Infection-induced coronary dysfunction and systemic inflammation in piglets are dampened in hypercholesterolemic milieu

Malene Muusfeldt Birck; Erkki Pesonen; Michal Odermarsky; Axel Jacob Kornerup Hansen; Kenneth Persson; Henriette Rønne Frikke-Schmidt; Peter M. H. Heegaard; Petru Liuba

doi:10.1152/ajpheart.01253.2010

Infection-induced coronary dysfunction and systemic inflammation in piglets are dampened in hypercholesterolemic milieu

Malene Muusfeldt Birck, Erkki Pesonen, Michal Odermarsky, Axel Jacob Kornerup Hansen, Kenneth Persson, Henriette Rønne Frikke-Schmidt, Peter M. H. Heegaard, Petru Liuba

14 Citationer (Scopus)

Abstract

The synergism of infection with conventional cardiovascular risk factors in atherosclerosis is much debated. We hypothesized that coronary arterial injury correlates with infection recurrence and pathogen burden and is further aggravated by hypercholesterolemia. Forty-two Göttingen minipigs were assigned to repeated intratracheal inoculation of PBS, Chlamydia pneumoniae (Cpn), or both Cpn and influenza virus at 8, 11, and 14 wk of age. Animals were fed either standard or 2% cholesterol diet (chol-diet). At 19 wk of age coronary vasomotor responses to acetylcholine (ACh) and adenosine were assessed in vivo and blood and tissue samples were collected. Nonparametric tests were used to compare the groups. In cholesterol-fed animals, total cholesterol/HDL was significantly increased in infected animals compared with noninfected animals [3.13 (2.17-3.38) vs. 2.03 (1.53- 2.41), respectively; P = 0.01]. C-reactive protein (CRP) rose in infected animals [10.60 (4.96 -18.00) vs. 2.47 (1.44 -3.01) μg/ml in noninfected; P < 0.01] without significant difference between the mono- and coinfected groups. Among coinfected animals, both CRP and haptoglobin were lower in those fed chol-diet than in those fed standard diet (P < 0.05). The vasoconstricting response to ACh was most prominent in coinfected animals {769.3 (594 -1,129) cm; P = 0.03 vs. noninfected [342 (309-455) cm] and P < 0.07 vs. monoinfected [415 (252.5-971.8) cm]}. Among monoinfected animals, similar to CRP, a trend for less vasoconstriction was observed in those fed chol-diet (P = 0.08). Coinfection of piglets appears to be associated with more pronounced coronary muscarinic vasomotor dysfunction. In monoinfected animals, use of chol-diet seems to dampen both coronary dysfunction and systemic inflammation induced by infection.

Originalsprog	Dansk
Tidsskrift	American Journal of Physiology: Heart and Circulatory Physiology
Vol/bind	300
Udgave nummer	5
Sider (fra-til)	H1595-H1601
Antal sider	7
ISSN	0363-6135
DOI	https://doi.org/10.1152/ajpheart.01253.2010
Status	Udgivet - maj 2011

Emneord

Det tidligere LIFE
Animal Model
Atherosclerosis
Pig
Infection
Cholesterol

Adgang til dokumentet

10.1152/ajpheart.01253.2010

Citationsformater

Birck, M. M., Pesonen, E., Odermarsky, M., Hansen, A. J. K., Persson, K., Frikke-Schmidt, H. R., Heegaard, P. M. H., & Liuba, P. (2011). Infection-induced coronary dysfunction and systemic inflammation in piglets are dampened in hypercholesterolemic milieu. American Journal of Physiology: Heart and Circulatory Physiology, 300(5), H1595-H1601. https://doi.org/10.1152/ajpheart.01253.2010

Infection-induced coronary dysfunction and systemic inflammation in piglets are dampened in hypercholesterolemic milieu. / Birck, Malene Muusfeldt; Pesonen, Erkki; Odermarsky, Michal et al.

I: American Journal of Physiology: Heart and Circulatory Physiology, Bind 300, Nr. 5, 05.2011, s. H1595-H1601.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

Birck, MM, Pesonen, E, Odermarsky, M, Hansen, AJK, Persson, K, Frikke-Schmidt, HR, Heegaard, PMH & Liuba, P 2011, 'Infection-induced coronary dysfunction and systemic inflammation in piglets are dampened in hypercholesterolemic milieu', American Journal of Physiology: Heart and Circulatory Physiology, bind 300, nr. 5, s. H1595-H1601. https://doi.org/10.1152/ajpheart.01253.2010

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title = "Infection-induced coronary dysfunction and systemic inflammation in piglets are dampened in hypercholesterolemic milieu",

abstract = "The synergism of infection with conventional cardiovascular risk factors in atherosclerosis is much debated. We hypothesized that coronary arterial injury correlates with infection recurrence and pathogen burden and is further aggravated by hypercholesterolemia. Forty-two G{\"o}ttingen minipigs were assigned to repeated intratracheal inoculation of PBS, Chlamydia pneumoniae (Cpn), or both Cpn and influenza virus at 8, 11, and 14 wk of age. Animals were fed either standard or 2% cholesterol diet (chol-diet). At 19 wk of age coronary vasomotor responses to acetylcholine (ACh) and adenosine were assessed in vivo and blood and tissue samples were collected. Nonparametric tests were used to compare the groups. In cholesterol-fed animals, total cholesterol/HDL was significantly increased in infected animals compared with noninfected animals [3.13 (2.17-3.38) vs. 2.03 (1.53- 2.41), respectively; P = 0.01]. C-reactive protein (CRP) rose in infected animals [10.60 (4.96 -18.00) vs. 2.47 (1.44 -3.01) μg/ml in noninfected; P < 0.01] without significant difference between the mono- and coinfected groups. Among coinfected animals, both CRP and haptoglobin were lower in those fed chol-diet than in those fed standard diet (P < 0.05). The vasoconstricting response to ACh was most prominent in coinfected animals {769.3 (594 -1,129) cm; P = 0.03 vs. noninfected [342 (309-455) cm] and P < 0.07 vs. monoinfected [415 (252.5-971.8) cm]}. Among monoinfected animals, similar to CRP, a trend for less vasoconstriction was observed in those fed chol-diet (P = 0.08). Coinfection of piglets appears to be associated with more pronounced coronary muscarinic vasomotor dysfunction. In monoinfected animals, use of chol-diet seems to dampen both coronary dysfunction and systemic inflammation induced by infection.",

keywords = "Det tidligere LIFE, Animal Model, Atherosclerosis, Pig, Infection, Cholesterol",

author = "Birck, {Malene Muusfeldt} and Erkki Pesonen and Michal Odermarsky and Hansen, {Axel Jacob Kornerup} and Kenneth Persson and Frikke-Schmidt, {Henriette R{\o}nne} and Heegaard, {Peter M. H.} and Petru Liuba",

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T1 - Infection-induced coronary dysfunction and systemic inflammation in piglets are dampened in hypercholesterolemic milieu

AU - Birck, Malene Muusfeldt

AU - Pesonen, Erkki

AU - Odermarsky, Michal

AU - Hansen, Axel Jacob Kornerup

AU - Persson, Kenneth

AU - Frikke-Schmidt, Henriette Rønne

AU - Heegaard, Peter M. H.

AU - Liuba, Petru

PY - 2011/5

Y1 - 2011/5

N2 - The synergism of infection with conventional cardiovascular risk factors in atherosclerosis is much debated. We hypothesized that coronary arterial injury correlates with infection recurrence and pathogen burden and is further aggravated by hypercholesterolemia. Forty-two Göttingen minipigs were assigned to repeated intratracheal inoculation of PBS, Chlamydia pneumoniae (Cpn), or both Cpn and influenza virus at 8, 11, and 14 wk of age. Animals were fed either standard or 2% cholesterol diet (chol-diet). At 19 wk of age coronary vasomotor responses to acetylcholine (ACh) and adenosine were assessed in vivo and blood and tissue samples were collected. Nonparametric tests were used to compare the groups. In cholesterol-fed animals, total cholesterol/HDL was significantly increased in infected animals compared with noninfected animals [3.13 (2.17-3.38) vs. 2.03 (1.53- 2.41), respectively; P = 0.01]. C-reactive protein (CRP) rose in infected animals [10.60 (4.96 -18.00) vs. 2.47 (1.44 -3.01) μg/ml in noninfected; P < 0.01] without significant difference between the mono- and coinfected groups. Among coinfected animals, both CRP and haptoglobin were lower in those fed chol-diet than in those fed standard diet (P < 0.05). The vasoconstricting response to ACh was most prominent in coinfected animals {769.3 (594 -1,129) cm; P = 0.03 vs. noninfected [342 (309-455) cm] and P < 0.07 vs. monoinfected [415 (252.5-971.8) cm]}. Among monoinfected animals, similar to CRP, a trend for less vasoconstriction was observed in those fed chol-diet (P = 0.08). Coinfection of piglets appears to be associated with more pronounced coronary muscarinic vasomotor dysfunction. In monoinfected animals, use of chol-diet seems to dampen both coronary dysfunction and systemic inflammation induced by infection.

AB - The synergism of infection with conventional cardiovascular risk factors in atherosclerosis is much debated. We hypothesized that coronary arterial injury correlates with infection recurrence and pathogen burden and is further aggravated by hypercholesterolemia. Forty-two Göttingen minipigs were assigned to repeated intratracheal inoculation of PBS, Chlamydia pneumoniae (Cpn), or both Cpn and influenza virus at 8, 11, and 14 wk of age. Animals were fed either standard or 2% cholesterol diet (chol-diet). At 19 wk of age coronary vasomotor responses to acetylcholine (ACh) and adenosine were assessed in vivo and blood and tissue samples were collected. Nonparametric tests were used to compare the groups. In cholesterol-fed animals, total cholesterol/HDL was significantly increased in infected animals compared with noninfected animals [3.13 (2.17-3.38) vs. 2.03 (1.53- 2.41), respectively; P = 0.01]. C-reactive protein (CRP) rose in infected animals [10.60 (4.96 -18.00) vs. 2.47 (1.44 -3.01) μg/ml in noninfected; P < 0.01] without significant difference between the mono- and coinfected groups. Among coinfected animals, both CRP and haptoglobin were lower in those fed chol-diet than in those fed standard diet (P < 0.05). The vasoconstricting response to ACh was most prominent in coinfected animals {769.3 (594 -1,129) cm; P = 0.03 vs. noninfected [342 (309-455) cm] and P < 0.07 vs. monoinfected [415 (252.5-971.8) cm]}. Among monoinfected animals, similar to CRP, a trend for less vasoconstriction was observed in those fed chol-diet (P = 0.08). Coinfection of piglets appears to be associated with more pronounced coronary muscarinic vasomotor dysfunction. In monoinfected animals, use of chol-diet seems to dampen both coronary dysfunction and systemic inflammation induced by infection.

KW - Det tidligere LIFE

KW - Animal Model

KW - Atherosclerosis

KW - Pig

KW - Infection

KW - Cholesterol

U2 - 10.1152/ajpheart.01253.2010

DO - 10.1152/ajpheart.01253.2010

M3 - Tidsskriftartikel

C2 - 21357512

SN - 0363-6135

VL - 300

SP - H1595-H1601

JO - American Journal of Physiology - Heart and Circulatory Physiology

JF - American Journal of Physiology - Heart and Circulatory Physiology

IS - 5

ER -