Thalidomide Attenuates Airway Hyperresponsiveness and Eosinophilic Inflammation in a Murine Model of Allergic Asthma
Asthma is characterized by chronic eosinophilic inflammation and hyperresponsiveness of the airways. We hypothesized that thalidomide, which has numerous immunomodulatory properties, may have anti-inflammatory effects in allergic asthma. BALB/c mice sensitized and challenged with ovalbumin (OVA) wer...
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| Veröffentlicht in: | Biological & pharmaceutical bulletin 2010/06/01, Vol.33(6), pp.1028-1032 |
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| creator | Asano, Toshiaki Kume, Hiroaki Taki, Fumitaka Ito, Satoru Hasegawa, Yoshinori |
| description | Asthma is characterized by chronic eosinophilic inflammation and hyperresponsiveness of the airways. We hypothesized that thalidomide, which has numerous immunomodulatory properties, may have anti-inflammatory effects in allergic asthma. BALB/c mice sensitized and challenged with ovalbumin (OVA) were treated orally with thalidomide (30, 100, or 300 mg/kg) or a vehicle. When thalidomide was administered to OVA-challenged mice, the number of eosinophils in bronchoalveolar lavage fluid (BALF) was significantly decreased. The numbers of inflammatory cells other than eosinophils were not reduced by thalidomide. Thalidomide inhibited the elevated levels of interleukin-5 (IL-5) and tumor necrosis factor-α (TNF-α) in BALF by OVA challenges. Histological analysis of the lung revealed that both the infiltration of inflammatory cells and the hyperplasia of goblet cells were significantly suppressed by thalidomide treatment. Furthermore, thalidomide significantly inhibited the response to methacholine induced by OVA challenges. Taken together, thalidomide treatment decreased airway inflammation and hyperresponsiveness in a murine model of allergic asthma. These results might provide an opportunity for the development of novel therapeutics to treat severe asthma. |
| doi_str_mv | 10.1248/bpb.33.1028 |
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We hypothesized that thalidomide, which has numerous immunomodulatory properties, may have anti-inflammatory effects in allergic asthma. BALB/c mice sensitized and challenged with ovalbumin (OVA) were treated orally with thalidomide (30, 100, or 300 mg/kg) or a vehicle. When thalidomide was administered to OVA-challenged mice, the number of eosinophils in bronchoalveolar lavage fluid (BALF) was significantly decreased. The numbers of inflammatory cells other than eosinophils were not reduced by thalidomide. Thalidomide inhibited the elevated levels of interleukin-5 (IL-5) and tumor necrosis factor-α (TNF-α) in BALF by OVA challenges. Histological analysis of the lung revealed that both the infiltration of inflammatory cells and the hyperplasia of goblet cells were significantly suppressed by thalidomide treatment. Furthermore, thalidomide significantly inhibited the response to methacholine induced by OVA challenges. Taken together, thalidomide treatment decreased airway inflammation and hyperresponsiveness in a murine model of allergic asthma. These results might provide an opportunity for the development of novel therapeutics to treat severe asthma.</description><identifier>ISSN: 0918-6158</identifier><identifier>EISSN: 1347-5215</identifier><identifier>DOI: 10.1248/bpb.33.1028</identifier><identifier>PMID: 20522972</identifier><language>eng</language><publisher>Japan: The Pharmaceutical Society of Japan</publisher><subject>airway hyperresponsiveness ; Animals ; Anti-Inflammatory Agents - pharmacology ; Anti-Inflammatory Agents - therapeutic use ; asthma ; Asthma - drug therapy ; Asthma - metabolism ; Asthma - pathology ; Bronchial Hyperreactivity - drug therapy ; Bronchial Hyperreactivity - metabolism ; Bronchial Hyperreactivity - pathology ; Bronchoalveolar Lavage Fluid ; cytokine ; Disease Models, Animal ; eosinophilic infiltration ; Eosinophils - drug effects ; Eosinophils - metabolism ; Female ; Goblet Cells - pathology ; Hyperplasia ; Inflammation - drug therapy ; Interleukin-5 - metabolism ; Lung - drug effects ; Lung - metabolism ; Lung - pathology ; Methacholine Chloride - metabolism ; Mice ; Mice, Inbred BALB C ; Ovalbumin ; thalidomide ; Thalidomide - pharmacology ; Thalidomide - therapeutic use ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>Biological and Pharmaceutical Bulletin, 2010/06/01, Vol.33(6), pp.1028-1032</ispartof><rights>2010 The Pharmaceutical Society of Japan</rights><rights>Copyright Japan Science and Technology Agency 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c557t-c5036f28250285b6acc47962c868b1372267555b7bda73575ed0fd05f59b58123</citedby><cites>FETCH-LOGICAL-c557t-c5036f28250285b6acc47962c868b1372267555b7bda73575ed0fd05f59b58123</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1877,4010,27900,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20522972$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Asano, Toshiaki</creatorcontrib><creatorcontrib>Kume, Hiroaki</creatorcontrib><creatorcontrib>Taki, Fumitaka</creatorcontrib><creatorcontrib>Ito, Satoru</creatorcontrib><creatorcontrib>Hasegawa, Yoshinori</creatorcontrib><title>Thalidomide Attenuates Airway Hyperresponsiveness and Eosinophilic Inflammation in a Murine Model of Allergic Asthma</title><title>Biological & pharmaceutical bulletin</title><addtitle>Biol Pharm Bull</addtitle><description>Asthma is characterized by chronic eosinophilic inflammation and hyperresponsiveness of the airways. We hypothesized that thalidomide, which has numerous immunomodulatory properties, may have anti-inflammatory effects in allergic asthma. BALB/c mice sensitized and challenged with ovalbumin (OVA) were treated orally with thalidomide (30, 100, or 300 mg/kg) or a vehicle. When thalidomide was administered to OVA-challenged mice, the number of eosinophils in bronchoalveolar lavage fluid (BALF) was significantly decreased. The numbers of inflammatory cells other than eosinophils were not reduced by thalidomide. Thalidomide inhibited the elevated levels of interleukin-5 (IL-5) and tumor necrosis factor-α (TNF-α) in BALF by OVA challenges. Histological analysis of the lung revealed that both the infiltration of inflammatory cells and the hyperplasia of goblet cells were significantly suppressed by thalidomide treatment. Furthermore, thalidomide significantly inhibited the response to methacholine induced by OVA challenges. Taken together, thalidomide treatment decreased airway inflammation and hyperresponsiveness in a murine model of allergic asthma. These results might provide an opportunity for the development of novel therapeutics to treat severe asthma.</description><subject>airway hyperresponsiveness</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Anti-Inflammatory Agents - therapeutic use</subject><subject>asthma</subject><subject>Asthma - drug therapy</subject><subject>Asthma - metabolism</subject><subject>Asthma - pathology</subject><subject>Bronchial Hyperreactivity - drug therapy</subject><subject>Bronchial Hyperreactivity - metabolism</subject><subject>Bronchial Hyperreactivity - pathology</subject><subject>Bronchoalveolar Lavage Fluid</subject><subject>cytokine</subject><subject>Disease Models, Animal</subject><subject>eosinophilic infiltration</subject><subject>Eosinophils - drug effects</subject><subject>Eosinophils - metabolism</subject><subject>Female</subject><subject>Goblet Cells - pathology</subject><subject>Hyperplasia</subject><subject>Inflammation - drug therapy</subject><subject>Interleukin-5 - metabolism</subject><subject>Lung - drug effects</subject><subject>Lung - metabolism</subject><subject>Lung - pathology</subject><subject>Methacholine Chloride - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Ovalbumin</subject><subject>thalidomide</subject><subject>Thalidomide - pharmacology</subject><subject>Thalidomide - therapeutic use</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>0918-6158</issn><issn>1347-5215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpd0b1v3CAYBnAUtUquaafuFVKHDtVd-DAGb7WitImUqEsyI2y_znHC4AJOdf99OV1yQ5eXgZ8ewfsg9JmSDWWVuurmbsP5hhKmztCK8kquBaPiHVqRhqp1TYW6QB9S2hFCJGH8HF0wIhhrJFuh_Lg1zg5hsgPgNmfwi8mQcGvjX7PHt_sZYoQ0B5_sC3hICRs_4JuQrA_z1jrb4zs_OjNNJtvgsfXY4IclWg_4IQzgcBhx6xzE50LblLeT-Yjej8Yl-PR6XqKnnzeP17fr-9-_7q7b-3UvhMxlEl6PTDFRvia62vR9JZua9apWHeWSsVoKITrZDUZyIQUMZByIGEXTCUUZv0TfjrlzDH8WSFlPNvXgnPEQlqQl57SsSh3k1__kLizRl8dpWlUNl1JyVdT3o-pjSCnCqOdoJxP3mhJ96EKXLjTn-tBF0V9eM5duguFk35ZfwI8j2KVsnuEETMy2d_AWVh_HIfN01W9N1OD5PzACm4U</recordid><startdate>2010</startdate><enddate>2010</enddate><creator>Asano, Toshiaki</creator><creator>Kume, Hiroaki</creator><creator>Taki, Fumitaka</creator><creator>Ito, Satoru</creator><creator>Hasegawa, Yoshinori</creator><general>The Pharmaceutical Society of Japan</general><general>Japan Science and Technology Agency</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>2010</creationdate><title>Thalidomide Attenuates Airway Hyperresponsiveness and Eosinophilic Inflammation in a Murine Model of Allergic Asthma</title><author>Asano, Toshiaki ; Kume, Hiroaki ; Taki, Fumitaka ; Ito, Satoru ; Hasegawa, Yoshinori</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c557t-c5036f28250285b6acc47962c868b1372267555b7bda73575ed0fd05f59b58123</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>airway hyperresponsiveness</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Anti-Inflammatory Agents - therapeutic use</topic><topic>asthma</topic><topic>Asthma - drug therapy</topic><topic>Asthma - metabolism</topic><topic>Asthma - pathology</topic><topic>Bronchial Hyperreactivity - drug therapy</topic><topic>Bronchial Hyperreactivity - metabolism</topic><topic>Bronchial Hyperreactivity - pathology</topic><topic>Bronchoalveolar Lavage Fluid</topic><topic>cytokine</topic><topic>Disease Models, Animal</topic><topic>eosinophilic infiltration</topic><topic>Eosinophils - drug effects</topic><topic>Eosinophils - metabolism</topic><topic>Female</topic><topic>Goblet Cells - pathology</topic><topic>Hyperplasia</topic><topic>Inflammation - drug therapy</topic><topic>Interleukin-5 - metabolism</topic><topic>Lung - drug effects</topic><topic>Lung - metabolism</topic><topic>Lung - pathology</topic><topic>Methacholine Chloride - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Ovalbumin</topic><topic>thalidomide</topic><topic>Thalidomide - pharmacology</topic><topic>Thalidomide - therapeutic use</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Asano, Toshiaki</creatorcontrib><creatorcontrib>Kume, Hiroaki</creatorcontrib><creatorcontrib>Taki, Fumitaka</creatorcontrib><creatorcontrib>Ito, Satoru</creatorcontrib><creatorcontrib>Hasegawa, Yoshinori</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biological & pharmaceutical bulletin</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Asano, Toshiaki</au><au>Kume, Hiroaki</au><au>Taki, Fumitaka</au><au>Ito, Satoru</au><au>Hasegawa, Yoshinori</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Thalidomide Attenuates Airway Hyperresponsiveness and Eosinophilic Inflammation in a Murine Model of Allergic Asthma</atitle><jtitle>Biological & pharmaceutical bulletin</jtitle><addtitle>Biol Pharm Bull</addtitle><date>2010</date><risdate>2010</risdate><volume>33</volume><issue>6</issue><spage>1028</spage><epage>1032</epage><pages>1028-1032</pages><issn>0918-6158</issn><eissn>1347-5215</eissn><abstract>Asthma is characterized by chronic eosinophilic inflammation and hyperresponsiveness of the airways. We hypothesized that thalidomide, which has numerous immunomodulatory properties, may have anti-inflammatory effects in allergic asthma. BALB/c mice sensitized and challenged with ovalbumin (OVA) were treated orally with thalidomide (30, 100, or 300 mg/kg) or a vehicle. When thalidomide was administered to OVA-challenged mice, the number of eosinophils in bronchoalveolar lavage fluid (BALF) was significantly decreased. The numbers of inflammatory cells other than eosinophils were not reduced by thalidomide. Thalidomide inhibited the elevated levels of interleukin-5 (IL-5) and tumor necrosis factor-α (TNF-α) in BALF by OVA challenges. Histological analysis of the lung revealed that both the infiltration of inflammatory cells and the hyperplasia of goblet cells were significantly suppressed by thalidomide treatment. Furthermore, thalidomide significantly inhibited the response to methacholine induced by OVA challenges. Taken together, thalidomide treatment decreased airway inflammation and hyperresponsiveness in a murine model of allergic asthma. These results might provide an opportunity for the development of novel therapeutics to treat severe asthma.</abstract><cop>Japan</cop><pub>The Pharmaceutical Society of Japan</pub><pmid>20522972</pmid><doi>10.1248/bpb.33.1028</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| source | J-STAGE Free; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Free Full-Text Journals in Chemistry |
| subjects | airway hyperresponsiveness Animals Anti-Inflammatory Agents - pharmacology Anti-Inflammatory Agents - therapeutic use asthma Asthma - drug therapy Asthma - metabolism Asthma - pathology Bronchial Hyperreactivity - drug therapy Bronchial Hyperreactivity - metabolism Bronchial Hyperreactivity - pathology Bronchoalveolar Lavage Fluid cytokine Disease Models, Animal eosinophilic infiltration Eosinophils - drug effects Eosinophils - metabolism Female Goblet Cells - pathology Hyperplasia Inflammation - drug therapy Interleukin-5 - metabolism Lung - drug effects Lung - metabolism Lung - pathology Methacholine Chloride - metabolism Mice Mice, Inbred BALB C Ovalbumin thalidomide Thalidomide - pharmacology Thalidomide - therapeutic use Tumor Necrosis Factor-alpha - metabolism |
| title | Thalidomide Attenuates Airway Hyperresponsiveness and Eosinophilic Inflammation in a Murine Model of Allergic Asthma |
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