Maintenance of NF-κB activation in T-lymphocytes and a naive T-cell population in autoimmune-prone (NZB/NZW)F1 mice by feeding a food-restricted diet enriched with n-3 fatty acids

Christopher A. Jolly, Alagarraju Muthukumar, C. P. Reddy Avula, Gabriel Fernandes

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

We have previously shown that feeding a fish oil (FO) supplemented diet in combination with 40% food restriction (FO/FR) has a greater impact on extending life span in lupus-prone (NZB × NZW)F1 mice than either FO ad libitum (FO/AL) or corn oil food restricted (CO/FR) alone. Lupus disease is associated with increased Th-2 (i.e., IL-6 and IL-10) cytokine production and reduced IL-2 production and NF-κB activation. We hypothesized that the mechanism of action by which FO/FR increases life span may involve alterations in T-lymphocyte signaling and subsequent cytokine production. To test this hypothesis, we isolated and then stimulated splenic T-lymphocytes ex vivo with anti-CD3 and -CD28 monoclonal antibodies. We report here that CO/FR and FO/FR and to a lesser extent FO/AL offset disease-associated losses in Th-1 cytokine production, CD69 expression, and NF-κB activation in splenic T-lymphocytes activated ex vivo. Similarly, CO/FR and FO/FR prevented the disease-dependent rise in Th-2 cytokine production ex vivo and CD69 expression in vivo. In essence, the T-lymphocyte phenotype in the old CO/FR and FO/FR groups was identical to that in the young disease-free mice. Taken together, the data suggest that both CO/FR and FO/FR increase life span, in part, by maintaining a youthful immune phenotype in autoimmune-prone mice. However, FO/FR appears to represent a more potent dietary strategy in delaying disease-associated immune dysregulation than CO/FR.

Original languageEnglish (US)
Pages (from-to)122-133
Number of pages12
JournalCellular Immunology
Volume213
Issue number2
DOIs
StatePublished - Nov 1 2001

Fingerprint

Fish Oils
Omega-3 Fatty Acids
Maintenance
Corn Oil
Diet
T-Lymphocytes
Food
Population
Cytokines
Phenotype
Immune System Diseases
Interleukin-10
Interleukin-2
Interleukin-6
Monoclonal Antibodies

ASJC Scopus subject areas

  • Cell Biology
  • Immunology

Cite this

Maintenance of NF-κB activation in T-lymphocytes and a naive T-cell population in autoimmune-prone (NZB/NZW)F1 mice by feeding a food-restricted diet enriched with n-3 fatty acids. / Jolly, Christopher A.; Muthukumar, Alagarraju; Reddy Avula, C. P.; Fernandes, Gabriel.

In: Cellular Immunology, Vol. 213, No. 2, 01.11.2001, p. 122-133.

Research output: Contribution to journalArticle

@article{f27404e5fe1f4a589769f9e8b42f7687,
title = "Maintenance of NF-κB activation in T-lymphocytes and a naive T-cell population in autoimmune-prone (NZB/NZW)F1 mice by feeding a food-restricted diet enriched with n-3 fatty acids",
abstract = "We have previously shown that feeding a fish oil (FO) supplemented diet in combination with 40{\%} food restriction (FO/FR) has a greater impact on extending life span in lupus-prone (NZB × NZW)F1 mice than either FO ad libitum (FO/AL) or corn oil food restricted (CO/FR) alone. Lupus disease is associated with increased Th-2 (i.e., IL-6 and IL-10) cytokine production and reduced IL-2 production and NF-κB activation. We hypothesized that the mechanism of action by which FO/FR increases life span may involve alterations in T-lymphocyte signaling and subsequent cytokine production. To test this hypothesis, we isolated and then stimulated splenic T-lymphocytes ex vivo with anti-CD3 and -CD28 monoclonal antibodies. We report here that CO/FR and FO/FR and to a lesser extent FO/AL offset disease-associated losses in Th-1 cytokine production, CD69 expression, and NF-κB activation in splenic T-lymphocytes activated ex vivo. Similarly, CO/FR and FO/FR prevented the disease-dependent rise in Th-2 cytokine production ex vivo and CD69 expression in vivo. In essence, the T-lymphocyte phenotype in the old CO/FR and FO/FR groups was identical to that in the young disease-free mice. Taken together, the data suggest that both CO/FR and FO/FR increase life span, in part, by maintaining a youthful immune phenotype in autoimmune-prone mice. However, FO/FR appears to represent a more potent dietary strategy in delaying disease-associated immune dysregulation than CO/FR.",
author = "Jolly, {Christopher A.} and Alagarraju Muthukumar and {Reddy Avula}, {C. P.} and Gabriel Fernandes",
year = "2001",
month = "11",
day = "1",
doi = "10.1006/cimm.2001.1866",
language = "English (US)",
volume = "213",
pages = "122--133",
journal = "Cellular Immunology",
issn = "0008-8749",
publisher = "Academic Press Inc.",
number = "2",

}

TY - JOUR

T1 - Maintenance of NF-κB activation in T-lymphocytes and a naive T-cell population in autoimmune-prone (NZB/NZW)F1 mice by feeding a food-restricted diet enriched with n-3 fatty acids

AU - Jolly, Christopher A.

AU - Muthukumar, Alagarraju

AU - Reddy Avula, C. P.

AU - Fernandes, Gabriel

PY - 2001/11/1

Y1 - 2001/11/1

N2 - We have previously shown that feeding a fish oil (FO) supplemented diet in combination with 40% food restriction (FO/FR) has a greater impact on extending life span in lupus-prone (NZB × NZW)F1 mice than either FO ad libitum (FO/AL) or corn oil food restricted (CO/FR) alone. Lupus disease is associated with increased Th-2 (i.e., IL-6 and IL-10) cytokine production and reduced IL-2 production and NF-κB activation. We hypothesized that the mechanism of action by which FO/FR increases life span may involve alterations in T-lymphocyte signaling and subsequent cytokine production. To test this hypothesis, we isolated and then stimulated splenic T-lymphocytes ex vivo with anti-CD3 and -CD28 monoclonal antibodies. We report here that CO/FR and FO/FR and to a lesser extent FO/AL offset disease-associated losses in Th-1 cytokine production, CD69 expression, and NF-κB activation in splenic T-lymphocytes activated ex vivo. Similarly, CO/FR and FO/FR prevented the disease-dependent rise in Th-2 cytokine production ex vivo and CD69 expression in vivo. In essence, the T-lymphocyte phenotype in the old CO/FR and FO/FR groups was identical to that in the young disease-free mice. Taken together, the data suggest that both CO/FR and FO/FR increase life span, in part, by maintaining a youthful immune phenotype in autoimmune-prone mice. However, FO/FR appears to represent a more potent dietary strategy in delaying disease-associated immune dysregulation than CO/FR.

AB - We have previously shown that feeding a fish oil (FO) supplemented diet in combination with 40% food restriction (FO/FR) has a greater impact on extending life span in lupus-prone (NZB × NZW)F1 mice than either FO ad libitum (FO/AL) or corn oil food restricted (CO/FR) alone. Lupus disease is associated with increased Th-2 (i.e., IL-6 and IL-10) cytokine production and reduced IL-2 production and NF-κB activation. We hypothesized that the mechanism of action by which FO/FR increases life span may involve alterations in T-lymphocyte signaling and subsequent cytokine production. To test this hypothesis, we isolated and then stimulated splenic T-lymphocytes ex vivo with anti-CD3 and -CD28 monoclonal antibodies. We report here that CO/FR and FO/FR and to a lesser extent FO/AL offset disease-associated losses in Th-1 cytokine production, CD69 expression, and NF-κB activation in splenic T-lymphocytes activated ex vivo. Similarly, CO/FR and FO/FR prevented the disease-dependent rise in Th-2 cytokine production ex vivo and CD69 expression in vivo. In essence, the T-lymphocyte phenotype in the old CO/FR and FO/FR groups was identical to that in the young disease-free mice. Taken together, the data suggest that both CO/FR and FO/FR increase life span, in part, by maintaining a youthful immune phenotype in autoimmune-prone mice. However, FO/FR appears to represent a more potent dietary strategy in delaying disease-associated immune dysregulation than CO/FR.

UR - http://www.scopus.com/inward/record.url?scp=0035498438&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035498438&partnerID=8YFLogxK

U2 - 10.1006/cimm.2001.1866

DO - 10.1006/cimm.2001.1866

M3 - Article

C2 - 11831874

AN - SCOPUS:0035498438

VL - 213

SP - 122

EP - 133

JO - Cellular Immunology

JF - Cellular Immunology

SN - 0008-8749

IS - 2

ER -