Biomedical subjects

A N Taylor

Publications and source records attributed to A N Taylor.

At least 19 recordsLinked to original sources

PubMed2004

Association of HLA-DQ5 and HLA-DR1 with sensitization to organic acid anhydrides.

BACKGROUND: Organic acid anhydrides are low molecular weight industrial chemicals, able to cause rhinoconjunctivitis and asthma associated with specific IgE against hapten-carrier protein conjugate. Only a proportion of exposed workers develop IgE-associated allergy to acid anhydrides. OBJECTIVE: We determined whether genetic susceptibility, in particular, HLA Class II alleles may be a risk factor. METHODS: We undertook HLA typing in 52 cases who had confirmed specific IgE and in 73 referents matched on site, age and duration of acid anhydride exposure identified in cross-sectional studies of workers exposed to hexahydrophthalic (HHPA), methylhexahydrophthalic (MHHPA) and methyltetrahydrophthalic (MTHPA) anhydrides. RESULTS: The linked alleles DQ5 (odds ratio [OR]=4.3; 95% confidence interval [95% CI]=1.7, 11) and DR1 (OR 3.0; 95% CI 1.2, 11) were more prevalent in cases than in referents. Within DQ5, DQB1(*)0501 was particularly frequent (OR 3.0; 95% CI 1.2, 7.4). CONCLUSION: DQB1(*)05 gene confers susceptibility to develop specific IgE antibodies against HHPA, MHHPA and a non-significant trend with MTHPA. DQB1(*)0501 is protective for other low molecular chemical sensitizers (isocyanates and plicatic acid) which may indicate varying affinities for the corresponding specific class II molecules.

Adult↗

PubMed2003

Serum levels of sex hormones and corticosterone throughout 4- and 5-day estrous cycles in Fischer 344 rats and their simulation in ovariectomized females.

Among inbred strains of rats, the Fischer 344 (F344) is commonly used in immunological and behavioral studies. However, little is known about patterns of sex hormones and corticosterone (CORT) secretion throughout the estrous cycle in this strain, which is characterized by a marked CORT response to stress and variable length of cycles. In the current study, using radioimmunoassays, we assessed serum levels of progesterone, estradiol, LH, testosterone, prolactin and CORT, at 1-h intervals throughout the estrous cycle in F344 female rats with 4- and 5-day cycles, as well as in males. Vaginal smears were obtained from 268 females for 15 consecutive days to determine individual length of the estrous cycle and the exact estrous phase upon blood withdrawal, which was conducted once in each rat on the 12th day of smearing. The results indicated that both 4- and 5-day cyclers have two distinct and marked surges of progesterone, one on proestrus day and the other on diestrous-1 day. Testosterone levels in 5-day cyclers peaked on diestrus-3, one day earlier than in 4-day cyclers. Daily peak levels of CORT gradually increased from estrus day to proestrous day, whereas daily nadir levels of CORT remained unchanged. To simulate the natural kinetics of specific sex hormones in ovariectomized females, different doses of estradiol, progesterone, testosterone, prolactin or CORT were injected s.c. or i.p., or 90-day sustained release pellets containing different doses of estradiol or progesterone were implanted. The findings indicated dose- and time-dependent effects, suggesting regimens for modeling the estrous cycle or replacement therapy.

Animals↗

PubMed2001

Intracerebroventricular interleukin-1beta impairs clearance of tumor cells from the lungs: role of brain prostaglandins.

We have previously demonstrated that central administration of interleukin (IL)-1beta suppresses natural killer (NK) cell activity, impairs NK-mediated lung clearance of tumor cells, and enhances tumor colonization. The central pathways activated by IL-1beta are as yet unknown. Using an in vivo model of tumor colonization, this study examined the role of central noradrenergic, opioid and prostaglandin mechanisms in mediating the effect of IL-1beta on lung clearance of tumor cells. We demonstrate that central noradrenergic and opioid systems are not critically involved in this effect. Neither depletion of central noradrenergic pathways, or administration of the opioid antagonist, naltrexone (50 ug), blocked the impaired lung clearance of MADB106 tumor cells induced by central administration of IL-1beta (20 ng). Central prostaglandins (PGs) do, however, appear to play a critical role. Central administration of the prostaglandin antagonist, diclofenac (250 ug), but not ibuprofen, completely blocked the effect of IL-1beta on lung clearance of tumor cells. Antagonism of the effects of IL-1beta was shown to be due to the effects of centrally and not of peripherally acting prostaglandins.

Adenocarcinoma↗

PubMed2001

The glossopharyngeal nerve as a novel pathway in immune-to-brain communication: relevance to neuroimmune surveillance of the oral cavity.

Glossopharyngeal afferents may be the neural channel by which immune challenge of the posterior oral cavity conveys information to the brain. If this is the case, then bilateral transection of the glossopharyngeal nerves (GLOx) should disrupt this communication. Injection of lipopolysaccharide (LPS) or interleukin (IL)-1beta into the soft palate (ISP) of sham-operated rats induced a dose-related febrile response. GLOx significantly attenuated the febrile response induced by ISP injection of both LPS and IL-1beta. In contrast, GLOx did not affect the febrile response when LPS or IL-1beta were injected intraperitoneally, indicating that the effect of GLOx is not systemic. These results provide experimental evidence for a novel neural pathway for immune-to-brain communication.

Afferent Pathways↗

PubMed2001

Role of human leukocyte antigen phenotype and exposure in development of occupational asthma.

Studies of factory workforces in the past decade, exposed to both inhaled protein allergens (e.g. enzymes) and low molecular weight sensitisers (e.g. acid anhydrides), have provided consistent evidence of exposure-response relationships for both sensitisation (IgE production) and asthma. The development of molecular techniques has allowed investigation of candidate gene, in particular HLA Class 2 alleles, as risk factors contributing to individual susceptibility, in particular to low molecular weight chemicals. The frequency of HLA DR3 in cases of sensitisation to trimellitic anhydride and ammonium hexachloroplatinate is increased as compared to referents who have experienced a comparable intensity and duration of exposure. Similarly, HLA DQB1Asp57 is consistently more frequent in cases of isocyanate induced asthma. These observations indicate HLA Class 2 molecules contribute to individual susceptibility to sensitisation and asthma caused by low molecular weight chemicals. A study of platinum refinery workers suggested the relative risk associated with HLA phenotype was greater at lower levels of exposure.

Animals↗

PubMed2001

Interstitial lung diseases: an epidemiological overview.

Epidemiological studies on interstitial lung diseases (ILDs) may be schematically subdivided into the following major types: 1) quantifications of disease, broken down into incidence, prevalence and mortality data; 2) identification of aetiological factors; and 3) clinical epidemiological studies. Epidemiological data may be obtained from different sources or population groups, using different study designs such as systematic national statistics, population-based data and registries, and large case series of specific diseases. Differences in results between epidemiological studies may be due to real differences in incidence, but may also be due to changes in disease definitions and classifications, differences in the epidemiological design of the studies, or even registration bias. Comparative epidemiological data of different ILDs are almost limited to the general population study in Bernalillo County and to national mortality statistics, which should be interpreted with great caution. Also, some, mostly national registries of the different ILDs have been carried out by specific medical profession groups (especially pulmonologists), which clearly underestimate the real incidence of ILDs, but in which the comparison of the relative frequencies is probably accurate. Based on all these comparative studies, sarcoidosis and idiopathic pulmonary fibrosis appear to be the most frequent ILDs, followed by hypersensitivity pneumonitis and ILD in collagen vascular disease, when classical pneumoconioses are not included. There is also a relatively large group of nonspecific fibrosis. Much more data have been published on the epidemiology of specific forms of interstitial lung disease. Most information is available on the epidemiology of sarcoidosis, and those data are probably the most accurate. Data on idiopathic pulmonary fibrosis have the disadvantage of the recent changes in definition and classification of this disease. Hypersensitivity pneumonitis has been studied epidemiologically, especially in some exposure groups such as farmers and pigeon breeders, and in some regions in North America, UK, France and Scandinavia. Estimates of frequencies of interstitial lung disease in collagen vascular disease or of drug-induced interstitial lung disease are less accurate and more variable, depending on diagnostic criteria. Notwithstanding the aforementioned problems, this report tries to provide a balanced overview of the epidemiology of different interstitial lung diseases.

Humans↗

PubMed2000

Identification of four novel interleukin-13 gene polymorphisms.

The development of allergic asthma is thought to involve environmental and inherited genetic components and has pathophysiological features reflecting in part the activity of T cell cytokines. Interleukin-13, a product primarily of activated lymphocytes, is considered to be a critical effector molecule in allergic airway response and has been found to be overexpressed in the airways of patients with asthma. The IL-13 gene is located on chromosome 5q31, one of the major loci to be linked to asthma susceptibility, and amongst a cluster of genes which dominate the immunopathology of allergic disease. Recently, an IL-13 promoter polymorphism was found to be associated with allergic asthma. In the present study we report the identification of four novel biallelic polymorphisms in the IL-13 gene, two intronic and two exonic, one of which results in a basic to hydrophilic amino acid change. We characterised the frequencies of these four biallelic polymorphisms and the frequencies of the haplotypes, resulting from the combination of these four biallelic polymorphisms, in a population of 196 UK Caucasoid healthy individuals.

Alleles↗

PubMed1999

Fetal alcohol exposure attenuates interleukin-1beta-induced fever: neuroimmune mechanisms.

Central mechanisms for the attenuating effects of fetal alcohol exposure (FAE) on interleukin-1beta (IL-1beta)-induced fever were studied in adult male offspring of dams fed a liquid diet supplemented with ethanol (E), in pair-fed (P) control and in normal (N) offspring. Hypothalamic levels of IL-1 were significantly lower in E than in N rats at 2 h, but not at 4 and 6 h, after intraperitoneal administration of lipopolysaccharide. Fever induced by intracerebroventricular (i.c.v.) IL-1 was significantly lower in E than in N and P rats. In contrast, E rats showed a normal febrile response to i.c.v. prostaglandin-E2. Thus, whereas FAE does not affect central thermoregulatory mechanisms, per se, FAE alters the kinetics of hypothalamic IL-1 production/appearance and decreases the responsiveness of central mechanisms which mediate the febrile response to IL-1.

Adrenocorticotropic Hormone↗

PubMed1999

Intracerebral interleukin-1beta impairs response to tumor invasion: involvement of adrenal catecholamines.

Interleukin-1beta (IL-1beta) is released within the brain following stress, trauma, infection, and in specific brain disorders. This centrally acting IL-1beta has recently been shown to impair peripheral immunity. Central administration of IL-1beta suppresses natural killer (NK) cell activity impairs lung clearance of tumor cells and enhances tumor colonization. Using an in vivo model of tumor colonization (lung clearance of NK-sensitive MADB106 adenocarcinoma cells), this study examined the role of the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS) in mediating these effects. We demonstrate that adrenalectomy significantly attenuated the impaired lung clearance of MADB106 tumor cells induced by intracerebroventricular (i.c.v.) administration of IL-1beta (20 ng). Supplementing adrenalectomized animals with corticosterone did not reinstate the effect. The effect of IL-1beta on lung clearance was blocked by pretreatment with the beta-adrenergic antagonist, nadolol (0.5 mg/kg), but not by the alpha-antagonist phentolamine (5 mg/kg). Peripheral noradrenergic pathways are not implicated given that systemic administration of the noradrenergic neurotoxin, 6-hydroxydopamine, did not block the effect of IL-1beta. Taken together, these findings indicate that IL-1beta impairs lung clearance of MADB106 tumor cells via the actions of adrenal catecholamines, most likely epinephrine, acting at beta-adrenergic receptors in the periphery.

Adrenal Glands↗

PubMed1999

Lysosphingomyelin prevents behavioral aberrations and hippocampal neuron loss induced by the metabotropic glutamate receptor agonist quisqualate.

1. Excessive excitation of brain neurons by the excitatory neurotransmitter, glutamate, induces a cascade of events leading to increased intracellular Ca++, neuronal degeneration and death. 2. Recent in vitro research has demonstrated that a natural cationic amphiphile in the brain, lysosphingomyelin, may be able to prevent neuronal degeneration by repressing phosphosinositidase-C overactivation induced by excessive excitation of the metabotropic glutamate receptor. 3. This research tested the latter finding in vivo in a rat model of glutamate excitotoxicity. Intracerebroventricular (i.c.v.) administration of the Group 1 metabotropic glutamate receptor (mGluR) agonist, quisqualate, produced seizures, akinesia, destruction of hippocampal pyramidal cell dendritic microtubule-associated protein-2, and major loss of hippocampal CA sector neurons. 4. Prophylactic i.c.v. infusion of lysosphingomyelin powerfully attenuates these quisqualate-induced behaviors and prevents neuronal degeneration. 5. Lysosphingomyelin may be of clinical use in allaying progressive Group 1 mGluR-induced hippocampal cognitive and motor disorders including Alzheimer's disease, brain seizure, and stroke.

Animals↗

PubMed1999

Thymocyte development in male fetal alcohol-exposed rats.

We previously reported altered responses of thymocytes to mitogen stimulation after fetal alcohol exposure (FAE) in prepubertal male Sprague-Dawley rats. The purpose of this study was to examine the effect of FAE on the developmental pattern of thymocyte subsets. In the first experiment, we found that the proportion of double-labeled CD4+CD8+ thymocytes is identical in fetal alcohol-exposed (E) and control (C) animals at 34 and 45 days of age. In the second experiment--at 20, 28, 35, and 48 days of age--we examined the proportion of CD4+ and CD8+ thymocytes that express or are devoid of the maturational markers, the alpha/beta configuration of the T-cell receptor (TcR), and the restriction fragment C of the common leukocyte antigen (CD45RC). We found significant age-dependent effects on the numbers of total double-positive CD4-TcR and CD8-TcR or CD45RC thymocytes, and significantly lower numbers of total CD4+ and CD8+ cells in E than in C rats throughout this period--a finding consistent with the significantly lower total number of thymocytes in E than in C rats. The developmental patterns for both markers were similar in E and C groups, in both the rising (days 20 to 28) and declining (days 35 to 48) phases. However, on day 35, E rats had significantly lower numbers of double-positive CD8-TcR and CD8-CD45RC cells than C rats. It therefore seems that FAE tends to accelerate the decline of double-positive CD8-TcR and CD8-CD45RC cells. The contribution of this phenotypic change to the thymic functional alterations induced by FAE remains to be determined.

Animals↗

PubMed1998

Psychosine blocks quisqualate-induced glutamate excitotoxicity in hippocampal CA sector neurons.

Quisqualate is a potent specific agonist for Group 1 metabotropic glutamate receptors (mGluR's), that activate G protein-coupled phospholipase C (PLC) in a molecular signal-transduction mechanism that raises cytoplasmic Ca2+ and, when excessive, damages hippocampal neurons. Psychosine (beta-galactosylsphingosine), a cationic lysosphingolipid occurring naturally in nervous tissues, dose-dependently inhibited PLC activation induced by metabotropic alpha 1-adrenergic receptor signaling in cultured rat brain astrocytes in vitro. In the present study, we have tested neuroprotective efficacy of psychosine in vivo, in a rat model of glutamate excitotoxicity induced by intracerebroventricular (i.c.v.) administration of quisqualate. A sublethal i.c.v. dose of quisqualate caused episodes of prolonged akinesia and convulsions, and major damage to pyramidal neurons of the hippocampal CA1 and CA3 sector, but not to granule cell neurons of the dentate gyrus. Prior infusion of psychosine greatly attenuated quisqualate-induced behaviors, and fully prevented destruction by quisqualate of vulnerable hippocampal neurons. Psychosine may prove useful in prophylaxis of neurodegenerative disorders that arise from intensive hippocampal Group 1 mGluR stimulation.

Animals↗

PubMed1998

Intracerebral HIV glycoprotein (gp120) enhances tumor metastasis via centrally released interleukin-1.

Infection with the human immunodeficiency virus (HIV) is associated with a high incidence of cancers. This relationship does not appear to be due to a direct effect of the virus, and may be mediated by neuroimmune interactions since the HIV glycoprotein, gp120, enters the brain soon after infection with HIV, and intracerebroventricular (i.c.v.) infusion of gp120 suppresses aspects of cellular and tumor immunity. It has been speculated that this suppression may be attributed to the release of interleukin-1 (IL-1) in the brain induced by gp120. Using an in vivo tumor model, we examined the effect of centrally administered gp120 on tumor metastasis and lung clearance of mammary adenocarcinoma (MADB106) tumor cells in rats, and the role played by brain IL-1 in mediating these effects. We demonstrate that central administration of gp120 (4 microg) significantly (p<0.05) increased the retention of tumor cells in the lungs and significantly (p<0.02) enhanced the development of tumor metastases. Central administration of IL-1beta (10 ng) also significantly (p<0.05) increased retention of tumor cells in the lungs. The effect of gp120 on lung retention of tumor cells was blocked by co-administration of alpha-melanocyte stimulating hormone (alpha-MSH, 20 ng), a hormone that blocks many of the biological effects of IL-1, or the IL-1 receptor antagonist (50 microg). Given that systemic administration of gp120 or IL-1beta had no effect on the retention of tumor cells in the lungs, these findings indicate that gp120-induced secretion of IL-1 within the brain most likely mediates the effects of gp120 on tumor metastasis. These findings suggest a possible neuroimmune mechanism to account for the increased incidence and aggressiveness of tumors in HIV-infected patients.

Adenocarcinoma↗

PubMed1998

Immunologic cross-reactivity between respiratory chemical sensitizers: reactive dyes and cyanuric chloride.

BACKGROUND: CyCl is a low molecular weight reactive chemical used as an intermediate in the production of plastics, herbicides, pharmaceuticals, and fiber-reactive dyes. It is a potent inducer of specific IgE antibody. The CyCl functionality is a structural component of monochlorotriazine and dichlorotriazine dyes. OBJECTIVE: We have investigated the immunologic cross-reactivity between cyanuric chloride (CyCl) and reactive dyes and it was hypothesized that this moiety might be a dye epitope and that it might stimulate an allergic antibody response in dye-exposed workers. METHODS: To test this hypothesis, we have used sera with IgE antibodies to CyCl and also sera from dye-exposed workers who have IgE antibodies to Procion Orange MX2R, an azo dye containing the dichlorotriazine group. As a control group we have used dye-exposed workers with IgE antibody to Remazol Black B, a diazo dye containing the vinyl sulfone-reactive group. RESULTS: Using RAST and RAST inhibitions, we identified negligible cross-reactivity between CyCl and dichlorotriazine dye. CONCLUSION: The results of this study imply that the allergenic moiety on the dye residue resides in the chromophore rather than in the common structural component of CyCl and dichlorotriazine dyes.

Antibody Specificity↗

PubMed1998

Effects of prenatal alcohol and pair feeding on lipopolysaccharide-induced secretion of TNF-alpha and corticosterone.

Fetal alcohol exposure (FAE) produces profound alterations in immunological and neuroendocrine functions. The present study examined the effects of FAE on the secretion of tumor necrosis factor (TNF-alpha) and corticosterone following administration of lipopolysaccharide (LPS) in normal (N) adult rats, in adult offspring of dams fed a liquid diet supplemented with ethanol (E), and in pair-fed control offspring (P). LPS-induced TNF-alpha secretion was not affected by either gender or prenatal treatment. In contrast, LPS-induced corticosterone secretion was significantly greater in female than in male rats, and at 60-min post-LPS was significantly higher in E and P, compared to N females. Ovariectomy significantly inhibited LPS-induced TNF-alpha secretion in E, but not in P and N, rats and chronic replacement with 17-beta-estradiol markedly inhibited TNF-alpha secretion in ovariectomized E and N, but not in P, rats. In contrast, ovariectomy reduced the effects of LPS on corticosterone secretion in all groups, and chronic replacement with 17-beta-estradiol reversed this effect. These findings indicate that LPS-induced secretion of corticosterone, but not TNF-alpha, is affected by prenatal manipulations and by gender. In addition, alterations in the hormonal environment in females modulate LPS-induced corticosterone secretion in all prenatal treatment groups, but differentially influence TNF-alpha secretion in rats exposed to alcohol, restricted feeding, or normal diets in utero.

Animals↗

PubMed1997

Chronic dietary restriction influences tumor metastasis in the rat: parametric considerations.

Chronic dietary restriction is a well-documented means of inhibiting tumor growth. This study examines the effects of chronic dietary restriction on tumor metastasis in the rat. We investigate the effect of 1) the degree of food restriction, 2) the effect of preexposure to food restriction, and 3) the duration of food restriction after tumor inoculation on tumor metastasis. We also compare two methods of dietary restriction: 1) the time that food is available and 2) the amount of food available. Our findings demonstrate that rats restricted to 50% of ad libitum diet for one week before inoculation with MADB106 tumor cells and for three weeks after inoculation exhibit a significant (p < 0.001) reduction in lung colonization compared with animals fed ad libitum. Animals restricted to access to food for 4 hrs/day (60% of ad libitum) for the same period of time exhibit significantly (p < 0.005) greater lung tumor colonization than animals fed ad libitum. Preadaptation to the feeding regimen for one week before tumor inoculation proved to be critical in inhibiting tumor metastasis. The tumor-inhibitory effect was not significantly influenced by the duration of restriction after inoculation or by the manner in which food restriction was implemented. Finally, we demonstrate that inhibition of tumor colonization may be mediated by enhanced natural killer cell activity in the early postinoculation period.

Adenocarcinoma↗

PubMed1997

Fetal alcohol exposure augments the blunting of tumor necrosis factor production in vitro resulting from in vivo priming with lipopolysaccharide in young adult male but not female rats.

We previously reported altered responses of thymocytes and splenocytes to mitogen stimulation in fetal alcohol-exposed (FAE) male Sprague-Dawley rats. We also reported enhanced neuroendocrine responses to stressful stimuli in these animals. The experiments we describe herein aimed at testing whether young adult FAE rats manifest a notable dysregulation in the neuroendocrine-immune response to pathogen administration. We tested the effect of in vivo priming of the animal with a low dose of endotoxin [lipopolysaccharide (LPS), 5 micrograms/kg], considered to be suboptimal from the perspective of mounting detectable levels of circulating monokines several hours after administration, upon the production of immunoreactive tumor necrosis factor (TNF-alpha) in response to a further in vitro challenge of peripheral blood mononuclear cells with 2.5 micrograms/ml of LPS 90 min after priming. We show that the response to the LPS pathogen in vitro after priming is significantly blunted (p < 0.01) in male rats exposed prenatally to alcohol, compared with control male animals. FAE female rats and FAE ovariectomized female rats do not show significant differences in the priming response, compared with control animals. We also show that there is no correspondence between plasma corticosterone levels and TNF-alpha production after priming in any of the groups tested.

Animals↗

PubMed1996

Effects of fetal alcohol exposure on fever, sickness behavior, and pituitary-adrenal activation induced by interleukin-1 beta in young adult rats.

Exposure to alcohol in utero can lead to long-lasting impairments of immune functions and to decreased resistance to infectious agents. We have previously reported that fetal alcohol-exposed rats show markedly decreased lipopolysaccharide-induced fever and suggested that fetal alcohol exposure (FAE) impairs the communication between the immune and the nervous systems. The present study examined the effects of interleukin-1 beta (IL-1) on body temperature, motor activity, ingestive behavior, and pituitary-adrenal activation in fetal alcohol-exposed and control rats. Transmitters for continuous biotelemetric recording of body temperature and motor activity were implanted i.p. in normal (N) adult rats, offspring of dams fed a liquid diet supplemented with ethanol (E), and pair-fed control offspring (P). In one experiment, rats were injected with either IL-1 (2 micrograms/kg, i.p.) or saline at the beginning of the light period. IL-1 produced a marked increase in body temperature, which was significantly lower in E rats than in N and P rats. In a second experiment, rats were administered either IL-1 (10 micrograms/kg, i.p.) or saline at the beginning of the dark period. IL-1 produced an initial transient hypothermia followed by a longer-lasting hyperthermia. During the hyperthermic phase, fever in the E rats was lower than in the P rats, but comparable to fever in the N rats. IL-1 significantly reduced motor activity, during both the hypothermic and hyperthermic phases. This effect was similar in all prenatal treatment groups. IL-1 also suppressed 24-h food consumption in N and P rats and water consumption in P rats, but it did not produce significant anorexia and adypsia in E rats. A third experiment demonstrated that IL-1 (2 micrograms/ kg, ip) significantly increased ACTH and corticosterone release in all prenatal treatment groups. IL-1-induced corticosterone secretion was attenuated in P offspring, compared to both E and N rats. Together, these findings indicate that exposure to ethanol in utero produces impairments in mechanisms that mediate the effects of IL-1 on body temperature (particularly during the light period) and ingestive behavior, but not on motor activity and pituitary-adrenal activation. In view of the adaptive role of IL-1-induced fever and anorexia, these impairments may contribute to the decreased resistance to infections observed in animals and humans following FAE.

Adrenocorticotropic Hormone↗