No abstract available.
Chemokines* ; Dermatitis, Atopic*

During study in HIV/AIDS, US researchers of National Institute of Allergy and Infectious Diseases found that sometime gene mutations in immune-competent cells could help body have better resistance to cardiovascular diseases. These mutations are in some receptors of chemokines in membrane of immune cells. Results of experimental trial in mouse had gene mutation in receptor CX3CR1 showed that this mutant could make better resistance to high-risk factors and genetic factors in pathogenesis of cardiovascular diseases. This finding provided a new way to study drugs that have effects right on chemokine receptor CX3CR1 of high-risk patients with atherosclerosis
Cardiovascular Diseases ; Chemokines ; Mutation

Chemokines ; Humans ; Pain

PURPOSE: Chemokines are potent regulators of the host inflammatory or immune responses. Mucosal synthesis of chemokines may be important in the pathogenesis of mucosal inflammation in ulcerative colitis (UC). We performed this study to investigate the expression of C-X-C chemokine genes in UC. METHODS: Mucosal tissues were obtained from six normal controls and six UC patients by endoscopic biopsies. In patients with UC, mucosal tissues were separately obtained from both involved and uninvolved regions. RNA was extracted and mRNA levels of five C-X-C chemokines were determined by quantitative reverse transcription-PCR using internal RNA standards. RESULTS: Mucosal mRNA levels of all chemokines tested increased in the involved region of UC compared with the uninvolved region of UC or normal controls. CONCLUSION: Our data suggest that mucosal expression of C-X-C chemokines contributes to the pathogenesis of UC
Biopsy ; Chemokines ; Chemokines, CXC ; Colitis, Ulcerative* ; Colon* ; Humans ; Inflammation ; Mucous Membrane* ; RNA ; RNA, Messenger ; Ulcer*

BACKGROUND: Psoriatic keratinocytes express CXC chemokines like IL-8 and GRO-alpha, and CC chemokines like MCP-1 and RANTES, which have a significant role in the accumulation of inflammatory cells in psoriatic skin and both CXCR1 and CXCR2 receptors are also expressed in psoriatic keratinocytes, which suggests that IL-8 and GRO-alpha could have a role in the characteristic epidermal changes through binding to their receptors in psoriatic keratinocytes. OBJECTIVE: The purpose is to understand the pathogenetic mechanisms of psoriasis by comparing immunoreactivity of various chemokines and chemokine receptors between lesional and non-lesional skin of psoriasis. METHODS:We have performed immunohistochemical studies with mouse anti-human IL-8, mouse anti-human GRO, anti-huamn MCP-1, mouse anti-human RANTES, anti-human CDw 128 IL-8RA/ CXCR1, and anti-human IL-8RB/CXCR2 for lesional and non-lesional skin of ten psoriatic patients. RESULTS: 1.Immunohistochemical reactivity for IL-8 is stronger in lesional epidermis than non-lesional epidermis(p<0.05) and immunohistochemical reactivity for GRO-alpha is stronger in lesional epidermis than non-lesional epidermis(p<0.05). 2.Immunohistochemical reactivity for MCP-1 is stronger in lesional epidermis than non-lesional epidermis(p<0.05), and immunohistochemical reactivity for RANTES is stronger in lesional epidermis than non-lesional epidermis(p<0.05). 3.Immunohistochemical reactivity for CXCR1 is stronger in lesional epidermis than non-lesional epidermis(p<0.05) and immunohistochemical reactivity for CXCR2 is stronger in lesional epidermis than non-lesional epidermis(p<0.05). 4.Immunofluorescent staining reveals positive finding in epidermis of lesional psoriasis, but negative finding in CXCR2. CONCLUSION: These results suggest that psoriatic keratinocytes express CXC chemokines like IL-8 and GRO-alpha, and CC chemokines like MCP-1 and RANTES, which have a significant role in the accumulation of inflammatory cells in psoriatic skin and that both CXCR1 and CXCR2 receptors are also expressed in psoriatic keratinocytes, which suggests that IL-8 and GRO-alpha could have a role in the characteristic epidermal changes through binding to their receptors in psoriatic keratinocytes.
Animals ; Chemokine CCL5 ; Chemokines* ; Chemokines, CC ; Chemokines, CXC ; Epidermis ; Humans ; Interleukin-8 ; Keratinocytes ; Mice ; Psoriasis* ; Receptors, Chemokine* ; Receptors, Interleukin-8B ; Skin

BACKGROUND: Psoriatic keratinocytes express CXC chemokines like IL-8 and GRO-alpha, and CC chemokines like MCP-1 and RANTES, which have a significant role in the accumulation of inflammatory cells in psoriatic skin and both CXCR1 and CXCR2 receptors are also expressed in psoriatic keratinocytes, which suggests that IL-8 and GRO-alpha could have a role in the characteristic epidermal changes through binding to their receptors in psoriatic keratinocytes. OBJECTIVE: The purpose is to understand the pathogenetic mechanisms of psoriasis by comparing immunoreactivity of various chemokines and chemokine receptors between lesional and non-lesional skin of psoriasis. METHODS:We have performed immunohistochemical studies with mouse anti-human IL-8, mouse anti-human GRO, anti-huamn MCP-1, mouse anti-human RANTES, anti-human CDw 128 IL-8RA/ CXCR1, and anti-human IL-8RB/CXCR2 for lesional and non-lesional skin of ten psoriatic patients. RESULTS: 1.Immunohistochemical reactivity for IL-8 is stronger in lesional epidermis than non-lesional epidermis(p<0.05) and immunohistochemical reactivity for GRO-alpha is stronger in lesional epidermis than non-lesional epidermis(p<0.05). 2.Immunohistochemical reactivity for MCP-1 is stronger in lesional epidermis than non-lesional epidermis(p<0.05), and immunohistochemical reactivity for RANTES is stronger in lesional epidermis than non-lesional epidermis(p<0.05). 3.Immunohistochemical reactivity for CXCR1 is stronger in lesional epidermis than non-lesional epidermis(p<0.05) and immunohistochemical reactivity for CXCR2 is stronger in lesional epidermis than non-lesional epidermis(p<0.05). 4.Immunofluorescent staining reveals positive finding in epidermis of lesional psoriasis, but negative finding in CXCR2. CONCLUSION: These results suggest that psoriatic keratinocytes express CXC chemokines like IL-8 and GRO-alpha, and CC chemokines like MCP-1 and RANTES, which have a significant role in the accumulation of inflammatory cells in psoriatic skin and that both CXCR1 and CXCR2 receptors are also expressed in psoriatic keratinocytes, which suggests that IL-8 and GRO-alpha could have a role in the characteristic epidermal changes through binding to their receptors in psoriatic keratinocytes.
Animals ; Chemokine CCL5 ; Chemokines* ; Chemokines, CC ; Chemokines, CXC ; Epidermis ; Humans ; Interleukin-8 ; Keratinocytes ; Mice ; Psoriasis* ; Receptors, Chemokine* ; Receptors, Interleukin-8B ; Skin

BACKGROUND AND OBJECTIVES: The cause of nasal polyp is unsure but inflammation is thought to be an important factor in the development of nasal poyps. CC chemokine is a powerful chemotactic cytokine for inflammatory cells. We designed this study to investigate whether specific CC chemokines are associated with different forms of nasal polyps and their changes according to antibiotic treatment. MATERIALS AND METHODS: Nasal polyp from patients with atopy (AP group, n=12) and without atopy (NP group, n=20) were sampled. Expressions of RANTES, eotaxin, MCP-2, MCP-3 and MIP-1alpha were studied by an immunohistochemical study. Specimens of non-allergic nasal turbinates were used as the control group from 14 patients who were operated for nasal blockage. All patients were divided into 2 groups. One group was treated with antibiotics for 10 days before operation. The other was non-treated. RESULTS: Between the NP and AP group, the ratio of stained cells except anti-MCP 2 monoclonal antibody in the AP group was more increased than that of the NP group. Among them, RANTES and eotaxin were increased significantly (p<0.05). There was a significant difference of the expression of 5 CC chemokines between the treated and non-treated groups (p<0.05). CONCLUSIONS: These results suggest that chemokines play an important role in the development of nasal polyps, and different kinds of chemokines can be involved according to the cause of nasal polyps and CC chemokines affected by antibiotic treatment.
Anti-Bacterial Agents ; Chemokine CCL3 ; Chemokine CCL5 ; Chemokines ; Chemokines, CC ; Humans ; Inflammation ; Nasal Obstruction ; Nasal Polyps* ; Turbinates

BACKGROUND AND OBJECTIVES: The cause of nasal polyp is unsure but inflammation is thought to be an important factor in the development of nasal poyps. CC chemokine is a powerful chemotactic cytokine for inflammatory cells. We designed this study to investigate whether specific CC chemokines are associated with different forms of nasal polyps and their changes according to antibiotic treatment. MATERIALS AND METHODS: Nasal polyp from patients with atopy (AP group, n=12) and without atopy (NP group, n=20) were sampled. Expressions of RANTES, eotaxin, MCP-2, MCP-3 and MIP-1alpha were studied by an immunohistochemical study. Specimens of non-allergic nasal turbinates were used as the control group from 14 patients who were operated for nasal blockage. All patients were divided into 2 groups. One group was treated with antibiotics for 10 days before operation. The other was non-treated. RESULTS: Between the NP and AP group, the ratio of stained cells except anti-MCP 2 monoclonal antibody in the AP group was more increased than that of the NP group. Among them, RANTES and eotaxin were increased significantly (p<0.05). There was a significant difference of the expression of 5 CC chemokines between the treated and non-treated groups (p<0.05). CONCLUSIONS: These results suggest that chemokines play an important role in the development of nasal polyps, and different kinds of chemokines can be involved according to the cause of nasal polyps and CC chemokines affected by antibiotic treatment.
Anti-Bacterial Agents ; Chemokine CCL3 ; Chemokine CCL5 ; Chemokines ; Chemokines, CC ; Humans ; Inflammation ; Nasal Obstruction ; Nasal Polyps* ; Turbinates

BACKGROUND AND OBJECTIVES: The number of eosinophil in nasal polyps has been reported to be strongly elevated when compared to non-affected nasal tissue, indicating an important role for eosinophils in the pathogenesis of nasal polyposis. The mechanisms determining selective eosinophilic tissue infiltration into diseased nasal mucosa as yet are specualtive. Panleukotactic factors also known to be present on nasal polyps cannot explain the type-selective tissue infiltration in eosinophilic or neutrophilic-featured diseases. Chemokines are known to have leukocyte subtype-selective chemotactic properties in vitro and thus are candidates explaining leukocytic characteristic tissue infiltration. The aim of this study was to investigate whether specific chemokines are associated with different forms of nasal polyps. This study was designed to demonstrate the expressions of various CC chemokines. MATERIALS AND METHODS: Nasal polyp from patients with systemic allergy (AP group, n=7) and negative allergic skin tests (NP group, n=10) were sampled. Expressions of RANTES, eotaxin, MCP-1, MIP-1alpha,beta were studies by RT-PCR and immunohistochemical studies. RESULTS: Expression and mean density of RANTES, MCP-1, MIP-1beta were significantly stronger in NP group than in AP group (p<0.05). However, those of eotaxin and MIP-1alpha were significantly stronger in AP group than in NP group (p<0.01). CONCLUSION: This results suggest that only selective chemokines could be involved to develop the pathologic conditions in different type of nasal polyp.
Chemokine CCL3 ; Chemokine CCL4 ; Chemokine CCL5 ; Chemokines ; Chemokines, CC* ; Eosinophils ; Humans ; Hypersensitivity ; Leukocytes ; Nasal Mucosa ; Nasal Polyps* ; Skin Tests

BACKGROUND: Although glucocorticoids (GCs) are effective in controlling asthma in the majority of patients, a subset of asthmatics fails to demonstrate a satisfactory response, even to systemic GC therapy. This population is referred to as being "steroid-resistant". The actual mechanism underlying steroid resistance in asthma remains to be elucidated. METHODS: We have investigated how dexamethasone (DEX) regulates asthmatic phenotypes in a murine model of asthma, in which mice received i.p. immunization twice, followed by two bronchoprovocations with aerosolized OVA with a one-week interval, which we have recently described. RESULTS: Pretreatment with DEX resulted in an inhibition of NF-kappaB activation in asthmatic lungs, and also inhibited bronchoalveolar lavage (BAL) levels of NF-kappaB-dependent cytokines such as TNF-alpha and CC chemokines [eotaxin and monocyte chemotactic protein (MCP)-1]. DEX was effective in suppressing airway hyperresponsiveness (AHR) at 10 h, Th2-dependent asthmatic phenotypes such as airway eosinophilia, BAL levels of Th2 cytokines (IL-5 and IL-13), and mucin production. However, DEX failed to suppress BAL levels of CXC chemokines [macrophage inflammatory protein-2 (MIP-2) and keratinocyte-derived chemokine (KC)] and airway neutrophilia. CONCLUSION: Airway neutrophilia is among the phenomena observed in patients with severe GC-resistant asthma. This study will provide insight into the molecular basis for airway neutrophila seen in steroid-resistant asthma. Further studies are required to delineate the underlying mechanism of CXC chemokine expression in asthma.
Animals ; Asthma* ; Bronchoalveolar Lavage ; Chemokines, CC ; Chemokines, CXC ; Cytokines ; Dexamethasone* ; Eosinophilia ; Glucocorticoids ; Humans ; Immunization ; Lung ; Mice ; Monocytes ; Mucins ; NF-kappa B ; Ovum ; Phenotype ; Tumor Necrosis Factor-alpha