrations, a biomarker of mast cell degranulation. Compared with pre-exercise, histamine was increased after exercise by Δ4.2 ± 1.8 ng ml-1 (P < 0.05), but not when α-FMH was administered (Δ-0.3 ± 1.3 ng ml-1, P = 0.9). Likewise, local blood flow after exercise was reduced to pre-exercise levels by both α-FMH and H1/H2 blockade. In addition, tryptase was elevated during exercise by Δ6.8 ± 1.1 ng ml-1 (P < 0.05). Taken together, these data suggest that interstitial histamine in skeletal muscle increases with exercise and results from both de novo formation and mast cell degranulation. This suggests that exercise produces an anaphylactoid signal which affects recovery, and may influence skeletal muscle blood flow during exercise.

Copyright © 2016, Journal of Applied Physiology

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Lactic Acid Suppresses IL-33-Mediated Mast Cell Inflammatory Responses via Hypoxia-Inducible Factor-1a-Dependent miR -155 Suppression


The Journal of Immunology August 24, 2016

Daniel Abebayehu, Andrew J. Spence, Amina Abdul Qayum, Marcela T. Taruselli, Jamie J. A. McLeod, Heather L. Caslin, Alena P. Chumanevich, Elizabeth Motunrayo Kolawole, Anuya Paranjape, Bianca Baker, Victor S. Ndaw, Brian O. Barnstein, Carole A. Oskeritzian, Scott A. Sell and John J. Ryan (Department of Biomedical Engineering, Virginia Commonwealth University, Richmond, VA 23284; Department of Biology, Virginia Commonwealth University, Richmond, VA 23284; Department of Pathology, Microbiology, and Immunology, University of South Carolina School of Medicine, Columbia, SC 29208; and Department of Biomedical Engineering, Saint Louis University, St. Louis, MO 63103)


Lactic acid (LA) is present in tumors, asthma, and wound healing, environments with elevated IL-33 and mast cell infiltration. Although IL-33 is a potent mast cell activator, how LA affects IL-33–mediated mast cell function is unknown. To investigate this, mouse bone marrow–derived mast cells were cultured with or without LA and activated with IL-33. LA reduced IL-33–mediated cytokine and chemokine production. Using inhibitors for monocarboxylate transporters (MCT) or replacing LA with sodium lactate revealed that LA effects are MCT-1– and pH-dependent. LA selectively altered IL-33 signaling, suppressing TGF-β–activated kinase-1, JNK, ERK, and NF-κB phosphorylation, but not p38 phosphorylation. LA effects in other contexts have been linked to hypoxia-inducible factor (HIF)-1α, which was enhanced in bone marrow–derived mast cells treated with LA. Because HIF-1α has been shown to regulate the microRNA miR-155 in other systems, LA effects on miR-155-5p and miR-155-3p species were measured. In fact, LA selectively suppressed miR-155-5p in an HIF-1α–dependent manner. Moreover, overexpressing miR-155-5p, but not miR-155-3p, abolished LA effects on IL-33–induced cytokine production. These in vitro effects of reducing cytokines were consistent in vivo, because LA injected i.p. into C57BL/6 mice suppressed IL-33–induced plasma cytokine levels. Lastly, IL-33 effects on primary human mast cells were suppressed by LA in an MCT-dependent manner. Our data demonstrate that LA, present in inflammatory and malignant microenvironments, can alter mast cell behavior to suppress inflammation.

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Allergen specific immunotherapy: is it vaccination against toxins after all?


Allergy, Accepted manuscript online: 24 August 2016


IgE-mediated allergies, in particular allergic rhino-conjunctivitis and asthma, have reached epidemic proportions, affecting about one third of the population in developed countries. The most effective treatment for allergies is specific immunotherapy (SIT), which involves the injection of increasing doses of an allergen extract to allergic individuals.

The current form of SIT was first introduced 1911 and recently celebrated its 100th birthday for the treatment of hay fever. The concept of this therapy at the time was straight-forward, since it was believed that pollen contained toxins against which the patient could be vaccinated. However, the understanding became blurred with the discovery that IgE antibodies were the effector molecules of the allergic response. Subsequent research focused on the idea that SIT should induce tolerance keeping the IgE antibodies at bay. In this review, we will discuss the various hypotheses for the mechanism of SIT and we will put forward the concept that allergens may be viewed as “protoxins” which need to be activated by IgE antibodies. Within this framework, protoxin-neutralizing antibodies are the key effector molecules while a shift to Th1 or Treg cells mainly contributes to the efficacy of SIT by helping B cells to produce neutralizing IgG antibodies.

This article is protected by copyright. All rights reserved.

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International Archive of Allergy Immunology, Vol 170: Various articles


Int Arch Allergy Immunol 170(2) 69–140 (2016)

A Critical Evaluation of Anti-IL-13 and Anti-IL-4 Strategies in Severe Asthma

Bagnasco, D.; Ferrando, M. (Genoa); Varricchi, G. (Naples); Passalacqua, G.; Canonica, G.W. (Genoa)

Real-Life Study for the Diagnosis of House Dust Mite Allergy – The Value of Recombinant Allergen-Based IgE Serology

Becker, S. (Mainz/Munich); Schlederer, T. (Vienna); Kramer, M.F.; Haack, M. (Munich); Vrtala, S.; Resch, Y.; Lupinek, C.; Valenta, R. (Vienna); Gröger, M. (Munich)

Changes in the Expression of MicroRNA in the Buildup Phase of Wasp Venom Immunotherapy: A Pilot Study

Specjalski, K.; Maciejewska, A.; Pawłowski, R.; Chełmińska, M.; Jassem, E. (Gdansk)

Disagreement between Skin Prick Tests and Specific IgE in Early Childhood

Chauveau, A.; Dalphin, M.-L.; Kaulek, V. (Besançon); Roduit, C. (Zurich); Pugin, A. (Besançon); von Mutius, E. (Munich); Vuitton, D.A.; Dalphin, J.-C. (Besançon)

Blood Coagulation and Asthma Exacerbation in Children

Manuyakorn, W.; Mairiang, D.; Sirachainan, N.; Kadegasem, P.; Kamchaisatian, W.; Benjaponpitak, S.; Chuansumrit, A. (Bangkok)

Immediate Wheal Reactivity to Autologous Sweat in Atopic Dermatitis Is Associated with Clinical Severity, Serum Total and Specific IgE and Sweat Tryptase Activity

Ilves, T. (Kuopio/Mikkeli); Virolainen, A. (Pori); Harvima, I.T. (Kuopio)

Shortened Activated Partial Thromboplastin Time May Help in Diagnosing Hereditary and Acquired Angioedema

Bork, K.; Witzke, G. (Mainz)

BIOBRAD Study: The Search for Biomarkers of Bradykinin-Mediated Angio-Oedema Attacks

Deroux, A.; Dumestre-Perard, C.; Khalil-Mgharbel, A.; Maignan, M.; Boccon-Gibod, I.; Fevre, M.-C.; Vilgrain, I.; Bouillet, L. (Grenoble)

The Relevance of Nasal Provocation Testing in Children with Nonallergic Rhinitis

Duman, H.; Bostanci, I.; Ozmen, S.; Dogru, M. (Ankara)

Atopic Predilection among Kawasaki Disease Patients: A Cross-Sectional Study of 1,187,757 Teenagers

Hassidim, A. (Jerusalem); Merdler, I. (Tel Aviv); Chorin, O. (Holon); Merdler-Rabinowicz, R. (Tel Hashomer); Dallal, I. (Holon); Perlman, M. (Tel Hashomer); Chorin, E. (Tel Aviv)

Symptomatic Primary Selective Immunoglobulin M Deficiency with Nonprotective Pneumococcal Titers Responsive to Subcutaneous Immunoglobulin Treatment

Patel, S.S.; Fergeson, J.E.; Glaum, M.C.; Lockey, R.F. (Tampa, Fla.)

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