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Article: Huo-Luo-Xiao-Ling Dan modulates antigen-directed immune response in adjuvant-induced inflammation

TitleHuo-Luo-Xiao-Ling Dan modulates antigen-directed immune response in adjuvant-induced inflammation
Authors
KeywordsAntibodies
Cytokines
Huo-Luo-Xiao-Ling Dan
Immune modulation
Inflammation
T cells
Issue Date2009
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/jethpharm
Citation
Journal Of Ethnopharmacology, 2009, v. 123 n. 1, p. 40-44 How to Cite?
AbstractEthnopharmacological relevance: HLXL is a traditional Chinese medicine that has long been used in folk medicine for the treatment of chronic inflammatory diseases. However, the precise immunological mechanisms by which HLXL mediates its anti-inflammatory activity are not fully defined. Aim of the study: To determine the effects of HLXL on antigen-specific immune parameters in adjuvant-induced inflammation model in the Lewis rat. Materials and methods: Rats were fed daily with either HLXL (2.3 g/kg) or vehicle (water) beginning 3 days before subcutaneous injection of heat-killed Mycobacterium tuberculosis H37Ra (Mtb), and then continued for another 6 days. After 9 days of Mtb injection, the draining lymph node cells were tested for T cell proliferative and cytokine responses against mycobacterial heat-shock protein 65 (Bhsp65). Moreover, sera were tested for anti-Bhsp65 antibodies and nitric oxide (NO). Results: HLXL-treated rats showed reduced T cell proliferative response to Bhsp65 compared to control rats. Furthermore, HLXL suppressed IL-17 response but enhanced IL-10 response without much effect on IFN-γ. HLXL treatment also reduced the levels of anti-Bhsp65 antibodies but not that of NO. Conclusions: HLXL feeding modulated both the cellular and the humoral immune response to Bhsp65 favoring an anti-inflammatory milieu for the suppression of adjuvant-induced inflammation. © 2009 Elsevier Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/188611
ISSN
2023 Impact Factor: 4.8
2023 SCImago Journal Rankings: 0.936
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorRajaiah, Ren_US
dc.contributor.authorLee, DYWen_US
dc.contributor.authorMa, Zen_US
dc.contributor.authorFan, AYen_US
dc.contributor.authorLao, Len_US
dc.contributor.authorFong, HHSen_US
dc.contributor.authorBerman, BMen_US
dc.contributor.authorMoudgil, KDen_US
dc.date.accessioned2013-09-03T04:10:35Z-
dc.date.available2013-09-03T04:10:35Z-
dc.date.issued2009en_US
dc.identifier.citationJournal Of Ethnopharmacology, 2009, v. 123 n. 1, p. 40-44en_US
dc.identifier.issn0378-8741en_US
dc.identifier.urihttp://hdl.handle.net/10722/188611-
dc.description.abstractEthnopharmacological relevance: HLXL is a traditional Chinese medicine that has long been used in folk medicine for the treatment of chronic inflammatory diseases. However, the precise immunological mechanisms by which HLXL mediates its anti-inflammatory activity are not fully defined. Aim of the study: To determine the effects of HLXL on antigen-specific immune parameters in adjuvant-induced inflammation model in the Lewis rat. Materials and methods: Rats were fed daily with either HLXL (2.3 g/kg) or vehicle (water) beginning 3 days before subcutaneous injection of heat-killed Mycobacterium tuberculosis H37Ra (Mtb), and then continued for another 6 days. After 9 days of Mtb injection, the draining lymph node cells were tested for T cell proliferative and cytokine responses against mycobacterial heat-shock protein 65 (Bhsp65). Moreover, sera were tested for anti-Bhsp65 antibodies and nitric oxide (NO). Results: HLXL-treated rats showed reduced T cell proliferative response to Bhsp65 compared to control rats. Furthermore, HLXL suppressed IL-17 response but enhanced IL-10 response without much effect on IFN-γ. HLXL treatment also reduced the levels of anti-Bhsp65 antibodies but not that of NO. Conclusions: HLXL feeding modulated both the cellular and the humoral immune response to Bhsp65 favoring an anti-inflammatory milieu for the suppression of adjuvant-induced inflammation. © 2009 Elsevier Ireland Ltd. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/jethpharmen_US
dc.relation.ispartofJournal of Ethnopharmacologyen_US
dc.subjectAntibodies-
dc.subjectCytokines-
dc.subjectHuo-Luo-Xiao-Ling Dan-
dc.subjectImmune modulation-
dc.subjectInflammation-
dc.subjectT cells-
dc.subject.meshAnimalsen_US
dc.subject.meshAntibody Formationen_US
dc.subject.meshAntigens - Immunologyen_US
dc.subject.meshCytokines - Metabolismen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshInflammation - Chemically Induced - Immunology - Therapyen_US
dc.subject.meshInflammation Mediators - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshMedicine, Chinese Traditionalen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Lewen_US
dc.titleHuo-Luo-Xiao-Ling Dan modulates antigen-directed immune response in adjuvant-induced inflammationen_US
dc.typeArticleen_US
dc.identifier.emailLao, L: lxlao1@hku.hken_US
dc.identifier.authorityLao, L=rp01784en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.jep.2009.02.032en_US
dc.identifier.pmid19429337en_US
dc.identifier.scopuseid_2-s2.0-64549090605en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-64549090605&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume123en_US
dc.identifier.issue1en_US
dc.identifier.spage40en_US
dc.identifier.epage44en_US
dc.identifier.isiWOS:000266124600007-
dc.publisher.placeIrelanden_US
dc.identifier.scopusauthoridRajaiah, R=24329548500en_US
dc.identifier.scopusauthoridLee, DYW=55808069921en_US
dc.identifier.scopusauthoridMa, Z=8709903000en_US
dc.identifier.scopusauthoridFan, AY=7005672886en_US
dc.identifier.scopusauthoridLao, L=7005681883en_US
dc.identifier.scopusauthoridFong, HHS=34569199300en_US
dc.identifier.scopusauthoridBerman, BM=35458606800en_US
dc.identifier.scopusauthoridMoudgil, KD=7003544028en_US
dc.identifier.issnl0378-8741-

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