Decreasing lysophosholipids accompany the activation of inflammation and the immune system after higher fat intake in the NUGAT (NUtriGenomics Analysis in Twins) study

Previous studies have linked certain types of gut mucosal immune cells with fat intake. We determined whether fat absorption activates intestinal mucosal mast cells (MMC), a key component of the gut mucosal immune system. Conscious intestinal lymph fistula rats were used. The mesenteric lymph ducts were cannulated, and the intraduodenal (i.d.) tubes were installed for the infusion of Liposyn II 20% (an intralipid emulsion). Lymphatic concentrations of histamine, rat MMC protease II (RMCPII), a specific marker of rat intestinal MMC degranulation, and prostaglandin D2 (PGD2) were measured by ELISA. Intestinal MMC degranulation was visualized by immunofluorescent microscopy of jejunum sections taken at 1 h after Liposyn II gavage. Intraduodenal bolus infusion of Liposyn II 20% (4.4 kcal/3 ml) induced approximately a onefold increase in lymphatic histamine and PGD2, ∼20-fold increase in lymphatic RMCPII, but only onefold increase in peripheral serum RMCPII concentrations. Release of RMCPII into lymph increased dose dependently with the amount of lipid fed. In addition, i.d. infusion of long-chain triacylglycerol trilinolein (C18:2 n-6, the major composite in Liposyn II) significantly increased the lymphatic RMCPII concentration, whereas medium-chain triacylglycerol tricaprylin (C8:0) did not alter lymph RMCPII secretion. Immunohistochemistry image revealed the degranulation of MMC into lamina propria after lipid feeding. These novel findings indicate that intestinal MMC are activated and degranulate to release MMC mediators to the circulation during fat absorption. This action of fatty acid is dose and chain length dependent.

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Effect of Prednisolone, Physical Activity, Fat Intake, Choleretic Agents on the Serum Bilirubin Level in a Case of Constitutional Hepatic Dysfunction (Gilbert's Disease)

Gastroenterology ◽

10.1016/s0016-5085(57)80142-5 ◽

1957 ◽

Vol 32 (2) ◽

pp. 325-331 ◽

Cited By ~ 2

Author(s):

F. Gilbert McMahon

Keyword(s):

Physical Activity ◽

Bilirubin Level ◽

Hepatic Dysfunction ◽

Serum Bilirubin ◽

Serum Bilirubin Level ◽

Fat Intake

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Parasite Evolution and the Immune System

Allergy & Clinical Immunology International - Journal of the World Allergy Organization ◽

10.1027/0838-1925.17.6.229 ◽

2005 ◽

Vol 17 (06) ◽

pp. 229-236

Author(s):

Kathleen Barnes

Keyword(s):

Immune System ◽

Parasite Evolution

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Learned Placebo Effects in the Immune System

Zeitschrift für Psychologie ◽

10.1027/2151-2604/a000184 ◽

2014 ◽

Vol 222 (3) ◽

pp. 148-153 ◽

Cited By ~ 2

Author(s):

Sabine Vits ◽

Manfred Schedlowski

Keyword(s):

Nervous System ◽

Immune System ◽

Associative Learning ◽

Placebo Response ◽

Immunosuppressive Drug ◽

Immune Functions ◽

Placebo Effects ◽

New Therapeutic Approaches ◽

Biological Variables ◽

Experimental Approaches

Associative learning processes are one of the major neuropsychological mechanisms steering the placebo response in different physiological systems and end organ functions. Learned placebo effects on immune functions are based on the bidirectional communication between the central nervous system (CNS) and the peripheral immune system. Based on this “hardware,” experimental evidence in animals and humans showed that humoral and cellular immune functions can be affected by behavioral conditioning processes. We will first highlight and summarize data documenting the variety of experimental approaches conditioning protocols employed, affecting different immunological functions by associative learning. Taking a well-established paradigm employing a conditioned taste aversion model in rats with the immunosuppressive drug cyclosporine A (CsA) as an unconditioned stimulus (US) as an example, we will then summarize the efferent and afferent communication pathways as well as central processes activated during a learned immunosuppression. In addition, the potential clinical relevance of learned placebo effects on the outcome of immune-related diseases has been demonstrated in a number of different clinical conditions in rodents. More importantly, the learned immunosuppression is not restricted to experimental animals but can be also induced in humans. These data so far show that (i) behavioral conditioned immunosuppression is not limited to a single event but can be reproduced over time, (ii) immunosuppression cannot be induced by mere expectation, (iii) psychological and biological variables can be identified as predictors for this learned immunosuppression. Together with experimental approaches employing a placebo-controlled dose reduction these data provide a basis for new therapeutic approaches to the treatment of diseases where a suppression of immune functions is required via modulation of nervous system-immune system communication by learned placebo effects.

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