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Lack of enteral nutrition blunts extracellular-regulated kinase phosphorylation in gut-associated lymphoid tissue

Yoshinori Maeshima1, Kazuhiko Fukatsu, Woodae Kang

  • 1Department of Surgery, National Defense Medical College Research Institute, Saitama, Japan.

Shock (Augusta, Ga.)
|February 17, 2007
PubMed

Insights

Lack of enteral nutrition impairs gut-associated lymphoid tissue (GALT) function by reducing extracellular signal-regulated kinase (ERK) activation and cell proliferation in effector sites. This highlights a key mechanism behind compromised host defense without gut feeding.

Area of Science:

  • Immunology
  • Gastroenterology
  • Nutrition Science

Background:

  • Mitogen-activated protein kinase (MAPK) signaling pathways, including extracellular signal-regulated kinase (ERK) and p38, are crucial for immune cell function and host defense.
  • Gut-associated lymphoid tissue (GALT) plays a vital role in intestinal immunity, and its function may be influenced by nutritional status.
  • Impaired GALT function is suspected in the absence of enteral nutrition, potentially linked to altered MAPK signaling.

Purpose of the Study:

  • To investigate the hypothesis that impaired GALT function due to lack of enteral nutrition is associated with reduced MAPK phosphorylation in GALT cells.
  • To compare the effects of ad libitum chow, intragastric (i.g.)-total parenteral nutrition (TPN), and intravenous (i.v.)-TPN on MAPK phosphorylation and lymphocyte proliferation in GALT.

Main Methods:

  • Male Institute of Cancer Research mice were randomized into three groups: ad libitum chow, i.g.-TPN, and i.v.-TPN for 5 days.
  • Lymphocytes were isolated from Peyer patches (PPs), lamina propria (LP), and intraepithelial (IE) spaces.
  • Phosphorylated ERK (p-ERK) and p38 (p-p38) levels were measured using laser scanning cytometry after phorbol myristate acetate (PMA) stimulation. In vitro lymphocyte proliferation was assessed using BrdU.

Main Results:

  • ERK phosphorylation increased after PMA stimulation in PP lymphocytes across all groups.
  • PMA-induced ERK phosphorylation in GALT effector sites (IE and LP) was enhanced only in the enteral feeding groups (chow and i.g.-TPN).
  • p38 phosphorylation did not increase in response to PMA in any GALT site or feeding group. Lymphocyte proliferation was maintained in chow and i.g.-TPN groups but remained low in the i.v.-TPN group.

Conclusions:

  • The absence of enteral feeding blunts ERK activation and cell proliferation in response to stimulation in GALT effector sites.
  • This reduction in ERK signaling and proliferation may be a significant mechanism contributing to impaired GALT function without enteral nutrition.
  • Further research is needed to assess the influence of nutrition on GALT p38 phosphorylation using different stimulants.

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