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Biomedical subjects

D S Lin

Publications and source records attributed to D S Lin.

At least 19 recordsLinked to original sources
PubMed1992

Antibody responses to Toxoplasma gondii antigens in aqueous and cerebrospinal fluids of cats infected with T. gondii and FIV.

Antibodies to antigens of Toxoplasma gondii were measured in the aqueous and cerebrospinal fluid (CSF) of 16 specific-pathogen free kittens experimentally infected with feline immunodeficiency virus (FIV), T. gondii, or both pathogens. The results indicated that all cats infected with T. gondii had antibody responses to antigens of T. gondii in both aqueous fluids and CSF. Co-infection with FIV did not affect antibody levels. Aqueous fluids from eyes of cats with toxoplasmic retinochoroiditis did not necessarily have higher antibody levels than those from eyes without lesions. Antibodies to T. gondii were also detected in the CSF of two cats from whose brains no parasites were isolated by in vivo mouse inoculation. Total IgG did not increase significantly in the aqueous fluids and CSF of cats infected with T. gondii whether or not they were also infected with FIV.

Animals↗
PubMed1992

Change in interleukin 2 production by lymphocytes during maturation of young cats.

Lymphocytes from four specific-pathogen free cats were tested for their interleukin 2 activity every week beginning when the cats were 12 weeks old and ending when they were 26 weeks old. Lymphocytes from cats > or = 20 weeks old released significantly more interleukin 2 than those obtained from these cats at earlier ages when stimulated with calcium ionophore A23187 and phorbol myristate acetate. The change of interleukin 2 levels with maturation of young cats may represent an important difference in their level of defense to infections with various pathogens.

Aging↗
PubMed1992

Feline immune system.

Immunological features of feline lymphocytes, immunoglobulins, monocytes/macrophages, cytokines, major histocompatibility complex and delayed-type hypersensitivity are reviewed. Attention is given to the comparison of the feline immune system with the immune systems of humans and other animals. Also presented is information on the modification of feline immunity by pathogens.

Animals↗
PubMed1992

Macrophage functions in cats experimentally infected with feline immunodeficiency virus and Toxoplasma gondii.

It was suspected that feline immunodeficiency virus (FIV) infection would affect the function of feline macrophages, and that the concomitant infection of cats with FIV and Toxoplasma gondii would cause even greater changes in macrophage function. Sixteen specific-pathogen-free kittens, four per group, were infected either with FIV, T. gondii, both pathogens, or neither pathogen. After the cats had been infected with FIV for 14 weeks (8 weeks after T. gondii infection), peritoneal macrophages were collected. Some macrophages were stimulated with lipopolysaccharide and supernatants were collected for the measurement of interleukin-1 production. Other macrophages were infected with T. gondii in a microbiocidal assay. Peritoneal macrophages from cats infected with FIV had decreased interleukin-1 secretion and increased antimicrobial activity. Co-infection with T. gondii apparently had no effect on these modifications of macrophage activity. Thus, acute FIV infection alone caused significant changes in macrophage functions that were not affected by concomitant T. gondii infection.

Animals↗
PubMed1992

Toxoplasma gondii: an AIDS enhancing cofactor.

Disseminated toxoplasmosis, one of the most severe acquired immune deficiency syndrome (AIDS)-associated infections in humans, is believed to develop from a latent infection after the cellular immune system is suppressed by human immunodeficiency virus type 1 (HIV-1). However, Toxoplasma gondii may serve as a cofactor in enhancing the immunodeficiency induced by HIV-1. This hypothesis is supported by the facts that: 1) co-infection with other pathogens in humans infected with HIV-1 may enhance the progression of the disease to AIDS; and 2) concomitant infection with T. gondii enhances feline immunodeficiency virus-induced immune dysfunction and is likely to cause a more rapid disease onset than an infection with HIV alone. It is possible that T. gondii infection induces tumor necrosis factor (TNF) production. TNF then stimulates the induction of T-cell proteins that bind to the long terminal repeat of HIV-1. This binding at the repeat site then leads to increased HIV-1 activation which causes the dysfunction of CD4 cells and a resulting immunodeficiency that allows even greater amounts of T. gondii replication.

AIDS-Related Opportunistic Infections↗
PubMed1992

Immunological changes in cats with concurrent Toxoplasma gondii and feline immunodeficiency virus infections.

To examine the immunological changes in cats concurrently infected with feline immunodeficiency virus (FIV) and Toxoplasma gondii, kittens (four per group) were inoculated with FIV, T. gondii, both agents, or no pathogens. Blood mononuclear cells and plasma were collected weekly for lymphocyte assays and serology. At week 14, spleen and lymph node cells were used for lymphocyte assays; brains and mesenteric lymph nodes were used for isolation of T. gondii. More T. gondii organisms were present in tissues of the dually infected cats than in tissues of cats with toxoplasmosis alone. Two dually infected cats and one cat infected with T. gondii developed chorioretinitis. Spleen, lymph node, and blood mononuclear cells from dually infected cats had the greatest reduction in mitogenic responses. By week 3, cats infected with FIV underwent a decrease in the number of CD4 cells that was not changed by concurrent T. gondii infection; the number of CD8 cells increased only in cats infected with T. gondii alone. For cats infected with T. gondii, the responses of lymphocytes to T. gondii antigen were not affected by FIV infection; the responses to FIV antigen were negligible in all groups. Overall, this study indicates that FIV infection favors T. gondii proliferation. Also, the establishment of toxoplasmosis may enhance FIV-induced immunodeficiency and is likely to cause a more rapid disease progression than that from infection with FIV alone.

Animals↗
PubMed1991

High levels of the (n-6) fatty acid 4,7,10,13,16-docosapentaenoate in the retinas of rabbits are reduced by feeding dietary fish oil from birth to adult life.

High levels of 4,7,10,13,16-docosapentaenoic acid [22:5(n-6)], a fatty acid usually associated with (n-3) fatty acid deficiency, have been reported in the retina of young rabbits. We studied the fatty acid composition of the rabbit retina throughout development, from birth to adult life. We also attempted to modify the fatty acid composition of the retina by the feeding of fish oil, high in docosahexaenoic acid [22:6(n-3), DHA]. Female rabbits were fed either a control or 2% fish oil diet through pregnancy and the nursing period. Weaned rabbits received the mothers' diet. In the retinas of control rabbits, 22:5(n-6) represented 3.7% of total fatty acids at birth, reached 15.1% at 9 wk and declined to 5.6% in adult rabbits. However, 22:6(n-3) increased steadily from birth onwards, from 3.8% of total fatty acids at birth to 19.6% in adults. Dietary fish oil increased the trace concentrations of long-chain (n-3) fatty acids in the milk to 10% of total fatty acids, reduced retinal 22:5(n-6) to less than or equal to 0.5% at all ages, and increased DHA to approximately 30% by 9 wk. Retinal phosphatidylethanolamine was even more sensitive to the impact of the fish oil diet, with DHA levels in newborn rabbits rising from 10% (control diet) to 43% of total fatty acids. These results demonstrated that 22:5(n-6) in the normal rabbit retina remains elevated (compared with other species) at all ages even as retinal DHA increases. The great increase of DHA in newborns whose mothers were fed fish oil suggests placental transfer of DHA and incorporation into retinal lipids.

Animals↗
PubMed1991

The incorporation of n-3 and n-6 essential fatty acids into the chick embryo from egg yolks having vastly different fatty acid compositions.

The effect of egg yolk fatty acid composition on essential fatty acid utilization by the developing chick embryo was studied by feeding laying hens a fat-free diet supplemented with oils containing widely divergent contents of the essential n-6 and n-3 fatty acids. A control hen was fed a commercial feed for laying hens. The diets contained 20 to 4370 mg/100 g n-3 fatty acids and 360 to 8020 mg/100 g n-6 fatty acids. Fertile eggs were collected in pairs: one was incubated and the other served as an unincubated control. The fatty acid content of the unincubated egg and the newly hatched chick from each pair was compared. Some 50% of the total fatty acids in the egg yolk were incorporated into the tissues of the newly hatched chick. Regardless of diet, more yolk n-6 fatty acids were incorporated into the chick compared to saturated or monounsaturated fatty acids. The percentage of incorporation especially increased from the eggs containing relatively low amounts of n-6 fatty acid. The percentage of incorporation of n-3 fatty acids was similar to that of saturated and monounsaturated fatty acids when n-3 fatty acids were plentiful in the egg yolk, but increased significantly when n-3 fatty acids were low in the eggs. There was a generally linear relationship between essential fatty acids in the egg and in the chick, although levels of docosahexaenoic acid [DHA; 22:6(n-3)] in the brain did not respond proportionally.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Cellular responses of cats with primary toxoplasmosis.

The cellular responses of 8 kittens (4 inoculated orally with mouse brains containing Toxoplasma gondii cysts and 4 uninfected controls) were studied. Oocyst numbers, body weight, and rectal temperature were monitored daily. Blood was collected weekly for serology and mononuclear cell purification. At necropsy, peritoneal and alveolar macrophages, spleen, and lymph node cells were harvested. Infected cats shed oocysts 4-15 days postinfection, maintained normal body weight and rectal temperature, and developed anti-T. gondii immunoglobulin M and G. Infected cats had normal surface immunoglobulin-positive cell populations and peripheral blood lymphocyte functions. The infected cats differed in their responses from control cats in that they developed circulating T. gondii antigen-specific lymphocytes, had increased interleukin 1 secretion by monocytes, had spleen and lymph node cells with depressed mitogenic responses and interleukin 2 production, and had macrophages with enhanced abilities in preventing the intracellular proliferation of T. gondii. Overall, the primary response of the cat to an infection with T. gondii appeared similar to that of other hosts.

Animals↗
PubMed1991

Effects of nitroscanate on adult Taenia pisiformis in dogs with experimentally induced infections.

Twenty-four specific-pathogen-free Beagles were each given 50 cysticerci of Taenia pisiformis that had been harvested from experimentally infected rabbits. Quantitative fecal egg counts and fecal screening for recovery of passed segments were performed on postinoculation days 56 through 70. Twenty-three of 24 dogs fed cysticerci developed patent infections. The 23 dogs with patent infections were assigned to 1 of 2 groups and treated with nitroscanate or a placebo 60 days after inoculation. Egg counts in the treated dogs had markedly decreased by the second day after treatment, and by the sixth day after treatment, segments were not found in the feces of any of the treated animals. The control dogs continued to pass eggs and segments in their feces throughout the 9 days after treatment. The dogs were euthanatized and necropsied 70 days after being inoculated. At necropsy, the mean number of scolices recovered from control dogs was 24.6, the mean number of scolices recovered from treated dogs was 0.25. Worms recovered from the control dogs were intact, gravid cestodes. Efficacy of treatment with nitroscanate at a mean dosage of 56 mg/kg of body weight was 98.9%.

Animals↗
PubMed1990

Are the n-3 fatty acids from dietary fish oil deposited in the triglyceride stores of adipose tissue?

Adipose tissue is the chief reservoir of the essential fatty acids (n-3 and n-6). To study the incorporation of the dietary n-3 fatty acids eicosapentaenoic acid (EPA) (20:5) and docosahexaenoic acid (DHA) (22:6), and a unique monounsaturated fatty acid, cetoleic acid (22:1n-11), into adipose tissue, rabbits were fed two different processed fish oils: MaxEPA (high in EPA and DHA; Seven Sea Ltd, Hull, UK) and herring oil (high in cetoleic acid). EPA and DHA increased from 0% of total adipose tissue fatty acid, in the adipose tissue of control rabbits to 2.2% and 4.9%, respectively, in MaxEPA-fed rabbits. The DHA-to-EPA ratio in the adipose tissue was higher than that in the diet, indicating alternative metabolic pathways for EPA. In the adipose tissue of herring-oil-fed rabbits, cetoleic acid increased from 0% to 7.9% of total fatty acids. The deposition of EPA and DHA was 1.8% and 2.8%, respectively. Our data indicated that these unique long-chain unsaturated fatty acids from dietary fish oils were readily incorporated into the fat stores from whence they could be mobilized.

Adipose Tissue↗
PubMed1990

Effects of dietary n-3 fatty acids on the phospholipid molecular species of monkey brain.

We examined the changes in the molecular species of brain ethanolamine glycerophospholipids of monkeys fed diets containing widely ranging amounts of n-3 fatty acids. Two groups of rhesus monkeys were fed pre- and postnatally either a control diet (soy oil; containing 8% of fatty acids as 18:3n-3) or a deficient diet (safflower oil; containing less than 0.3% 18:3n-3). The brains of these animals were analyzed at 22 months of age. A third group of monkeys was fed the safflower oil diet to 22 months of age and then switched to a fish oil diet (28% long-chain n-3 fatty acids) for 1-2 years before autopsy. The molecular species of the diacyl, alkylacyl, and alkenylacyl ethanolamine glycerophospholipids from frontal cortex were separated by HPLC. A total of 24 molecular species were identified. Fatty acids in the sn-2 position differed markedly among the diet groups, but the sn-1 position always contained only 16:0, 18:0, or 18:1. In the diacyl subclass of the control brain, the n-3 molecular species represented 41% of total and the n-6 species 45%, whereas in the deficient brain the n-3 molecular species decreased to 9% and n-6 molecular species increased to 77%. The fatty acid 22:5n-6 did not replace 22:6n-3 in a symmetrical fashion in the molecular species of the deficient brain. In the brains of the fish oil-fed monkeys, the n-3 molecular species amounted to 61% and n-6 molecular species were reduced to 25%. The species 18:1-22:6, 16:0-22:6, and 18:0-22:6 generally changed proportionally in response to diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Dietary effects on brain fatty acid composition: the reversibility of n-3 fatty acid deficiency and turnover of docosahexaenoic acid in the brain, erythrocytes, and plasma of rhesus monkeys.

Rhesus monkeys given pre- and postnatal diets deficient in n-3 essential fatty acids develop low levels of docosahexaenoic acid (22:6 n-3, DHA) in the cerebral cortex and retina and impaired visual function. This highly polyunsaturated fatty acid is an important component of retinal photoreceptors and brain synaptic membranes. To study the turnover of polyunsaturated fatty acids in the brain and the reversibility of n-3 fatty acid deficiency, we fed five deficient juvenile rhesus monkeys a fish oil diet rich in DHA and other n-3 fatty acids for up to 129 weeks. The results of serial biopsy samples of the cerebral cortex indicated that the changes of brain fatty acid composition began as early as 1 week after fish oil feeding and stabilized at 12 weeks. The DHA content of the phosphatidylethanolamine of the frontal cortex increased progressively from 3.9 +/- 1.2 to 28.4 +/- 1.7 percent of total fatty acids. The n-6 fatty acid, 22:5, abnormally high in the cerebral cortex of n-3 deficient monkeys, decreased reciprocally from 16.2 +/- 3.1 to 1.6 +/- 0.4%. The half-life (t 1/2) of DHA in brain phosphatidylethanolamine was estimated to be 21 days. The fatty acids of other phospholipids in the brain (phosphatidylcholine, -serine, and -inositol) showed similar changes. The DHA content of plasma and erythrocyte phospholipids also increased greatly, with estimated half-lives of 29 and 21 days, respectively. We conclude that monkey cerebral cortex with an abnormal fatty acid composition produced by dietary n-3 fatty acid deficiency has a remarkable capacity to change its fatty acid content after dietary fish oil, both to increase 22:6 n-3 and to decrease 22:5 n-6 fatty acids. The biochemical evidence of n-3 fatty acid deficiency was completely corrected. These data imply a greater lability of the fatty acids of the phospholipids of the cerebral cortex than has been hitherto appreciated.

Animals↗
PubMed1989

Rapid modulation of the n-3 docosahexaenoic acid levels in the brain and retina of the newly hatched chick.

The newly hatched chick obtains its fatty acids almost completely from the lipids of the egg yolk as these are transferred to the developing embryo during its 21-day period of incubation. Since the diet of the laying hen greatly influences the fatty acid composition of the egg lipids, and presumably also the fatty acid composition of the resulting chick, we tested how quickly and to what extent varying the amount of n-3 fatty acids in the diet of the hen would modulate the level of n-3 fatty acids in the brain and retina of the newly hatched chick. White Leghorn hens were fed commercial or semi-purified diets supplemented with 10% fish oil, linseed oil, soy oil, or safflower oil. Eggs, together with the brain, retina, and serum of newly hatched chicks, were then analyzed for fatty acid composition. The fatty acids of egg yolk responded quickly to the hen's diet with most of the change occurring by 4 weeks. There was a linear relationship between the linolenic acid content of the diets and levels of this fatty acid in egg yolk and chick serum. In chicks from hens fed the fish oil diet, the total n-3 fatty acids, including 22:6(n-3), were elevated twofold in the brain and retina and sevenfold in serum relative to commercial diet controls. The safflower oil diet led to a very low n-3 fatty acid content in egg yolks and only 25% of the control n-3 fatty acid content in the brain and retina of chicks.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗