{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/15514"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/15514","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Effects of mannan oligosaccharide on immune function and disease resistance in pigs","abstract":"The 3 studies described below demonstrate the effects of mannan oligosaccharide (MOS) on immune function and disease resistance in pigs. Study 1 evaluated whether MOS in both in vivo and in vitro systems regulates cytokine production by alveolar macrophages (AMφ) in response to in vitro microbial challenge models. The lipopolysaccharide (LPS)- stimulated AMφ from MOS-fed pigs produced less tumor necrosis factor-α (TNF-α) (P < 0.01) and more IL-10 (P = 0.051) than AMφ from the control-fed pigs. Dietary MOS did not affect AMφ-produced cytokines induced by polyinosinic:polycytidylic acid (Poly I:C). When applied in vitro, MOS suppressed LPS-induced TNF-α (P < 0.001), but enhanced LPS-induced IL-10 (P < 0.05). Further, TNF-α production by AMφ stimulated with LPS (P < 0.05) or Poly I:C (P < 0.001) was suppressed by a mannan-rich fraction (MRF). In order to learn if MOS interacts with LPS receptors, AMφ were cultured with Polymyxin B, an inhibitor of LPS-activated toll-like receptor (TLR) 4. Although Polymyxin B completely inhibited AMφ-produced TNF-α induced by LPS, it did not affect the ability of MOS to regulate cytokine production in the absence of LPS. When added in vitro, both MOS and MRF were also able to regulate constitutive production of TNF-α in the absence of LPS. Study 2 determined if various levels of dietary MOS affect growth and serum cytokine levels in nursery pigs. No effect of MOS on growth was found. There were no differences in serum levels of TNF-α and IL-10, although these levels changed over time. Study 3 showed that MOS altered nursery pigs‟ immune response to a porcine reproductive and respiratory syndrome virus (PRRSV). Infection of PRRSV reduced pig performance and leukocytes (P < 0.01), but increased serum inflammatory mediators and fever (P < 0.01). Dietary MOS prevented leukopenia at d 3 and 7 postinfection (PI) and tended to improve feed efficiency. In infected pigs, MOS reduced fever at d 7 PI (P < 0.01) and serum TNF-α at d 14 PI (P = 0.06). The gene expression profile in peripheral blood mononuclear cells and bronchoalveolar lavage fluid cells at d 7 PI was characterized by using microarray and real time RT-PCR. The MOS x PRRSV interaction altered the gene expression in the above leukocytes (P < 0.05). In peripheral blood mononuclear cells, MOS increased the gene expression of pattern recognition receptors, cytokines, and intracellular signaling molecules in uninfected pigs, but reduced the gene expression of TLR4 and various types of key cytokines and chemokines in infected pigs (P < 0.05). In bronchoalveolar lavage fluid cells, MOS may promote a cytotoxic T cell immune response by enhancing MHCI mRNA expression, but reduce the expression of complement system-associated molecules and 2’,5’-oligoadenylate synthetase-1. The downregulation of inflammatory responses regulated by MOS at d 7 PI was associated with several important canonical pathways such as triggering receptor expressed on myeloid cells-1 signaling, hypoxia signaling, IL-4 signaling, macropinocytosis signaling, and perhaps the alternative activation of macrophages. In summary, MOS is a potent immunomodulator in both in vitro and in vivo systems. Dietary inclusion of MOS in diets for pigs may bring benefits by boosting and maintaining the host’s disease resistance while preventing over-stimulation of the immune system.","abstract_html":"The 3 studies described below demonstrate the effects of mannan oligosaccharide (MOS) on immune function and disease resistance in pigs. Study 1 evaluated whether MOS in both in vivo and in vitro systems regulates cytokine production by alveolar macrophages (AMφ) in response to in vitro microbial challenge models. The lipopolysaccharide (LPS)- stimulated AMφ from MOS-fed pigs produced less tumor necrosis factor-α (TNF-α) (P &lt; 0.01) and more IL-10 (P = 0.051) than AMφ from the control-fed pigs. Dietary MOS did not affect AMφ-produced cytokines induced by polyinosinic:polycytidylic acid (Poly I:C). When applied in vitro, MOS suppressed LPS-induced TNF-α (P &lt; 0.001), but enhanced LPS-induced IL-10 (P &lt; 0.05). Further, TNF-α production by AMφ stimulated with LPS (P &lt; 0.05) or Poly I:C (P &lt; 0.001) was suppressed by a mannan-rich fraction (MRF). In order to learn if MOS interacts with LPS receptors, AMφ were cultured with Polymyxin B, an inhibitor of LPS-activated toll-like receptor (TLR) 4. Although Polymyxin B completely inhibited AMφ-produced TNF-α induced by LPS, it did not affect the ability of MOS to regulate cytokine production in the absence of LPS. When added in vitro, both MOS and MRF were also able to regulate constitutive production of TNF-α in the absence of LPS. Study 2 determined if various levels of dietary MOS affect growth and serum cytokine levels in nursery pigs. No effect of MOS on growth was found. There were no differences in serum levels of TNF-α and IL-10, although these levels changed over time. Study 3 showed that MOS altered nursery pigs‟ immune response to a porcine reproductive and respiratory syndrome virus (PRRSV). Infection of PRRSV reduced pig performance and leukocytes (P &lt; 0.01), but increased serum inflammatory mediators and fever (P &lt; 0.01). Dietary MOS prevented leukopenia at d 3 and 7 postinfection (PI) and tended to improve feed efficiency. In infected pigs, MOS reduced fever at d 7 PI (P &lt; 0.01) and serum TNF-α at d 14 PI (P = 0.06). The gene expression profile in peripheral blood mononuclear cells and bronchoalveolar lavage fluid cells at d 7 PI was characterized by using microarray and real time RT-PCR. The MOS x PRRSV interaction altered the gene expression in the above leukocytes (P &lt; 0.05). In peripheral blood mononuclear cells, MOS increased the gene expression of pattern recognition receptors, cytokines, and intracellular signaling molecules in uninfected pigs, but reduced the gene expression of TLR4 and various types of key cytokines and chemokines in infected pigs (P &lt; 0.05). In bronchoalveolar lavage fluid cells, MOS may promote a cytotoxic T cell immune response by enhancing MHCI mRNA expression, but reduce the expression of complement system-associated molecules and 2’,5’-oligoadenylate synthetase-1. The downregulation of inflammatory responses regulated by MOS at d 7 PI was associated with several important canonical pathways such as triggering receptor expressed on myeloid cells-1 signaling, hypoxia signaling, IL-4 signaling, macropinocytosis signaling, and perhaps the alternative activation of macrophages. In summary, MOS is a potent immunomodulator in both in vitro and in vivo systems. Dietary inclusion of MOS in diets for pigs may bring benefits by boosting and maintaining the host’s disease resistance while preventing over-stimulation of the immune system.","abstract_has_math":false,"creators":["Che, Tung M."],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Animal Sciences","degree_department":null,"school":null,"contributors":["Pettigrew, James E.","Kelley, Keith W.","Johnson, Rodney W.","Van Alstine, William G.","Stein, Hans H."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2010,"date_issued":"2010-05-14T20:43:44Z","date_published":"2010-05-14T20:43:44Z","updated_at":"2026-07-22T22:25:08Z","subjects":["Alveolar macrophages and cytokine secretion","disease resistance","immunomodulation","mannan oligosaccharide","pigs","porcine reproductive and respiratory syndrome virus (PRRSV)"],"languages":["en"],"rights":["Copyright 2010 Tung Che"],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/2142/15514","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Pettigrew, James E.","Kelley, Keith W.","Johnson, Rodney W.","Van Alstine, William G.","Stein, Hans H."]},{"key":"dc:creator","label":"Author","values":["Che, Tung M."]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2010-05-14T20:43:44Z","2012-05-15T10:00:21Z","2010-5"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Animal Sciences"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois at Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Alveolar macrophages and cytokine secretion","disease resistance","immunomodulation","mannan oligosaccharide","pigs","porcine reproductive and respiratory syndrome virus (PRRSV)"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["en"]},{"key":"dc:rights","label":"Dc Rights","values":["Copyright 2010 Tung Che"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/2142/15514"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["The 3 studies described below demonstrate the effects of mannan oligosaccharide (MOS) on immune function and disease resistance in pigs. Study 1 evaluated whether MOS in both in vivo and in vitro systems regulates cytokine production by alveolar macrophages (AMφ) in response to in vitro microbial challenge models. The lipopolysaccharide (LPS)- stimulated AMφ from MOS-fed pigs produced less tumor necrosis factor-α (TNF-α) (P < 0.01) and more IL-10 (P = 0.051) than AMφ from the control-fed pigs. Dietary MOS did not affect AMφ-produced cytokines induced by polyinosinic:polycytidylic acid (Poly I:C). When applied in vitro, MOS suppressed LPS-induced TNF-α (P < 0.001), but enhanced LPS-induced IL-10 (P < 0.05). Further, TNF-α production by AMφ stimulated with LPS (P < 0.05) or Poly I:C (P < 0.001) was suppressed by a mannan-rich fraction (MRF). In order to learn if MOS interacts with LPS receptors, AMφ were cultured with Polymyxin B, an inhibitor of LPS-activated toll-like receptor (TLR) 4. Although Polymyxin B completely inhibited AMφ-produced TNF-α induced by LPS, it did not affect the ability of MOS to regulate cytokine production in the absence of LPS. When added in vitro, both MOS and MRF were also able to regulate constitutive production of TNF-α in the absence of LPS. Study 2 determined if various levels of dietary MOS affect growth and serum cytokine levels in nursery pigs. No effect of MOS on growth was found. There were no differences in serum levels of TNF-α and IL-10, although these levels changed over time. Study 3 showed that MOS altered nursery pigs‟ immune response to a porcine reproductive and respiratory syndrome virus (PRRSV). Infection of PRRSV reduced pig performance and leukocytes (P < 0.01), but increased serum inflammatory mediators and fever (P < 0.01). Dietary MOS prevented leukopenia at d 3 and 7 postinfection (PI) and tended to improve feed efficiency. In infected pigs, MOS reduced fever at d 7 PI (P < 0.01) and serum TNF-α at d 14 PI (P = 0.06). The gene expression profile in peripheral blood mononuclear cells and bronchoalveolar lavage fluid cells at d 7 PI was characterized by using microarray and real time RT-PCR. The MOS x PRRSV interaction altered the gene expression in the above leukocytes (P < 0.05). In peripheral blood mononuclear cells, MOS increased the gene expression of pattern recognition receptors, cytokines, and intracellular signaling molecules in uninfected pigs, but reduced the gene expression of TLR4 and various types of key cytokines and chemokines in infected pigs (P < 0.05). In bronchoalveolar lavage fluid cells, MOS may promote a cytotoxic T cell immune response by enhancing MHCI mRNA expression, but reduce the expression of complement system-associated molecules and 2’,5’-oligoadenylate synthetase-1. The downregulation of inflammatory responses regulated by MOS at d 7 PI was associated with several important canonical pathways such as triggering receptor expressed on myeloid cells-1 signaling, hypoxia signaling, IL-4 signaling, macropinocytosis signaling, and perhaps the alternative activation of macrophages. In summary, MOS is a potent immunomodulator in both in vitro and in vivo systems. Dietary inclusion of MOS in diets for pigs may bring benefits by boosting and maintaining the host’s disease resistance while preventing over-stimulation of the immune system.","Item withdrawn by Mark Zulauf (zulauf@illinois.edu) on 2010-03-01T14:09:33Z Item was in collections: University of Illinois Theses & Dissertations (ID: 1) No. of bitstreams: 2 Che_Tung.pdf: 1385862 bytes, checksum: 0af203c36c2208aa6c3ab6e3b610521f (MD5) Che_Tung.docx: 1214173 bytes, checksum: 674c3a0171c3ee02bef86da5292bebce (MD5)","Made available in DSpace on 2010-05-14T20:43:44Z (GMT). No. of bitstreams: 4 Che_Tung.pdf: 1385862 bytes, checksum: 0af203c36c2208aa6c3ab6e3b610521f (MD5) Che_Tung.docx: 1214173 bytes, checksum: 674c3a0171c3ee02bef86da5292bebce (MD5) 1_Che_Tung.pdf: 1390274 bytes, checksum: 502f09ee217e7415451edb5576cc704a (MD5) license.txt: 4058 bytes, checksum: deb4bc1a6f03671a36a3752f2bc5d70b (MD5)","Item marked as restricted to the 'Administrator' Group (id=1) by William Ingram (wingram2@illinois.edu) on 2010-05-14T20:45:16Z Item is restricted until 2012-05-14T20:45:13Z","Item reinstated by Sarah Shreeves (sshreeve@illinois.edu) on 2012-05-15T10:00:21Z Item was in collections: University of Illinois Dissertations and Theses (ID: 204) Dissertations and Theses - Animal Sciences (ID: 673) No. of bitstreams: 5 Che_Tung.pdf: 1385862 bytes, checksum: 0af203c36c2208aa6c3ab6e3b610521f (MD5) Che_Tung.docx: 1214173 bytes, checksum: 674c3a0171c3ee02bef86da5292bebce (MD5) 1_Che_Tung.pdf: 1390274 bytes, checksum: 502f09ee217e7415451edb5576cc704a (MD5) license.txt: 4058 bytes, checksum: deb4bc1a6f03671a36a3752f2bc5d70b (MD5) 1_Che_Tung.pdf.txt: 249705 bytes, checksum: a798903ff407f959aa0d08b57ca1058a (MD5)","Item released from any restrictions by Sarah Shreeves (sshreeve@illinois.edu) on 2012-05-15T10:00:21Z"]},{"key":"dc:title","label":"Title","values":["Effects of mannan oligosaccharide on immune function and disease resistance in pigs"]}]}],"canonical_facts":{"dc:contributor":["Pettigrew, James E.","Kelley, Keith W.","Johnson, Rodney W.","Van Alstine, William G.","Stein, Hans H."],"dc:creator":["Che, Tung M."],"dc:date":["2010-05-14T20:43:44Z","2012-05-15T10:00:21Z","2010-5"],"dc:description":["The 3 studies described below demonstrate the effects of mannan oligosaccharide (MOS) on immune function and disease resistance in pigs. Study 1 evaluated whether MOS in both in vivo and in vitro systems regulates cytokine production by alveolar macrophages (AMφ) in response to in vitro microbial challenge models. The lipopolysaccharide (LPS)- stimulated AMφ from MOS-fed pigs produced less tumor necrosis factor-α (TNF-α) (P < 0.01) and more IL-10 (P = 0.051) than AMφ from the control-fed pigs. Dietary MOS did not affect AMφ-produced cytokines induced by polyinosinic:polycytidylic acid (Poly I:C). When applied in vitro, MOS suppressed LPS-induced TNF-α (P < 0.001), but enhanced LPS-induced IL-10 (P < 0.05). Further, TNF-α production by AMφ stimulated with LPS (P < 0.05) or Poly I:C (P < 0.001) was suppressed by a mannan-rich fraction (MRF). In order to learn if MOS interacts with LPS receptors, AMφ were cultured with Polymyxin B, an inhibitor of LPS-activated toll-like receptor (TLR) 4. Although Polymyxin B completely inhibited AMφ-produced TNF-α induced by LPS, it did not affect the ability of MOS to regulate cytokine production in the absence of LPS. When added in vitro, both MOS and MRF were also able to regulate constitutive production of TNF-α in the absence of LPS. Study 2 determined if various levels of dietary MOS affect growth and serum cytokine levels in nursery pigs. No effect of MOS on growth was found. There were no differences in serum levels of TNF-α and IL-10, although these levels changed over time. Study 3 showed that MOS altered nursery pigs‟ immune response to a porcine reproductive and respiratory syndrome virus (PRRSV). Infection of PRRSV reduced pig performance and leukocytes (P < 0.01), but increased serum inflammatory mediators and fever (P < 0.01). Dietary MOS prevented leukopenia at d 3 and 7 postinfection (PI) and tended to improve feed efficiency. In infected pigs, MOS reduced fever at d 7 PI (P < 0.01) and serum TNF-α at d 14 PI (P = 0.06). The gene expression profile in peripheral blood mononuclear cells and bronchoalveolar lavage fluid cells at d 7 PI was characterized by using microarray and real time RT-PCR. The MOS x PRRSV interaction altered the gene expression in the above leukocytes (P < 0.05). In peripheral blood mononuclear cells, MOS increased the gene expression of pattern recognition receptors, cytokines, and intracellular signaling molecules in uninfected pigs, but reduced the gene expression of TLR4 and various types of key cytokines and chemokines in infected pigs (P < 0.05). In bronchoalveolar lavage fluid cells, MOS may promote a cytotoxic T cell immune response by enhancing MHCI mRNA expression, but reduce the expression of complement system-associated molecules and 2’,5’-oligoadenylate synthetase-1. The downregulation of inflammatory responses regulated by MOS at d 7 PI was associated with several important canonical pathways such as triggering receptor expressed on myeloid cells-1 signaling, hypoxia signaling, IL-4 signaling, macropinocytosis signaling, and perhaps the alternative activation of macrophages. In summary, MOS is a potent immunomodulator in both in vitro and in vivo systems. Dietary inclusion of MOS in diets for pigs may bring benefits by boosting and maintaining the host’s disease resistance while preventing over-stimulation of the immune system.","Item withdrawn by Mark Zulauf (zulauf@illinois.edu) on 2010-03-01T14:09:33Z Item was in collections: University of Illinois Theses & Dissertations (ID: 1) No. of bitstreams: 2 Che_Tung.pdf: 1385862 bytes, checksum: 0af203c36c2208aa6c3ab6e3b610521f (MD5) Che_Tung.docx: 1214173 bytes, checksum: 674c3a0171c3ee02bef86da5292bebce (MD5)","Made available in DSpace on 2010-05-14T20:43:44Z (GMT). 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