The effect of adding fish oil to parenteral nutrition on hepatic mononuclear cell function and survival after intraportal bacterial challenge in mice.

Background: Parenteral nutrition (PN) is indispensable for meeting caloric and substrate needs of patients who cannot receive adequate amounts of enteral nutrition; however, PN impairs hepatic immunity. We examined the effects of ω-3 and -6 polyunsaturated fatty acids, added individually to fat-free PN, on hepatic immunity in a murine model. We focused on serum liver enzymes, cytokine production, histopathology, and the outcomes after intraportal bacterial challenge.

Influence of adding pyrroloquinoline quinone to parenteral nutrition on gut-associated lymphoid tissue.

Background: Experimental intravenous (IV) parenteral nutrition (PN) diminishes gut-associated lymphoid tissue (GALT) cell number and function. PN solution cannot maintain GALT at the same level as a normal diet, even when delivered intragastrically (IG). Previous studies demonstrated pyrroloquinoline quinone (PQQ)-deficient mice to be less immunologically responsive.

Neutrophil elastase inhibitor restores gut ischemia reperfusion-induced impairment of gut immunity with reduced plasma interleukin-6 concentrations in mice.

Background And Purpose: Gut-associated lymphoid tissue (GALT) is regarded as central mucosa-associated lymphoid tissue that influences systemic mucosal immunity. Our previous study revealed that gut ischemia and reperfusion (I/R) reduces GALT lymphocyte numbers. Because gut hypoperfusion frequently occurs in trauma, shock, and surgery patients, establishment of a therapeutic method to preserve GALT mass after gut I/R may be important for the prevention of infections.

Arginine-enriched total parenteral nutrition improves survival in peritonitis by normalizing NFkappaB activation in peritoneal resident and exudative leukocytes.

Background: Enteral nutrition maintains peritoneal defense more effectively than parenteral nutrition, at least partly by preserving NFkappaB activation in peritoneal cells. We hypothesized that arginine (ARG)-enriched parenteral nutrition would normalize NFkappaB activation in peritoneal leukocytes, thereby improving the survival of peritonitis models.

Methods: A total of 105 ICR mice were randomized to chow (n=33), IV feeding of a standard (STD) total parenteral nutrition (STD-TPN) solution (ARG 0.

Parenteral feeding depletes pulmonary lymphocyte populations.

Background: The effect of parenteral nutrition (PN) on lymphocyte mass in the lung is unknown, but reduced mucosal lymphocytes are hypothesized to play a role in the reduced immunoglobulin A-mediated immunity in both gut and lung. The ability to transfer and track cells between mice may allow study of diet-induced mucosal immune function. The objectives of this study are to characterize lung T-cell populations following parenteral feeding and to study distribution patterns of transferred donor lung T cells in recipient mice.

Enteral nutrition rapidly reverses total parenteral nutrition-induced impairment of hepatic immunity in a murine model.

Background & Aims: Total parenteral nutrition (TPN) impairs host immunocompetence, a mechanism possibly underlying the high morbidity of infectious complications in critically ill patients. Our recent study demonstrated TPN to reduce the number and function of hepatic mononuclear cells (MNCs) and to worsen survival after intraportal Pseudomonas challenge in mice. The present study examined the duration of enteral nutrition (EN) needed to reverse TPN-induced changes in hepatic MNCs in a murine model.

Parenteral nutrition maintains pulmonary IgA antibody transport capacity, but not active transport, following injury.

Background: Parenteral nutrition (PN) increases post-trauma pneumonia versus enteral feeding. PN impairs murine immunoglobulin A (IgA) airway defenses and abrogates a normal IgA increase following injury. This work investigates the effect of type/route of nutrition on lung IgA and its transport protein, polymeric immunoglobulin receptor (pIgR), after injury.

Reversal of parenteral nutrition-induced gut mucosal immunity impairment with small amounts of a complex enteral diet.

Background: Although parenteral nutrition (PN) prevents progressive malnutrition, lack of enteral nutrition (EN) during PN leads to gut associated lymphoid tissue (GALT) atrophy and dysfunction. Administering a small amount of EN with PN reportedly prevents increases in intestinal permeability. However, its effects on GALT remain unclear.

Parenteral nutrition induces organ specific alterations in polymeric immunoglobulin receptor levels.

Background: Secretory immunoglobulin A (IgA) prevents pathogen adherence at mucosal surfaces to prevent infection. Polymeric immunoglobulin receptor (pIgR), located on the basolateral surface of mucosal cells, binds dimeric IgA produced by B cells with the cooperation of T cells in the lamina propria. This IgA-pIgR complex is transported apically, where it is exocytosed as secretory IgA to the mucosal surface.

Parenteral nutrition inhibits tumor necrosis factor-alpha-mediated IgA response to injury.

Background: Parenteral nutrition (PN) increases the incidence of pneumonia in severely injured patients compared with enteral feeding (ENT). Injury induces an innate airway IgA response in severely injured patients; similar responses occur in mice. Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1beta) stimulate the production of polymeric immunoglobulin receptor (pIgR), the protein required to transport immunoglobulin A (IgA) to mucosal surfaces.

Detrimental effects of early nutrition administration after severe gut ischemia-reperfusion.

Background: Although early enteral nutrition after insult has many advantages, effects of early nutritional manipulation on outcome after gut ischemia-reperfusion (I/R) remain unclear. We hypothesize that early enteral nutrition would improve survival after severe gut I/R by reducing organ injury and leukocyte activation.

Materials And Methods: Mice were randomized to chow, intravenous (IV)-total parenteral nutrition (TPN), intragastric (IG)-TPN, or complex enteral diet (CED) for feeding after I/R.

Fish oil infusion reverses 5-fluorouracil-induced impairments in mucosal immunity in mice.

Background & Aims: Anticancer drugs frequently have deleterious effects on host defense against infection, limiting their clinical application. We previously demonstrated continuous infusion of 5-fluorouracil (5FU) to reduce gut associated lymphoid tissue (GALT) mass and secretory IgA levels. This study was designed to examine the effects of concomitant infusion of fish oil on gut mucosal immunity in mice receiving 5FU.

Decreased enteral stimulation alters mucosal immune chemokines.

Background: Migration of lymphocytes into and through the mucosal immune system depends upon adhesion molecules to attract circulating cells and chemokines to stimulate diapedesis into tissues. Decreased enteral stimulation significantly reduces mucosal addressin cellular adhesion molecule-1 (MAdCAM-1) levels, an adhesion molecule critical for homing of T and B cells to Peyer's patches (PP), which reduces PP and intestinal T and B cells. We studied the effect of type and route of nutrition on tissue specific chemokines in PP (CXCL-12, -13 and CCL-19, -20 and -21), small intestine (SI; CCL-20, -25 and -28) and lung (CXCL-12, CCL-28).

Intraluminal glutamine administration during ischemia worsens survival after gut ischemia-reperfusion.

Background: Glutamine (GLN) treatment prior to gut ischemia-reperfusion (I/R) reportedly preserves gut glutathione levels and gut barrier function. We hypothesized that intraluminal GLN during ischemia would also protect against gut I/R.

Material And Methods: After randomization to control and GLN groups, mice were exposed to 75 min (Exp 1) or 50 min (Exp 2 and 3) gut I/R.

Influence of adding fish oil to parenteral nutrition on gut-associated lymphoid tissue.

Background: Lack of enteral nutrition reduces gut-associated lymphoid tissue (GALT) mass and function, a mechanism underlying the increased morbidity of infectious complications in severely injured or critically ill patients. Strategies to restore parenteral nutrition (PN)-induced changes of GALT mass and function have been pursued. However, the influences of adding fish oil to PN on gut immunity remain to be clarified.

Effects of lymphotoxin beta receptor blockade on intestinal mucosal immunity.

Background: Mucosal addressin cellular adhesion molecule-1 (MAdCAM-1) directs lymphocyte migration into gut-associated lymphoid tissue (GALT) through Peyer's patches (PPs). Parenteral nutrition (PN) impairs mucosal immunity by reducing PPs MAdCAM-1 expression, T and B cells in GALT, and intestinal and respiratory immunoglobulin (Ig) A levels. We previously showed that PN reduces lymphotoxin beta receptor blockade (LTbetaR) in PPs and intestine, and that stimulation with LTbetaR agonist antibodies reverses these defects.

Intestinal polymeric immunoglobulin receptor is affected by type and route of nutrition.

Background: Secretory immunoglobulin A (SIgA) prevents adherence of pathogens at mucosal surfaces to prevent invasive infection. Polymeric immunoglobulin receptor (pIgR) is located on the basolateral surface of epithelial cells and binds dimeric immunoglobulin A (IgA) produced by plasma cells in the lamina propria. This IgA-pIgR complex is transported apically, where IgA is exocytosed as SIgA to the mucosal surface.

Nutritional route affects ERK phosphorylation and cytokine production in hepatic mononuclear cells.

Objective: To clarify the influence of nutritional route on hepatic immunity in a murine model.

Summary Background Data: Parenteral nutrition is disadvantageous for preventing infectious complications in critically ill and/or severely injured patients as compared with enteral nutrition. To date, lack of enteral nutrition has been demonstrated to impair mucosal immunity, gut barrier function, and the peritoneal defense system.

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

The mitogen-activated protein kinase (MAPK) family (extracellular-regulated kinase [ERK], p38, etc.) of signal transduction proteins includes important intracellular mediators of inflammation, playing critical roles in host defense. Phosphorylations of ERK and p38 are responsible for cell proliferation, cell differentiation, and cell death.

Influences of long-term antibiotic administration on Peyer's patch lymphocytes and mucosal immunoglobulin A levels in a mouse model.

Background: Long-term antibiotic administration is sometimes necessary to control bacterial infections during the perioperative period. However, antibiotic administration may alter gut bacterial flora, possibly impairing gut mucosal immunity. We hypothesized that 1 week of subcutaneous (SC) antibiotic injections would affect Peyer's patch (PP) lymphocyte numbers and phenotypes, as well as mucosal immunoglobulin A (IgA) levels.

Interleukin-7 dose-dependently restores parenteral nutrition-induced gut-associated lymphoid tissue cell loss but does not improve intestinal immunoglobulin a levels.

Background: Without enteral nutrition, the mass and function of gut-associated lymphoid tissue (GALT), a center of systemic mucosal immunity, are reduced. Therefore, new therapeutic methods, designed to preserve mucosal immunity during parenteral nutrition (PN), are needed. Our recent study revealed that exogenous interleukin-7 (IL-7; 1 microg/kg twice a day) restores the GALT cell mass lost during intravenous (IV) PN but does not improve secretory immunoglobulin A (IgA) levels.

Albumin infusion after reperfusion prevents gut ischemia-reperfusion-induced gut-associated lymphoid tissue atrophy.

Background: Our recent study clarified that gut ischemia-reperfusion (I/R) causes gut-associated lymphoid tissue (GALT) mass atrophy, a possible mechanism for increased morbidity of infectious complications after severe surgical insults. Because albumin administration reportedly reduces hemorrhagic shock-induced lung injury, we hypothesized that albumin treatment prevents GALT atrophy due to gut I/R.

Methods: Male mice (n = 37) were randomized to albumin, normal saline, and sham groups.

Lack of enteral nutrition delays nuclear factor kappa B activation in peritoneal exudative cells in a murine glycogen-induced peritonitis model.

Background: Early enteral nutrition is associated with a lower incidence of intraabdominal abscess in severely injured patients than parenteral nutrition (PN). We explored the underlying mechanisms by examining the influence of nutrition route on nuclear factor kappaB (NFkappaB) activation in peritoneal exudative cells (PECs) and peritoneal cytokine levels.

Methods: Thirty male Institute Cancer Research mice were randomized to chow (n = 10), IV PN (n = 10), or intragastric (IG) PN (n = 10) and fed for 5 days.

Gut ischemia-reperfusion affects gut mucosal immunity: a possible mechanism for infectious complications after severe surgical insults.

Objective: To examine influences of gut ischemia/reperfusion (I/R) on gut-associated lymphoid tissue (GALT) mass and function.

Design: Prospective, randomized controlled study.

Setting: Research laboratory.

Exogenous interleukin 7 affects gut-associated lymphoid tissue in mice receiving total parenteral nutrition.

In the absence of enteral nutrient delivery, gut-associated lymphoid tissue (GALT) mass and function are reduced. The purpose of this study was to examine whether exogenous interleukin (IL)-7 treatment reverses intravenous (IV)-total parenteral nutrition (TPN)-induced changes in GALT, immunoglobulin (Ig) A levels, and gut barrier function. Eighty-nine mice were randomized to chow, TPN, or TPN + IL-7 (1 microg/kg, administered IV twice a day) and treated for 5 days.