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Please use this identifier to cite or link to this item: http://hdl.handle.net/11375/6939
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dc.contributor.advisorMarshall, Jean S.en_US
dc.contributor.authorLeal-Berumen, Ireneen_US
dc.date.accessioned2014-06-18T16:37:33Z-
dc.date.available2014-06-18T16:37:33Z-
dc.date.created2010-06-28en_US
dc.date.issued1995-07en_US
dc.identifier.otheropendissertations/2242en_US
dc.identifier.other3312en_US
dc.identifier.other1373366en_US
dc.identifier.urihttp://hdl.handle.net/11375/6939-
dc.description.abstract<p>The mast cell has been implicated as an initiating cell in the immediate responses to allergen challenge where preformed mediators such as histamine play an important role. However, the role of mast cells is less well understood in severe allergic disorders such as asthma where chronic inflammatory changes are resent. Results presented in this thesis demonstrate that freshly isolated and highly purified rat peritoneal mast cells can release IL-6 without any necessity for histamine release. These observations were determined with the use of bacterial products such as LPS and CT which significantly enhanced IL-6 production in our system.</p> <p>Prostanoids of the E family (PGE₁ and PGE₂) were also used as stimulating agents which may also participate in inflammation. We observed that these prostaglandins selectively enhanced IL-6 production while TNF-α synthesis was significantly inhibited CT was observed to have very similar effects to PGE₁ on mast cells . These findings illustrate the potential role that mast cells may have during chronic inflammation and infectious disease.</p>en_US
dc.subjectMedical Sciencesen_US
dc.subjectMedical Sciencesen_US
dc.titleRegulation of Interleukin-6 and Tumor Necrosis Factor-α in Rat Peritoneal Mast Cells by Lipopolysaccharide, Prostaglandin E₁, Prostaglandin E₂ and Cholera Toxinen_US
dc.typethesisen_US
dc.contributor.departmentMedical Sciencesen_US
dc.description.degreeDoctor of Philosophy (PhD)en_US
Appears in Collections:Open Access Dissertations and Theses

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