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The role of chemokines and chemokine...

Hardison, Jenny Lynn.

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The role of chemokines and chemokine receptors in host defense and chronic inflammation following Trypanosoma cruzi infection.

Record Type:	Electronic resources : Monograph/item
Title/Author:	The role of chemokines and chemokine receptors in host defense and chronic inflammation following Trypanosoma cruzi infection./
Author:	Hardison, Jenny Lynn.
Description:	231 p.
Notes:	Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1764.
Contained By:	Dissertation Abstracts International65-04B.
Subject:	Health Sciences, Immunology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3131525
ISBN:	0496787667

The role of chemokines and chemokine receptors in host defense and chronic inflammation following Trypanosoma cruzi infection.
Hardison, Jenny Lynn.

The role of chemokines and chemokine receptors in host defense and chronic inflammation following Trypanosoma cruzi infection. - 231 p.

Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1764.

Thesis (Ph.D.)--University of California, Irvine, 2004.

We characterized the expression of chemokines and chemokine receptors in the heart following experimental infection of mice with the Colombiana strain of Trypanosoma cruzi. We found chemokines XCL1, CXCL1, CCL2, CCL3, and CCL4 were expressed in the heart primarily during acute infection or at day 30 p.i. The most highly expressed chemokines in the heart during acute infection, day 15 p.i., are CXCL9, CXCL10, CCL2, and CCL5. Chemokine receptors expressed in the heart during acute infection or at day 30 p.i. are CCR1, CCR2, CCR5, and CXCR3. Of these, the most highly expressed chemokine receptors at day 15 p.i. are CCR2 and CCR5. Chemokine receptors CCR2, CCR5, and CXCR3 remain highly expressed in the heart during chronic infection at day 120 p.i.{09}Expression of chemokines and their cognate receptors during acute and chronic T. cruzi infection suggests that these molecules play a role in directing infiltration of mononuclear cells to the heart. Further, we show that macrophages are the primary source of chemokines CXCL9, CXCL10, and CCL5 at day 15 p.i., suggesting that these cells are important for the initiation of inflammation in the heart. Infection of mice deficient in chemokine receptors most highly expressed in the heart during T. cruzi infection, CCR5 and CCR2, show different roles for these receptors in host defense and cardiac inflammation. We find that CCR5 is important for control of parasite replication and survival during acute infection, as well as directing infiltration of macrophages and T cells to the heart early in infection, at day 15 p.i. In the absence of CCR5, infiltration of inflammatory cells to the heart is delayed, and is not apparent until day 30 p.i., suggesting that signaling by other chemokines/chemokine receptors compensate for the loss of CCR5 to direct inflammation to the heart by day 30 p.i. Further, once mononuclear cells have infiltrated the heart, CCR5 is not essential for the maintenance of inflammation during chronic infection. In contrast, CCR2 is not essential for infiltration of mononuclear cells in the heart at any time during acute or chronic infection. However, we do find that CCR2 contributes to control of cardiac parasitism during peak infection, at day 30 p.i. Lastly, we assessed the contribution of the most highly expressed chemokines found in the heart during both acute and chronic infection by developing neutralizing monoclonal antibodies (mAbs) against CXCL9, CXCL10, and CCL5, and administering them during infection through day 60 p.i. We find that activity by a single chemokine (CXCL10 or CCL5) or chemokines that share a common receptor (CXCL9 and CXLC10) is not essential for the infiltration of mononuclear cells to the heart during acute infection with T. cruzi. However, CXCL9 and CXCL10, in combination, are important for control of parasite burden during acute and early chronic infection, through day 49 p.i. Finally, neutralization of CXCL10, CXCL9 + CXCL10, or CCL5 does not reduce inflammation in the heart during chronic infection.

ISBN: 0496787667Subjects--Topical Terms:

1017716
Health Sciences, Immunology.

The role of chemokines and chemokine receptors in host defense and chronic inflammation following Trypanosoma cruzi infection.
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100 1 $a Hardison, Jenny Lynn. $3 1935477
245 1 4 $a The role of chemokines and chemokine receptors in host defense and chronic inflammation following Trypanosoma cruzi infection.
300 $a 231 p.
500 $a Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1764.
500 $a Chair: Jerry E. Manning.
502 $a Thesis (Ph.D.)--University of California, Irvine, 2004.
520 $a We characterized the expression of chemokines and chemokine receptors in the heart following experimental infection of mice with the Colombiana strain of Trypanosoma cruzi. We found chemokines XCL1, CXCL1, CCL2, CCL3, and CCL4 were expressed in the heart primarily during acute infection or at day 30 p.i. The most highly expressed chemokines in the heart during acute infection, day 15 p.i., are CXCL9, CXCL10, CCL2, and CCL5. Chemokine receptors expressed in the heart during acute infection or at day 30 p.i. are CCR1, CCR2, CCR5, and CXCR3. Of these, the most highly expressed chemokine receptors at day 15 p.i. are CCR2 and CCR5. Chemokine receptors CCR2, CCR5, and CXCR3 remain highly expressed in the heart during chronic infection at day 120 p.i.{09}Expression of chemokines and their cognate receptors during acute and chronic T. cruzi infection suggests that these molecules play a role in directing infiltration of mononuclear cells to the heart. Further, we show that macrophages are the primary source of chemokines CXCL9, CXCL10, and CCL5 at day 15 p.i., suggesting that these cells are important for the initiation of inflammation in the heart. Infection of mice deficient in chemokine receptors most highly expressed in the heart during T. cruzi infection, CCR5 and CCR2, show different roles for these receptors in host defense and cardiac inflammation. We find that CCR5 is important for control of parasite replication and survival during acute infection, as well as directing infiltration of macrophages and T cells to the heart early in infection, at day 15 p.i. In the absence of CCR5, infiltration of inflammatory cells to the heart is delayed, and is not apparent until day 30 p.i., suggesting that signaling by other chemokines/chemokine receptors compensate for the loss of CCR5 to direct inflammation to the heart by day 30 p.i. Further, once mononuclear cells have infiltrated the heart, CCR5 is not essential for the maintenance of inflammation during chronic infection. In contrast, CCR2 is not essential for infiltration of mononuclear cells in the heart at any time during acute or chronic infection. However, we do find that CCR2 contributes to control of cardiac parasitism during peak infection, at day 30 p.i. Lastly, we assessed the contribution of the most highly expressed chemokines found in the heart during both acute and chronic infection by developing neutralizing monoclonal antibodies (mAbs) against CXCL9, CXCL10, and CCL5, and administering them during infection through day 60 p.i. We find that activity by a single chemokine (CXCL10 or CCL5) or chemokines that share a common receptor (CXCL9 and CXLC10) is not essential for the infiltration of mononuclear cells to the heart during acute infection with T. cruzi. However, CXCL9 and CXCL10, in combination, are important for control of parasite burden during acute and early chronic infection, through day 49 p.i. Finally, neutralization of CXCL10, CXCL9 + CXCL10, or CCL5 does not reduce inflammation in the heart during chronic infection.
590 $a School code: 0030.
650 4 $a Health Sciences, Immunology. $3 1017716
650 4 $a Biology, Microbiology. $3 1017734
650 4 $a Biology, Molecular. $3 1017719
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710 2 0 $a University of California, Irvine. $3 705821
773 0 $t Dissertation Abstracts International $g 65-04B.
790 1 0 $a Manning, Jerry E., $e advisor
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791 $a Ph.D.
792 $a 2004
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3131525