This study aims to explore the effect of Jingfang Mixture on the protein expression of urticaria in mice and explain the mechanism of Jingfang Mixture in the treatment of urticaria. Twenty-seven male Kunming mice were randomly divided into a normal group, a model group and a Jingfang Mixture group according to body weight. Except for the normal group, mice in the model group and the Jingfang Mixture group were injected with the mixture of ovalbumin and Al(OH)_3 gel for the first immunization, and the second immunization was performed on the 10 th day to induce the urticaria model. Mice in the Jingfang Mixture group started to be administered on the 6 th day after the initial immunization, and was administered continuously for 21 days. The normal group and the model group were replaced with the same amount of purified water. Twenty-four hours after the last administration, an appropriate amount of skin was taken, and label-free quantitative proteomics technology was used to detect the differences in protein expression in skin tissue. The signaling pathways involved in the differential proteins was further analyzed. The results of proteomics indicated that seventy-six proteins were involved in the intervention of Jingfang Mixture on mice with urticaria, and the differential proteins were mainly enriched in biological process(BP), molecular function(MF), and cellular component(CC). Kyoto Encyclopedia of Genes and Genomes(KEGG) analysis showed that the signaling pathways regulated by Jingfang Mixture mainly involved carbon metabolism, metabolic pathways, glucagon signaling pathway, glycolysis/gluconeogenesis, pentose phosphate pathway, hypoxia inducible factor-1(HIF-1) signaling pathway, purine metabolism, adherens junction, calcium signaling pathway, leukocyte transendothelial migration, and inflammatory mediator regulation of transient receptor potential(TRP) channels, which were involved in skin tissue energy metabolism and immune regulation. The findings of this study showed that the protective effect of Jingfang Mixture on mice with urticaria was closely related to the regulation of immune disorders, and the regulatory effect on immune system may be achieved through the regulation of energy metabolism by Jingfang Mixture.
Male ; Mice ; Animals ; Proteomics/methods* ; Metabolic Networks and Pathways ; Urticaria/genetics* ; Signal Transduction ; Technology

Human Leukocyte Antigen (HLA) typing of large groups of patients with various autoimmune diseases has demonstrated that some HLA alleles occur at higher frequencies in specific diseases than in the general population. Chronic urticaria has been shown to have an autoimmune basis by a previous study which found an association between chronic urticaria and specific HLA groups. We investigated the HLA subtypes of Turkish chronic urticaria patients. For this purpose 42 Turkish patients with chronic urticaria and 115 healthy controls were typed for HLA-DR and DQ by PCR-SSP (Polymerase Chain Reaction Sequence Specific Primers) low resolution DNA technique. We found an increased frequency of DR4 (42.9%, p=0.01) in chronic urticaria patients in comparison with that in healthy controls. This study supports the hypothesis that HLA alleles may be involved in the pathogenesis of chronic urticaria and that they appear to be directly involved in the initiation of the immune response.
Chronic Disease ; HLA-DQ Antigens/genetics ; HLA-DR Antigens/genetics ; HLA-DR4 Antigen/genetics ; Histocompatibility Antigens Class II/*genetics ; *Histocompatibility Testing ; Human ; Urticaria/*genetics/*immunology

In order to investigate the association of genotypes of HLA-DRB1 and HLA-DQB1 alleles with the genetic susceptibility of chronic urticaria (CU), genotypes of HLA-DRB1 and HLA-DQB1 genes were detected by polymerase chain reactions with sequence-specific primers (PCR-SSP) in 42 patients with CU (19 men and 23 women, mean age 30.67+/-12.45 y old as well as 193 racially matched healthy persons in ethnic Han from Hubei provinece. Gene frequencies of HLA-DRB1 * 12, * 0901 (RR=3.11, chi2=7. 579, P=0.006; RR= 2.47, chi2 =5.684, P=0.017) were significantly increased in CU patients as compared with that in healthy people. Gene frequencies of HLA-DQB1 * 05 (RR=0.26, chi2=6.683, P=0.01) were significantly decreased in CU patients. It was suggested that CU was found strongly associated with HLA-DRB1 * 12, * 0901 and HLA-DQB1 * 05, the former might be the genetic markers for susceptibility to CU, but the latter might play a resistive role.
Alleles ; Chronic Disease ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; HLA-DQ Antigens/*genetics ; HLA-DR Antigens/*genetics ; Polymerase Chain Reaction ; Urticaria/*genetics

Familial Mediterranean fever (FMF) is an autosomal recessive disease characterized by recurrent episodes of fever and serosal, synovial, or cutaneous inflammation, caused by a dysfunction of pyrin as a result of mutation within the MEFV gene. It occurs mainly among Mediterranean and Middle Eastern populations, including Jews, Arabs, and Turks. However, FMF cases have been reported outside the Mediterranean and Middle Eastern countries in recent years. Although FMF has been relatively rare in Korea until now, proper recognition of FMF might lead to more frequent diagnoses of FMF. We experienced an interesting case, a 31-year-old Korean man who presented with recurrent abdominal pain with fever and urticarial eruption for 10 years. DNA analysis showed complex mutations (p.Leu110Pro, p.Glu148Gln) in the MEFV gene. To date, three cases have been reported, and this case of FMF with skin conditions is the first case in Korea.
Abdominal Pain/*etiology ; Adult ; Base Sequence ; Cytoskeletal Proteins/genetics ; Familial Mediterranean Fever/complications/*diagnosis/genetics ; Humans ; Male ; Polymorphism, Single Nucleotide ; Recurrence ; Sequence Analysis, DNA ; Urticaria/*diagnosis

The genetic mechanism of aspirin intolerant acute urticaria (AIAU) is unknown. To demonstrate an association between the beta2 adrenergic receptor (ADRB2) polymorphism and the phenotype of AIAU, one hundred fourteen patients with AIAU, 110 patients with aspirin intolerant chronic urticaria (AICU), and 498 normal healthy controls (NC) based on a Korean population were enrolled. The genotype of ADRB2 at 46 A > G was analyzed using a direct sequencing method. The ADRB2 polymorphism at 46 A > G showed a significant difference between AIAU and NC; the frequency of the major genotype was significantly higher in the AIAU group (p= 0.017 in recessive model), while no differences were noted in allele and genotype frequencies between AICU and NC. In conclusion, the ADRB2 (46 A > G) gene polymorphism may contribute to the development of the phenotype of AIAU.
Adult ; Aspirin/*adverse effects ; Female ; Gene Frequency ; Genotype ; Humans ; Male ; Middle Aged ; Phenotype ; *Polymorphism, Single Nucleotide ; Receptors, Adrenergic, beta-2/*genetics ; Urticaria/chemically induced/*genetics/pathology

To investigate the relationship between single nucleotide polymorphisms (SNPs) of CACNA1C (SNPs rs58619945, rs7316246 and rs216008) and susceptibility of chronic spontaneous urticaria (CSU) as well as the curative effect of non-sedating antihistamine drugs.
 Methods: Peripheral blood were extracted from 191 CSU patients to collect DNA. Urticaria Activity Score 7 (UAS7) and Dermatology Life Quality Index (DLQI) changes were collected from these patients with different non-sedating antihistamine drugs. PubMed retrieval system was used to select the 3 SNPs (rs58619945, rs7316246 and rs216008) of CACNA1C. Susceptibility of CSU and curative effect of non-sedating antihistamine drugs (desloratadine, mizolastine, fisofenadine) in 189 CSU patients and 105 controls with different SNPs were compared with Chi-squared test. Data of 105 southern Chinese controls were extracted from the 1 000 genome database.
 Results: Frequency of rs58619945 G allele in the CSU patients was significantly higher than that in the controls [OR(95%CI)=0.660(0.470-0.925), P=0.016]. However, there was no significant differences in rs7316246 and rs216008 between the CSU patients and the controls. Meanwhile there was no significant difference in general curative effect of the 3 drugs in the 3 SNPs (rs58619945: OR=0.843, P=0.454; rs7316246: OR=2.103, P=0.102; rs216008: OR=0.237, P=0.363). There was significant difference in different alleles of rs216008 in the patients administered by desloratadine [OR(95%CI)=0.480(0.247-0.933), P=0.029]. No difference was shown in the 3 SNPs in patients administered by mizolastine.
 Conclusion: The rs58619945 A/G might be related to susceptibility of CSU, and the rs216008 mutation might affect drug response of desloratadine.
Calcium Channels, L-Type ; genetics ; Chronic Disease ; Genetic Predisposition to Disease ; Histamine H1 Antagonists, Non-Sedating ; therapeutic use ; Humans ; Loratadine ; analogs & derivatives ; therapeutic use ; Polymorphism, Single Nucleotide ; Prognosis ; Retrospective Studies ; Urticaria ; drug therapy ; genetics

The pathogenesis of aspirin (acetylsalicylic acid, ASA)-intolerant urticaria (AIU) is still poorly understood but it has recently been suggested that it is associated with the overproduction of leukotriene (LT). This is supported by evidence that cyclooxygenase 2 inhibitor is given safely to patients with AIU. The present study was designed to investigate the role of genetic polymorphism of LT related genes in the pathogenesis of AIU via a case-control study. We screened single nucleotide polymorphisms (SNPs) in genes encoding enzymes involved in leukotriene synthesis in the Korean population with AIU (n=101), ASA-intolerant asthma (AIA, n=95) and normal healthy controls (n=123). Genotype was determined by primer extension reactions using the SNapShot ddNTP primer extension kit. Among 8 SNPs of four LT related genes, the polymorphism of ALOX5 at positions of -1708 G>A showed significant difference in genotype frequency between AIU and AIA (p=0.01). Furthermore, there were significant differences observed in the frequencies of two ALOX5 haplotypes between the AIU group and AIA group (p<0.05). However, there were no differences in allele, genotype, or haplotype frequencies of ALOX5 between the AIU group and the normal control group. These results suggested that ALOX5 has a differing contribution in two major clinical pathogenesis related to ASA-sensitivity.
Adult ; Arachidonate 5-Lipoxygenase/*genetics ; Aspirin/*adverse effects ; Asthma/etiology/*genetics/metabolism ; Carrier Proteins/genetics ; Case-Control Studies ; Cyclooxygenase 2/genetics ; Female ; Gene Frequency ; Genotype ; Glutathione Transferase/genetics ; Humans ; Leukotrienes/*biosynthesis ; Male ; Membrane Proteins/genetics ; Middle Aged ; Polymorphism, Single Nucleotide ; Research Support, Non-U.S. Gov't ; Urticaria/etiology/*genetics/metabolism

Allergy was originally defined in 1906 in 1906 by Clemens von Pirquet as 'altered reactivity' to denote the different reaction which on second exposure to and antigen due to the formation fo antibodies, when compared to the first exposure. The term atopy decribes the clinical presentation of Type I hypersensitivity, which include asthna, eczema, hay fever and urticaria, These usually occur in subjects with a family history of these or similar conditions. The mechanism of allergy is the Type I hypersensitity reaction. contact with allergen results in its being processed by an antigen presenting cell and presented to T helper cells which then help B cells to IgE antibody. The IgE antibody is rapidly taken up via its Fc portion by mast cells and basophils, which are then senitized. Subsequent contact with same allergen will result in the cross-linking of IgE molecules by their fab portions which cause cell degranulation and mediator release. The contribution of genentic factors to the development of atopy has been an intriguing issue. The exact controlling mechanisms of the genetic factors are unknown, but there are many studies support the genetic controls of the development of atopy. Abnormally high levels of IgE synthesis and associated atopy often run in families. Althouth the full inhritance pattern is probably multigenic, family studies has shown that their is clear autosomal transmission of atopy. The ability to make specific IgE antibodies to certain antigens, e.g., ragweed pollen, is also inherited and may be linked to particular class II major histocompatibility complex alleles. Therefore, I think that the clinicians must consider the environmental and genetic factors when evaluate the atopic disease.
Alleles ; Ambrosia ; Antibodies ; B-Lymphocytes ; Basophils ; Cell Degranulation ; Eczema ; Genetics* ; Humans ; Hypersensitivity* ; Hypersensitivity, Immediate ; Immunoglobulin E ; Major Histocompatibility Complex ; Mast Cells ; Pollen ; Rhinitis, Allergic, Seasonal ; T-Lymphocytes, Helper-Inducer ; Urticaria

It has been well established that bacterial superantigens lead to the induction and aggravation of chronic inflammatory skin diseases. We investigated the clinical significance of serum specific immunoglobulin E (lgE) to the staphylococcal superantigens staphylococcal enterotoxin A (SEA), staphylococcal enterotoxin B (SEB), and toxic shock syndrome toxin (TSST)-1 in patients with chronic urticaria (CU), focusing on the differences in these prevalences between aspirin-intolerant CU (AICU) and aspirin-tolerant CU (ATCU) patients. Aspirin sensitivity was confirmed by oral aspirin provocation test. There were 66 patients AICU and 117 patients ATCU in the study. Serum IgE antibodies specific for SEA, SEB, and TSST-1 were measured by the ImmunoCAP test and the patients were compared with 93 normal controls (NC). The prevalences of serum specific IgE to staphylococcal superantigens were significantly higher in CU than in NC patients (IgE to SEA, 13.7% vs. 5.4%; IgE to SEB, 12.0% vs. 4.3%; IgE to TSST-1, 18.0% vs. 6.5%; p<0.05, respectively). The patients with specific IgE to SEA, SEB, and TSST-1 had higher serum total IgE levels and higher rates of atopy. Significant associations were noted between the prevalence of specific IgE to SEA and SEB and the HLA DQB1*0609 and DRB1*1302 alleles in the AICU group. We confirmed that a sub-population of patients with CU possesses serum IgE antibodies to SEA, SEB, and TSST- 1. Particularly, the IgE immune response to TSST-1 is associated with aspirin sensitivity in CU patients.
Adolescent ; Adult ; Aged ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology ; Antigens/*chemistry ; Aspirin/pharmacology ; Bacterial Toxins/metabolism ; Chronic Disease ; Enterotoxins/metabolism ; Female ; Humans ; Immunoglobulin E/*chemistry/metabolism ; Male ; Middle Aged ; Phenotype ; Staphylococcus/*genetics/immunology ; Superantigens/metabolism ; Urticaria/*immunology

BACKGROUND: The results of epidemiological studies are different from each other by genetics, social circumstances, climate, geographic localization, etc. There are few reports on prevalence of adolescent dermatoses in Korea. OBJECTIVES: We performed this study to know prevalence of dermatoses of 19-year-old conscriptees in Kangwon province, 2001 and to compare its distribution with results of other studies. METHOD: From Aug. 2001 to Dec. 2001, we have examined 12, 657 men who had visited the Chuncheon Military Manpower Administration for the purpose of physical examination for conscription in Kangwon province. We estimated the total, monthly and regional prevalence of dermatoses and the dermatoses were recorded by rank and analyzed by group of disease and disease itself. RESULTS: A total of 2, 324 patients with 2, 509 dermatological diseases were seen by a dermatologist from August 2001 to December 2001 at the Chuncheon Military Manpower Administration. The prevalence of dermatoses was 18.4%. The monthly number of patients was greatest in August, and September, October, November and December in the right order. The regional prevalence was greatest in Hwachun & Yanggu(33.9%) and the western area of Kangwon province was greater than the eastern area except Youngweol. The frequent dermatoses include acne, tattoo, melanocytic nevus, folliculitis, keratosis pilaris, dermatophytosis, contact dermatitis, bromhidrosis, atopic dermatitis, urticaria, tinea versicolor, other eczema, freckle and melasma, and keloid in the right order, respectively above 1% of total dermatoses. In the distribution of dermatoses as disease groups, diseases of skin appendages(37.6%), dermatoses due to physical agents(16.6%), melanocytic nevi(13.6%), dermatomycosis(8.7%), hereditary skin diseases(7.8%), eczema(6.6%), and pigment anomaly (2.3%) constituted 93.2% of the total. CONCLUSIONS: Prevalence surveillance of the dermatoses in Kangwon province shows that cosmetic diseases such as tattoo, melanocytic nevus and keratosis pilaris are more frequent compared with previous hospital-based study and when compared with soldiers, infectious disease and disease due to physical agent are significantly different.
Acne Vulgaris ; Adolescent ; Climate ; Communicable Diseases ; Dermatitis, Atopic ; Dermatitis, Contact ; Eczema ; Epidemiologic Studies* ; Folliculitis ; Gangwon-do* ; Genetics ; Humans ; Keloid ; Keratosis ; Korea ; Male ; Melanosis ; Military Personnel ; Nevus, Pigmented ; Physical Examination ; Prevalence ; Skin ; Skin Diseases* ; Tinea ; Tinea Versicolor ; Urticaria ; Young Adult