Gut lymphocyte phenotype changes after parenteral nutrition and neuropeptide administration

Mark A. Jonker, Aaron F. Heneghan, John H. Fechner, Joseph Pierre, Yoshifumi Sano, Jinggang Lan, Kenneth A. Kudsk

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Objective: To define gut-associated lymphoid tissue (GALT) phenotype changes with parenteral nutrition (PN) and PN with bombesin (BBS). Background: PN reduces respiratory tract (RT) and GALT Peyer patch and lamina propria lymphocytes, lowers gut and RT immunoglobulin A (IgA) levels, and destroys established RT antiviral and antibacterial immunity. BBS, an enteric nervous system neuropeptide, reverses PN-induced IgA and RT immune defects. Methods: Experiment 1: Intravenously cannulated ICR mice received chow, PN, or PN + BBS injections for 5 days. LSR-II flow cytometer analyzed Peyer patches and lamina propria isolated lymphocytes for homing phenotypes (L-selectin + and LPAM-1 + ) and state of activation (CD25 + , CD44 + ) in T (CD3 + )-cell subsets (CD4 + and CD8 + ) along with homing phenotype (L-selectin + and LPAM-1 + ) in naive B (IgD + ) and antigen-activated (IgD-or IgM + ) B (CD45R/B220 + ) cells. Experiment 2: Following the initial experiment 1 protocol, lamina propria T regulatory cell phenotype was evaluated by Foxp3 expression. Results: Experiment 1: PN significantly reduced lamina propria (1) CD4 + CD25 + (activated) and (2) CD4 + CD25 + LPAM-1 + (activated cells homed to the lamina propria) T cells, whereas PN-BBS assimilated chow levels. PN significantly reduced lamina propria (1) IgD + (naive), (2) IgD-LPAM + (antigen-activated homed to the lamina propria) and CD44 + memory B cells, whereas PN-BBS assimilated chow levels. Experiment 2: PN significantly reduced lamina propria CD4 + CD25 + Foxp3 + T regulatory cells compared with chow-fed mice, whereas PN + BBS assimilated chow levels. Conclusions: PN reduces lamina propria activated and T regulatory cells and also naive and memory B cells. BBS addition to PN maintains these cell phenotypes, demonstrating the intimate involvement of the enteric nervous system in mucosal immunity.

Original languageEnglish (US)
Pages (from-to)194-201
Number of pages8
JournalAnnals of surgery
Volume262
Issue number1
DOIs
StatePublished - Jul 1 2015

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Parenteral Nutrition
Neuropeptides
Lymphocytes
Phenotype
Bombesin
Mucous Membrane
Immunoglobulin D
Respiratory System
Regulatory T-Lymphocytes
Enteric Nervous System
L-Selectin
Peyer's Patches
Lymphoid Tissue
Immunoglobulin A
B-Lymphocytes
Antigens
Mucosal Immunity
Inbred ICR Mouse
T-Lymphocyte Subsets
Antiviral Agents

All Science Journal Classification (ASJC) codes

  • Surgery

Cite this

Jonker, M. A., Heneghan, A. F., Fechner, J. H., Pierre, J., Sano, Y., Lan, J., & Kudsk, K. A. (2015). Gut lymphocyte phenotype changes after parenteral nutrition and neuropeptide administration. Annals of surgery, 262(1), 194-201. https://doi.org/10.1097/SLA.0000000000000878

Gut lymphocyte phenotype changes after parenteral nutrition and neuropeptide administration. / Jonker, Mark A.; Heneghan, Aaron F.; Fechner, John H.; Pierre, Joseph; Sano, Yoshifumi; Lan, Jinggang; Kudsk, Kenneth A.

In: Annals of surgery, Vol. 262, No. 1, 01.07.2015, p. 194-201.

Research output: Contribution to journalArticle

Jonker, MA, Heneghan, AF, Fechner, JH, Pierre, J, Sano, Y, Lan, J & Kudsk, KA 2015, 'Gut lymphocyte phenotype changes after parenteral nutrition and neuropeptide administration', Annals of surgery, vol. 262, no. 1, pp. 194-201. https://doi.org/10.1097/SLA.0000000000000878
Jonker, Mark A. ; Heneghan, Aaron F. ; Fechner, John H. ; Pierre, Joseph ; Sano, Yoshifumi ; Lan, Jinggang ; Kudsk, Kenneth A. / Gut lymphocyte phenotype changes after parenteral nutrition and neuropeptide administration. In: Annals of surgery. 2015 ; Vol. 262, No. 1. pp. 194-201.
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abstract = "Objective: To define gut-associated lymphoid tissue (GALT) phenotype changes with parenteral nutrition (PN) and PN with bombesin (BBS). Background: PN reduces respiratory tract (RT) and GALT Peyer patch and lamina propria lymphocytes, lowers gut and RT immunoglobulin A (IgA) levels, and destroys established RT antiviral and antibacterial immunity. BBS, an enteric nervous system neuropeptide, reverses PN-induced IgA and RT immune defects. Methods: Experiment 1: Intravenously cannulated ICR mice received chow, PN, or PN + BBS injections for 5 days. LSR-II flow cytometer analyzed Peyer patches and lamina propria isolated lymphocytes for homing phenotypes (L-selectin + and LPAM-1 + ) and state of activation (CD25 + , CD44 + ) in T (CD3 + )-cell subsets (CD4 + and CD8 + ) along with homing phenotype (L-selectin + and LPAM-1 + ) in naive B (IgD + ) and antigen-activated (IgD-or IgM + ) B (CD45R/B220 + ) cells. Experiment 2: Following the initial experiment 1 protocol, lamina propria T regulatory cell phenotype was evaluated by Foxp3 expression. Results: Experiment 1: PN significantly reduced lamina propria (1) CD4 + CD25 + (activated) and (2) CD4 + CD25 + LPAM-1 + (activated cells homed to the lamina propria) T cells, whereas PN-BBS assimilated chow levels. PN significantly reduced lamina propria (1) IgD + (naive), (2) IgD-LPAM + (antigen-activated homed to the lamina propria) and CD44 + memory B cells, whereas PN-BBS assimilated chow levels. Experiment 2: PN significantly reduced lamina propria CD4 + CD25 + Foxp3 + T regulatory cells compared with chow-fed mice, whereas PN + BBS assimilated chow levels. Conclusions: PN reduces lamina propria activated and T regulatory cells and also naive and memory B cells. BBS addition to PN maintains these cell phenotypes, demonstrating the intimate involvement of the enteric nervous system in mucosal immunity.",
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AU - Jonker, Mark A.

AU - Heneghan, Aaron F.

AU - Fechner, John H.

AU - Pierre, Joseph

AU - Sano, Yoshifumi

AU - Lan, Jinggang

AU - Kudsk, Kenneth A.

PY - 2015/7/1

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N2 - Objective: To define gut-associated lymphoid tissue (GALT) phenotype changes with parenteral nutrition (PN) and PN with bombesin (BBS). Background: PN reduces respiratory tract (RT) and GALT Peyer patch and lamina propria lymphocytes, lowers gut and RT immunoglobulin A (IgA) levels, and destroys established RT antiviral and antibacterial immunity. BBS, an enteric nervous system neuropeptide, reverses PN-induced IgA and RT immune defects. Methods: Experiment 1: Intravenously cannulated ICR mice received chow, PN, or PN + BBS injections for 5 days. LSR-II flow cytometer analyzed Peyer patches and lamina propria isolated lymphocytes for homing phenotypes (L-selectin + and LPAM-1 + ) and state of activation (CD25 + , CD44 + ) in T (CD3 + )-cell subsets (CD4 + and CD8 + ) along with homing phenotype (L-selectin + and LPAM-1 + ) in naive B (IgD + ) and antigen-activated (IgD-or IgM + ) B (CD45R/B220 + ) cells. Experiment 2: Following the initial experiment 1 protocol, lamina propria T regulatory cell phenotype was evaluated by Foxp3 expression. Results: Experiment 1: PN significantly reduced lamina propria (1) CD4 + CD25 + (activated) and (2) CD4 + CD25 + LPAM-1 + (activated cells homed to the lamina propria) T cells, whereas PN-BBS assimilated chow levels. PN significantly reduced lamina propria (1) IgD + (naive), (2) IgD-LPAM + (antigen-activated homed to the lamina propria) and CD44 + memory B cells, whereas PN-BBS assimilated chow levels. Experiment 2: PN significantly reduced lamina propria CD4 + CD25 + Foxp3 + T regulatory cells compared with chow-fed mice, whereas PN + BBS assimilated chow levels. Conclusions: PN reduces lamina propria activated and T regulatory cells and also naive and memory B cells. BBS addition to PN maintains these cell phenotypes, demonstrating the intimate involvement of the enteric nervous system in mucosal immunity.

AB - Objective: To define gut-associated lymphoid tissue (GALT) phenotype changes with parenteral nutrition (PN) and PN with bombesin (BBS). Background: PN reduces respiratory tract (RT) and GALT Peyer patch and lamina propria lymphocytes, lowers gut and RT immunoglobulin A (IgA) levels, and destroys established RT antiviral and antibacterial immunity. BBS, an enteric nervous system neuropeptide, reverses PN-induced IgA and RT immune defects. Methods: Experiment 1: Intravenously cannulated ICR mice received chow, PN, or PN + BBS injections for 5 days. LSR-II flow cytometer analyzed Peyer patches and lamina propria isolated lymphocytes for homing phenotypes (L-selectin + and LPAM-1 + ) and state of activation (CD25 + , CD44 + ) in T (CD3 + )-cell subsets (CD4 + and CD8 + ) along with homing phenotype (L-selectin + and LPAM-1 + ) in naive B (IgD + ) and antigen-activated (IgD-or IgM + ) B (CD45R/B220 + ) cells. Experiment 2: Following the initial experiment 1 protocol, lamina propria T regulatory cell phenotype was evaluated by Foxp3 expression. Results: Experiment 1: PN significantly reduced lamina propria (1) CD4 + CD25 + (activated) and (2) CD4 + CD25 + LPAM-1 + (activated cells homed to the lamina propria) T cells, whereas PN-BBS assimilated chow levels. PN significantly reduced lamina propria (1) IgD + (naive), (2) IgD-LPAM + (antigen-activated homed to the lamina propria) and CD44 + memory B cells, whereas PN-BBS assimilated chow levels. Experiment 2: PN significantly reduced lamina propria CD4 + CD25 + Foxp3 + T regulatory cells compared with chow-fed mice, whereas PN + BBS assimilated chow levels. Conclusions: PN reduces lamina propria activated and T regulatory cells and also naive and memory B cells. BBS addition to PN maintains these cell phenotypes, demonstrating the intimate involvement of the enteric nervous system in mucosal immunity.

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