BACKGROUND AND OBJECTIVES: The nasal epithelium is the first barrier encountered by airborne allergens and is an active participant in airway inflammation. The aim of this study was to determine the activation mechanism of nasal epithelial cells with Alternaria and the effect of rhinovirus on the Alternaria induced activation of nasal epithelial cells. MATERIALS AND METHODS: Cultured epithelial cells were stimulated by Alternaria with or without rhinovirus-16 (RV-16) infection. Release of interleukin (IL)-6, IL-8, and granulocyte macrophage colony-stimulating factor (GM-CSF) into culture supernatants were measured to determine the activation of epithelial cells. Nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1) of the epithelial cells were analyzed using western blot analysis. Intracellular NF-kappaB and AP-1 activity were evaluated by enzyme-linked immunosorbent assay. To determine the epithelial cell activation mechanism, cytokine production was inhibited with NF-kB, AP-1, and mitogen activated protein kinase (MAPK) inhibitors. RESULTS: Exposure of epithelial cells to Alternaria enhanced the production of cytokines. Intracellular NF-kB expression and activity were significantly increased by Alternaria, but not by RV-16. AP-1 expression and activity were not influenced by Alternaria. Increased IL-6 production was significantly inhibited by transcription factor inhibitors. However, IL-8 and GM-CSF production were not inhibited by these transcription factor inhibitors. CONCLUSIONS: Our in-vitro results demonstrate that Alternaria activates nasal polyp epithelial cells via NF-kB pathway and that NF-kB, AP-1, and MAPK are involved in the production of IL-6.
Allergens ; Alternaria ; Blotting, Western ; Cytokines ; Enzyme-Linked Immunosorbent Assay ; Epithelial Cells ; Granulocyte-Macrophage Colony-Stimulating Factor ; Granulocytes ; Inflammation ; Interleukin-6 ; Interleukin-8 ; Interleukins ; Macrophage Colony-Stimulating Factor ; Nasal Mucosa ; Nasal Polyps ; NF-kappa B ; Protein Kinases ; Rhinovirus ; Transcription Factor AP-1 ; Transcription Factors

Anisakiasis of the gastrointestinal tract is caused by the ingestion of raw fish or uncooked foods infested with Anisakis larvae belonging to the subfamily Anisakidae. With the increasing popularity of Japanese cuisine such as sashimi in Korea, the incidence of anisakiasis is expected to increase. The entire gastrointestinal tract from the esophagus to the rectum can be involved. Colonic anisakiasis is rare in comparison with gastric involvement. We report the anisakiasis concurrently invading the stomach, ileocecal valve and transverse colon treated by endoscopy with a brief review of the relevant literature.
Anisakiasis* ; Anisakis ; Asian Continental Ancestry Group ; Colon ; Colon, Transverse* ; Eating ; Endoscopy ; Esophagus ; Gastrointestinal Tract ; Humans ; Ileocecal Valve* ; Incidence ; Korea ; Larva ; Rectum ; Stomach*

BACKGROUND AND OBJECTIVES: Eosinophil cationic protein (ECP) is one of the major granule-derived proteins with cytotoxic activity derived from eosinophils. It has also been used as a marker of allergic inflammation. In this study, we measured ECP levels in nasal secretion to evaluate its effect on nasal allergic symptoms. MATERIALS AND METHODS: ECP was measured in nasal secretion and in serum of 30 symptomatic allergic rhinitis patients, 20 non-allergic rhinitis patients, and 15 normal controls. We also measured symptom scores composed of sneezing, itching, rhinorrhea, nasal obstruction, and nasal blowing. RESULTS: The ECP level in the nasal secretion of allergic rhinitis was higher than those of non-allergic rhinitis and the normal control (p<0. 001). The difference of ECP levels in serum among three groups didn't have statistical significance, but there was statistically significant correlation between the ECP level in nasal secretion and the mean symptom scores in allergic rhinitis (p=0.006). CONCLUSION: The ECP level in nasal secretions seems to be a very useful parameter for monitoring and assessing the condition of nasal allergic inflammation in allergic rhinitis.
Eosinophil Cationic Protein* ; Eosinophils* ; Humans ; Inflammation ; Nasal Obstruction ; Pruritus ; Rhinitis* ; Sneezing

Endothelins secreted from keratinocytes are intrinsic mitogens and melanogens of human melanocytes in UVB-induced hyperpigmentation. To elucidate the cellular mechanism of antimelanogenic activity of bamboo extract, the effects of three ingredients of bamboo extract on endothelin 1 (ET-1) -induced Ca2+ mobilization were investigated in cultured human melanocytes. ET-1 receptors in human melanocytes were characterized by using specific antagonist, and ET-1 was found to increase intracellular Ca2+ concentration ([Ca2+]i) by activating ET-B receptor. SM709 (1, 2-O-diferulyl-glycerol), an ingredient of bamboo extract, inhibited ET-1-induced [Ca2+]i increase in a concentration- and time-dependent manner, although another ingredients SM707 and SM708 had no effect on ET-1-induced [Ca2+]i increase in human melanocytes. SM709 (100 microM), however, did not affect [Ca2+]i increase induced by thapsigargin and caffeine, suggesting that SM709 has no effect on the Ca2+ store in melanocytes. Furthermore, SM709 did not affect [Ca2+]i increase induced by LPA or ATP, known as G protein-mediated PLC activators like ET-1. Taken together, it is suggested that SM709 antagonizes ET-1-induced transmembrane signaling through ET-B receptor, which maybe a possible underlying mechanism of antimelanogenic activity of bamboo extract in human melanocytes.
Adenosine Triphosphate ; Caffeine ; Endothelin-1 ; Endothelins ; Humans* ; Hyperpigmentation ; Keratinocytes ; Melanocytes* ; Mitogens ; Thapsigargin

In addition to classical synaptic transmission, information is transmitted between cells via the activation of extrasynaptic receptors that generate persistent tonic current in the brain. While growing evidence supports the presence of tonic NMDA current (INMDA) generated by extrasynaptic NMDA receptors (eNMDARs), the functional significance of tonic I(NMDA) in various brain regions remains poorly understood. Here, we demonstrate that activation of eNMDARs that generate I(NMDA) facilitates the α-amino-3-hydroxy-5-methylisoxazole-4-proprionate receptor (AMPAR)-mediated steady-state current in supraoptic nucleus (SON) magnocellular neurosecretory cells (MNCs). In low-Mg2+ artificial cerebrospinal fluid (aCSF), glutamate induced an inward shift in I(holding) (I(GLU)) at a holding potential (V(holding)) of -70 mV which was partly blocked by an AMPAR antagonist, NBQX. NBQX-sensitive I(GLU) was observed even in normal aCSF at V(holding) of -40 mV or -20 mV. I(GLU) was completely abolished by pretreatment with an NMDAR blocker, AP5, under all tested conditions. AMPA induced a reproducible inward shift in I(holding) (I(AMPA)) in SON MNCs. Pretreatment with AP5 attenuated I(AMPA) amplitudes to ~60% of the control levels in low-Mg2+ aCSF, but not in normal aCSF at V(holding) of -70 mV. I(AMPA) attenuation by AP5 was also prominent in normal aCSF at depolarized holding potentials. Memantine, an eNMDAR blocker, mimicked the AP5-induced I(AMPA) attenuation in SON MNCs. Finally, chronic dehydration did not affect I(AMPA) attenuation by AP5 in the neurons. These results suggest that tonic I(NMDA), mediated by eNMDAR, facilitates AMPAR function, changing the postsynaptic response to its agonists in normal and osmotically challenged SON MNCs.
alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid* ; Brain ; Cerebrospinal Fluid ; Dehydration ; Glutamic Acid ; Memantine ; N-Methylaspartate* ; Neurons ; Receptors, AMPA ; Receptors, N-Methyl-D-Aspartate* ; Supraoptic Nucleus ; Synaptic Transmission