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Departments of 1 Nutritional Sciences and 6 Animal Sciences, College of Agriculture and Life Sciences; 2 Department of Medicine, Medical School; 4 Department of Surgical Sciences, School of Veterinary Medicine, and the 5 Food Research Institute, University of Wisconsin, Madison, Wisconsin 53706; and 3 Department of Internal Medicine, University of Texas, Galveston, Texas 77555
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Conjugated linoleic acid (CLA) has been shown to enhance immune reactions such as lymphocyte blastogenesis and delayed-type hypersensitivity. We investigated the role of CLA in type I (immediate) hypersensitivity, using a guinea pig tracheal superfusion model for measuring antigen-induced airway smooth muscle contraction and inflammatory mediator release. Female Hartley guinea pigs were fed a diet supplemented with 0.25 g corn oil or linoleic acid/100 g of diet (control) or 0.25 g CLA/100 g of diet for at least 1 wk before and during active sensitization to ovalbumin antigen. Tracheae from sensitized guinea pigs were suspended in air-filled water-jacketed (37°C) tissue chambers in a superfusion apparatus. Tracheae were superfused with buffer containing antigen, and tissue contraction was recorded. Superfusate was collected at 90-s intervals for evaluation of histamine and PGE2 release. CLA did not affect antigen-induced tracheal contractions when expressed as gram contraction per gram tissue. CLA significantly reduced antigen-induced histamine and PGE2 release. CLA appears to decrease release of some inflammatory mediators during type I hypersensitivity reactions.
type I hypersensitivity; conjugated linoleic acid; immunity; allergies; asthma
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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CONJUGATED LINOLEIC ACIDS (CLA) are naturally occurring isomers of linoleic acid in which the double bonds are in a conjugated formation (i.e., a 1,3-diene, not methylene interrupted). Notable biological effects include anticarcinogenesis (13), antiatherogenesis (15), body fat reduction (22), lean body mass enhancement (22), anticachectic effects (10), and immune enhancement, including increased lymphocyte blastogenesis (6, 10, 19, 32), increased lymphocyte cytotoxic activity (6), and increased delayed-type hypersensitivity (10).
The mechanism by which CLA affects these aspects of the immune system is not completely understood. The conversion of arachidonic acid into eicosanoids by cyclooxygenase or lipoxygenase is hypothesized to be affected by CLA (10). CLA is incorporated into the sn-2 position of phospholipids (21) and can be metabolized into 20 carbon molecules with either three or four double bonds (2, 26). However, to the best of our knowledge, no conjugated forms of cyclooxygenase or lipoxygenase products have been detected. Nugteren (20) showed that cis-8, trans-12, cis-14 eicosatrienoate and cis-5, cis-8, trans-12, cis-14 eicosatetraenoate (the elongated and desaturated fatty acid that would form from trans-10, cis-12 CLA) were able to competitively inhibit cyclooxygenase.
The use of CLA as a dietary supplement has increased in recent years, leading to a need for understanding the biological effects of CLA under different physiological conditions. Dietary fatty acids have been hypothesized to play a role in type I hypersensitivity reactions by affecting the eicosanoid pathway (3, 4). Because of the potential for CLA to modulate the eicosanoid pathway, its previously reported effects on immune function and the high incidence of type I hypersensitivity in humans [over 20% of the US population (1)], the present study was conducted to describe the effects of supplemental dietary CLA in a guinea pig model of type I hypersensitivity.
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MATERIALS AND METHODS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Diets and sensitization.
Female Hartley guinea pigs (Harlan Sprague Dawley, Madison, WI)
weighing 200-350 g were randomly divided into two dietary treatment groups, control and CLA. Because of experimental limitations in managing the number of tissues, the experiment was done in three
blocks. Diets consisted of standard commercial alfalfa-based guinea pig
chow1 (7006, Harlan-Teklad,
Madison, WI) supplemented with 0.25 g/100 g of either control oil or
CLA. The control oil was either corn oil (~55% linoleic acid) or
linoleic acid (95%, Nu-Check Prep, Elysian, MN). Both corn oil and
linoleic acid are typical control oils used in dietary CLA experiments
(5, 8, 23, 25). There were no statistical differences in
effects of the two control diets, so results were pooled (Fig. 1).
CLA2 was synthesized from
linoleic acid (Nu-Check Prep) by published methods (7).
Guinea pigs were housed in a temperature- and humidity-controlled room
with a 12:12-h light-dark cycle in compliance with the University of
Wisconsin-Madison Research Animal Resources Center. Guinea pigs were
given free access to the experimental diets at least 1 wk before and
during active sensitization to chicken egg ovalbumin (OVA, Sigma, St.
Louis, MO) antigen. Guinea pigs were sensitized with an initial
intraperitoneal injection of 50 µg OVA in PBS with 1 mg aluminum
hydroxide followed 2 wk later by a subcutaneous injection (flank) of
200 µg OVA in PBS emulsified with equal volume of incomplete
Freund's adjuvant. This sensitization protocol enhances production of
IgG1, the reaginic antibody in guinea pigs
(31). Guinea pigs were killed 4 days after the second
injection with an intraperitoneal injection of pentobarbital sodium
(100 mg/kg).
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Tracheal superfusion.
Tracheae (n = 15 per treatment) were removed, placed in
physiological saline solution (PSS), and trimmed of excess tissue with
care being taken not to stretch or abrade the tracheae. The PSS was a
bicarbonate buffer solution containing (in mM) 118 NaCl, 1.0 NaH2PO4, 4.7 KCl, 2.5 CaCl2, 0.5 MgCl2, 11 glucose, and 25 NaHCO3. Each trachea
was cut longitudinally into a spiral at a 45° angle (9)
and suspended isotonically in an air-filled, water-jacketed (37°C)
tissue chamber (30). The tracheae were superfused at a
rate of 2.2 ml/min with PSS (37°C; gassed with 95% O2
and 5% CO2) while being maintained at a constant tension of 5 g for an equilibration period of 90 min (11).
Changes in tensions (expressed as g of contraction) were measured with
Grass FT 03 electrical force-displacement transducers and plotted with a Grass polygraph (model 7D, Grass Instruments, Quincy, MA). After equilibration, tracheae were challenged by continuously superfusing PSS
containing 0.01 g/l OVA (2.2 ml/min). Superfusates were collected in
separate aliquots at 90-s intervals for 15 min beginning 90 s
before antigen challenge (designated collection period 0)
and stored at 4°C. Peak changes in tracheal tensions were determined for each 90-s collection period. After collection, superfusates were
stored at 
20°C until they were analyzed for histamine and PGE2 content (analyses were performed within 3 days of
superfusion). After antigen challenge, tracheae were continuously
superfused with PSS containing 10
5 M carbachol
(carbamylcholine chloride, Sigma) to produce maximal contraction. After
carbachol-induced contraction, tracheae were weighed, minced with
scissors, homogenized in 0.4 N perchloric acid, and placed in a boiling
water bath for 10 min. After centrifugation, the supernatants were
collected for determination of residual histamine.
Mediator analysis.
Histamine contents from superfusates and tracheae were determined by
enzyme immunoassay (EIA, Immunotech, Westbrook, ME) for nine guinea
pigs from each treatment. The sensitivity of the assay is 0.05 µg/l.
PGE2 contents of superfusates from 15 tracheae from each
treatment were analyzed using an EIA (Amersham Life Science, Arlington
Heights, IL) with a sensitivity of 40 pg/ml. In this assay,
cross-reactivity with PGE1, PGF2
,
6-keto-PGF1, and arachidonic acid is 25%, 0.04%,
<0.1%, and <0.001%, respectively.
Fatty acid analysis. Fatty acid composition of the diet and CLA isomer composition of the diet and tracheae were determined by gas chromatography using previously published methods (7). Tracheae used for CLA isomer analysis were obtained in a separate experiment using the same feeding and sensitization protocol described above.
Statistical analysis. Data were analyzed using SAS (Cary, NC). ANOVAs with repeated measures were performed to test for diet effect on tracheal contractions, histamine release, and PGE2 release.
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RESULTS |
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ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Tracheal contractions. Carbachol, an acetylcholine analog, is typically used in superfusion experiments to determine the maximal contraction of tissues to express contraction as a percent of the maximal carbachol-induced contraction. This method is frequently preferred, but assumes that the treatment being studied does not affect the maximum contraction. Another way to express contractions is as grams of contraction per gram of trachea. This method works best for tracheae of approximately the same size, and the assumption made is that muscle distribution is constant. In these experiments, there was a moderate treatment effect on the maximal carbachol-induced contractions (in g contraction/g trachea: control, 14.82; CLA, 17.37; SE = 0.94, P = 0.06). Therefore, contractions were expressed both as grams contraction per gram wet trachea and as a percent of maximal (carbachol induced) contraction. There were no significant differences in tracheal contraction due to diet (Fig. 1A) when expressed as gram per gram trachea, but the CLA-supplemented guinea pig tracheae had significantly lower contractions during time periods 1 and 2 relative to control guinea pigs when expressed as percent of maximal carbachol-induced contraction.
Histamine release. There was a significantly lower amount of histamine released by tracheae from CLA-supplemented guinea pigs relative to controls during the first 90 s of antigen challenge (Fig. 1B, collection period 1, P < 0.0001). The peak histamine release at this time point corresponded with peak tracheal contraction for both treatment groups. There were no significant differences in histamine release at all other time points measured. Total histamine release and total tissue histamine (total released plus residual in trachea) were not significantly different between groups (control, 7,355 ng/g; CLA, 7,075 ng/g; P > 0.5).
PGE2 release. Overall release of PGE2 was significantly lower in CLA-supplemented guinea pigs relative to controls (Fig. 1C). Peak PGE2 release (collection period 2) followed peak contraction and histamine release (collection period 1).
Weight gain, feed consumption, and tissue analysis. There were no significant differences between dietary treatments in weight gain or feed consumption during these experiments (data not shown). CLA content of control tracheae was in the ranges of 0-0.23% and 0.11-0.16% of total fatty acids for phospholipids and neutral lipids, respectively; and for CLA tracheae, 1.83-2.20% and 1.99-2.64% of total fatty acids for phospholipids and neutral lipids, respectively.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Histamine release from tracheae of CLA-supplemented guinea pigs was significantly reduced during the time interval of maximal release. Histamine is an inflammatory mediator released from antigen-activated mast cells in airway tissue, and histamine causes smooth muscle contraction, increased epithelial permeability, and increased mucous secretion (33). Despite higher levels of histamine release in the control group during the first 90-s interval after OVA challenge, tracheal contractions (g contraction per g trachea) were similar to the CLA group. It is possible that histamine was released at a greater concentration than required for maximal tracheal contractions or that other inflammatory mediators induced contraction or relaxation. CLA feeding did not affect total tissue histamine in our study. Sugano and coworkers (27) did not observe an influence of CLA on histamine release from rat peritoneal exudate cells, but did notice a decreased trend in stored histamine in cells with increasing dietary CLA levels. Noteworthy differences between the study by Sugano and coworkers and this study are that the animals used in the former study were not sensitized to an antigen, and isolated cells, not tissues, were used.
PGE2 release by tracheae from CLA-fed guinea pigs was
consistently decreased during superfusion. This is consistent with
other reports of CLA decreasing PGE2 in serum (27,
28), bone (17), spleen (28), and
cultured keratinocytes (19). PGE2 plays an important role in type I hypersensitivity by inhibiting the formation of interferon-
, a cytokine responsible for downregulating production of IgE (12). PGE2 can also act directly on B
cells to increase the formation of IgG1 (the reaginic Ig in
guinea pigs) and IgE (24). Therefore, decreased
PGE2 may result in decreased sensitization to the allergen.
In fact, previous reports (27) indicate that CLA-supplemented rats had decreased serum IgE (the reaginic Ig in rats)
compared with control-fed rats.
PGE2 is also an airway relaxant (14). We did not evaluate this effect in the current study. However, CLA decreased the release of both contractile (histamine) and relaxant (PGE2) substances, leading to a net mechanical response to antigen stimulation that was not different from controls.
The cis-9, trans-11 and trans-10, cis-12 isomers of CLA are the two most abundant CLA isomers in most commercial sources. Based on prior evidence that cis-8, trans-12, cis-14 eicosatrienoate and cis-5, cis-8, trans-12, cis-14 eicosatetraenoate inhibit cyclooxygenase (20), we hypothesize that the trans-10, cis-12 isomer of CLA is the isomer responsible for decreasing the amount of PGE2 measured. Recent availability of pure isomers will allow for the testing of this hypothesis.
Maximal contractions in response to carbachol were moderately increased in CLA-supplemented guinea pigs. CLA was previously shown to be incorporated into the phospholipids of cell membranes (21) and to decrease delta-9 desaturase (16). Membrane lipid composition has been shown to have an important effect on acetylcholine receptor function (29). Therefore, the increased carbachol contraction could reflect an altered responsiveness of the receptor due to changes in membrane fatty acid composition by CLA and/or by altered delta-9 desaturase activity. Alternatively, CLA has been shown to increase lean muscle mass (22), and, therefore, guinea pigs fed CLA may have increased smooth muscle mass, which in turn could have resulted in increased carbachol-induced contraction. The observed reduction in maximal contraction of tracheae when expressed as a percent of maximal carbachol-induced contraction appears to be the result of increased carbachol responsiveness of tracheae from CLA-supplemented guinea pigs.
In conclusion, in this guinea pig model of type I hypersensitivity, supplemental CLA reduced release of the inflammatory mediators measured (histamine and PGE2). Histamine release may be decreased as a result of decreased sensitization to the allergen. The reduction in PGE2 release is probably due to an altered eicosanoid synthesis pathway. CLA did not affect antigen-induced tracheal contractions (g/g trachea). These data suggest that CLA may play a role in downregulating type I hypersensitivity reactions.
Perspectives
The results from this study have an important broad implication. CLA, a naturally occurring component in our diet, may have downregulatory effects on type I hypersensitivity reactions such as allergies and asthma, conditions that affect a large number of people. The CLA isomer occurring at highest levels in our diet is the cis-9, trans-11/trans-9, cis-11. However, this study was done with a mixture of isomers containing approximately equal amounts of the trans-10, cis-12 and cis-9, trans 11/trans-9, cis-11 isomers, and at this point we do not know if one isomer or both are responsible for the effects seen. Further work is needed to better understand the interactions of the various CLA isomers with immune function and to determine if CLA downregulates type I hypersensitivity responses in other whole animal models and humans.| |
ACKNOWLEDGEMENTS |
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The authors thank James Fialkowski and Matt Zine for assistance with superfusion methods, Karen Albright for synthesis of CLA, and Yeonwha Park and Jayne Storkson for assistance with GC analysis of guinea pig tissues and diet.
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FOOTNOTES |
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Address for reprint requests and other correspondence: M. E. Cook, Dept. of Animal Sciences, 1675 Observatory Drive, Madison, WI 53706 (E-mail: mcook{at}facstaff.wisc.edu).
1 Proximate composition (provided by company; in g/kg): 17.0 crude protein, 2.5 crude fat, 16.0 crude fiber. Fatty acid composition by gas chromatography analysis of basal diet (as %total fatty acids): 34% 18:2, 28% 18:1, 20% 16:0, 7% 18:3, 6% 18:0, 2% 16:1.
2 Isomer composition of CLA: 43% trans-10, cis-12; 42% cis-9, trans-11/trans-9, cis-11; 10% trans,trans isomers, 3% cis,cis isomers. Pure isomers were not available in sufficient quantity.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 31 January 2000; accepted in final form 13 November 2000.
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REFERENCES |
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TOP
ABSTRACT
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MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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