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PubMed2002

Diabetes impairs hypothalamo-pituitary-adrenal (HPA) responses to hypoglycemia, and insulin treatment normalizes HPA but not epinephrine responses.

We recently established that in addition to plasma adrenocorticotrophic hormone (ACTH) and corticosterone, hypothalamic corticotrophin-releasing hormone (CRH) mRNA and hippocampal type 1 glucocorticoid receptor (GR1) mRNA were also upregulated in uncontrolled streptozotocin-induced diabetes. In the current study, control, diabetic, and insulin-treated diabetic rats underwent a hyperinsulinemic-hypoglycemic glucose clamp to evaluate central mechanisms of hypothalamo-pituitary-adrenal (HPA) and counterregulatory responses to insulin-induced hypoglycemia. Increases in plasma ACTH, corticosterone, and epinephrine were significantly lower in diabetic rats versus controls. Insulin treatment restored ACTH and corticosterone but not epinephrine responses to hypoglycemia in diabetic rats. Glucagon and norepinephrine responses to hypoglycemia were not affected by diabetes or insulin treatment. In response to hypoglycemia, hypothalamic CRH mRNA and pituitary proopiomelanocortin mRNA expression increased in control and insulin-treated but not in untreated diabetic rats. Arginine vasopressin mRNA was unaltered by hypoglycemia in all groups. Interestingly, hypoglycemia decreased hippocampal GR1 mRNA expression in control and insulin-treated diabetic rats but not in diabetic rats. In contrast, type 2 glucocortoid receptor (GR2) mRNA was not altered by hypoglycemia. In conclusion, despite increased basal HPA activity, HPA responses to hypoglycemia were markedly reduced in uncontrolled diabetes. We speculate that the defect in CRH response could be related to the defective GR1 response. It is intriguing that insulin treatment restored the HPA response to hypoglycemia but, surprisingly, not the deficient epinephrine response. This is important because during severe hypoglycemia, epinephrine is an important counterregulatory hormone.

Adrenal Glands↗
PubMed2006

Validity and reliability of Spanish versions of the Ruminative Responses Scale-Short Form and the Distraction Responses Scale in a sample of Spanish high school and college students.

This study investigated the construct validity and reliability of the Spanish Ruminative Responses Scale-Short From, and the Distraction Responses Scale of the Response Styles Questionnaire for a sample of 727 Spanish high school and college students who responded anonymously and voluntarily to a questionnaire (293 men, 434 women; ages 16 to 29 years, M=18.8, SD=3.0). In addition to the above scales, the questionnaire included the Spanish forms of the Beck Depression Inventory, the Trait Anxiety Scale from the State-Trait Anxiety Scale, the Satisfaction with Life Scale, and the Subjective Happiness Scale. The internal consistency of the scales was satisfactory (Cronbach alpha=.86 for the Ruminative Responses Scale and .78 for the Distraction Responses Scale). As expected, scores on the Spanish Ruminative Responses Scale showed positive correlations with those on the Beck Depression Inventory and the Trait Anxiety Scale and negative associations with the Satisfaction with Life Scale and the Subjective Happiness Scale. Conversely, the Spanish Distraction Responses Scale was negatively correlated with the Beck Depression Inventory and positively associated with the Satisfaction with Life Scale and the Subjective Happiness Scale. These results provide evidence of appropriate reliability for research purposes. Furthermore, the correlational analysis supported prior findings that ruminative response and distraction response styles are differentially associated with reported depressed and positive moods.

Adolescent↗
PubMed2002

Multivariate analysis of litter size for multiple parities with production traits in pigs: II. Response to selection for litter size and correlated response to production traits.

Litter size and production trait responses to experimental selection for increased litter size in a Landrace pig population are reported. The numbers of sows and litters available for the first cycle of selection were 3,034 and 961, respectively. Selection was carried out using a BLUP repeatability animal model for number of piglets born alive (NBA). The experiment included one selection and one control line, each with three nonoverlapping generations. The selection line (H) consisted of the 160 sows with the highest breeding values and one boar from each of 25 full-sib families with the highest breeding values. The control line (C) consisted of 160 sows and 25 boars randomly chosen. The two subsequent generations in each line were obtained by random selection. A Bayesian analysis of genetic response using a multivariate model was carried out by Gibbs sampler. Marginal posterior distributions were obtained for direct response in NBA, and for correlated response in weight (WT), and backfat thickness (BT) at 175 d of age. The posterior means and posterior standard deviation (PSD) for direct genetic response of NBA ranged from 0.32 (PSD 0.08) in the first parity to 0.64 (PSD 0.08) in the fourth. The posterior means for correlated genetic response in WT and BT were -0.66 kg (PSD 0.36) and 0.20 mm (PSD 0.10), respectively. For WT and BT, the 95% highest posterior density regions (HPD) contain zero-correlated genetic response. Marginal posterior distributions of selection differentials were investigated. The posterior means for standardized selection differentials for NBA in different parities ranged from 0.70 (PSD 0.12) to 0.94 (PSD 0.06) in females for line H, from 0.22 (PSD 0.19) to 0.34 (PSD 0.10) in males for line H, and from 0.08 (PSD 0.08) to 0.13 (PSD 0.07) in females for line C. All available males were used in line C. Results from this experiment showed that selection for increased litter size is effective. Responses to selection were heterogeneous across parities, suggesting that litter size in each parity may have a different genetic background. No correlated genetic response to growth and backfat thickness was observed.

Adipose Tissue↗
PubMed1992

N-benzylimidazole-mediated changes in hepatic drug-metabolizing enzyme activities in Ah-responsive and Ah-non-responsive mice.

1. The inductive effect of N-benzylimidazole (NBI) on hepatic microsomal and cytosolic drug-metabolizing enzyme activities in aryl hydrocarbon (Ah)-responsive C57BL/6N (B6) and Ah-non-responsive DBA/2N (D2) mouse strains was determined and compared with that caused by beta-naphthoflavone (BNF). 2. Relative Ah-responsiveness of the two strains was confirmed by measurement of BNF-induced ethoxyresorufin deethylase (EROD) activity and ELISA immunoquantification. BNF markedly induced EROD activity only in the Ah-responsive B6 mouse strain (65-fold increase). 3. NBI (150 mg/kg per day for 3 days) increased cytochrome P450 concentration similarly in both strains (40 and 60% in B6 and D2 strains, respectively). Compared with BNF treatment of the B6 strain, increases in EROD activity following NBI treatment were only minor. In addition, EROD activity increases were greater in the Ah-nonresponsive D2 strain (300%) than in the Ah-responsive B6 strain (100%) suggesting the possibility of an induction mechanism different from that of recognized Ah receptor agonists. 4. Induction of UDP-glucuronosyltransferase activity (p-nitrophenol acceptor) by BNF was greater in the Ah-responsive B6 strain than in the Ah-non-responsive D2 strain. NBI failed to induce this activity in either strain. 5. Induction of glutathione S-transferase activity towards 1-chloro-2,4-dinitrobenzene following NBI treatment occurred to the same extent (25% increase) as that seen following BNF treatment, in the Ah-responsive B6 strain. Neither xenobiotic affected this activity in the Ah-non-responsive D2 strain. 6. Although NBI is a major inducer, possessing Ah-like inducing properties in rat, it caused only minor changes in murine drug metabolizing enzymes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

The Visual Response Evaluation: a pilot study of an evaluation tool for assessing visual responses in low-level brain-injured patients.

The Visual Response Evaluation (VRE) was developed to meet the need for a formal and in-depth measure of visual responses in low-level brain-injured persons (Rancho Levels II and III) and to monitor and document minute changes in the recovery of these patients. Often, patients at these low functional levels exhibit little to no motoric or cognitive interaction with the environment, except that which occurs in response to sensory stimulation. Other tools have been developed to document responses to various types of stimulation; however, none contain the sensitivity to consistency and type of response that is necessary to show the small but vital progress that is characteristic of the Rancho II and II type patient. The VRE consists of 10 items separated into two general categories: (1) Observations. and (2) Response to Stimuli. The five items in the Observations section assess a patient's spontaneous responses, while the five items in the Response to Stimuli section document responses directly related to the presentation of a hierarchical order of stimuli. The VRE was administered to 10 patients with a mean age of 39.8 years at a mean time of 4.2 months post-injury. Statistical analyses of the pilot-study data show the VRE to be both internally reliable and criterion-related valid at the p less than 0.025 level of significance. The data supports further investigation in the areas of prognostic ability and implications for treatment. The VRE can be a useful tool for studying the recovery process and evaluating treatment programmes for low-level brain-injured persons.

Arousal↗
PubMed2004

Influences of multiple spatial stimulus and response codes on orthogonal stimulus-response compatibility.

When up-down stimuli are mapped to left-right responses, an up-right/down-left mapping advantage is found that is modified by response eccentricity and hand posture. These effects can be attributed to correspondence of asymmetric stimulus and response codes formed relative to multiple reference frames. We examined the influence of stimulus-set location on these orthogonal stimulus-response compatibility (SRC) effects. In Experiment 1, the stimulus set appeared in the upper or lower display positions. A spatial code for stimulus-set location was formed, producing Simon-type response eccentricity and hand posture effects, but this code had no influence on the coding of the relevant stimuli. In Experiment 2, the stimulus set appeared in the left, center, or right positions relative to the response location, which also varied, to dissociate the effects of response location, relative to the stimulus display and body midline. The former factor influenced the orthogonal SRC effect for both unimanual switch movements and bimanual keypresses, and the latter factor influenced the effect for only unimanual switch movements. Stimulus-set location causes orthogonal Simon-type effects when varied along the stimulus dimension and provides a referent for response coding when varied along the response dimension.

Choice Behavior↗
PubMed1982

Immune responses and immunoregulation in relation to human schistosomiasis in Egypt. I. Effect of treatment on in vitro cellular responsiveness.

Cell mediated immune reactivity of chronic schistosomiasis patients was tested in vitro by peripheral blood mononuclear cell (PBMN) responses against phytohemagglutinin P (PHA), Candida albicans extract, soluble schistosomal antigenic preparations derived from eggs (SEA), adult worms (SWAP) and cercariae (CAP), before and after treatment of the patients with parziquantel. The patient population was from villages in the Qalyub province, Egypt, that are endemic for Schistosoma mansoni and S. haematobium. Patients were studied immediately before, and at 1, 3, 6, and 9 months after chemotherapy. Egg counts were done on stool and urine specimens taken simultaneously with blood samples. There was a significant increase in PBMN responses to SWAP and CAP but not to SEA, PHA or C. albicans in 27 patients (age 8-65) 1 month after treatment. Eleven patients treated 1.5 years previously did not show such elevated responses 1 month after re-treatment. Three months after treatment higher mean responses were observed to SWAP, CAP, SEA, and PHA, but not to C. albicans in 24 patients (age 6-26). Significant increases in PBMN responses to SWAP and CAP, but not to SEA, PHA or C. albicans were obtained at 6 months after treatment in 12 patients (age 6-30). By 9 months after treatment in a group of 11 patients (age 8-25) SWAP and CAP responses were still elevated as were SEA and C. albicans induced reactivities. The PBMN responses of 10 patients were followed longitudinally at pretreatment, 3-, 6-, and 9-month post-treatment times. In general, elevated responses were maintained throughout this period to the schistosomal preparations. Unrelated responses occasionally fluctuated but were not consistently altered over time.

Adolescent↗
PubMed1999

Action of ethanol on responses to nicotine from cerebellar interneurons and medial septal neurons: relationship to methyllycaconitine inhibition of nicotine responses.

BACKGROUND: A majority of alcoholics also smoke, suggesting that alcohol and nicotine share a common action on nicotinic cholinergic receptors. METHODS: Extracellular single-unit recording was used to investigate the effects of ethanol on responses to nicotine from rat cerebellar interneurons and medial septal neurons. RESULTS: Nicotine produced inhibition from medial septal neurons, but increased neural activity of cerebellar interneurons. When ethanol was applied locally to cerebellar interneurons, the excitatory response to nicotine was enhanced in a dose-related manner. Nicotine-induced inhibition from medial septal neurons was reduced by ethanol from the majority of neurons, but a dose relationship for this inhibition by ethanol was not observed. Ethanol affected responses to nicotine from over 90% of all neurons investigated at these sites. Initially, it was established that the nicotinic antagonists, methyllycaconitine (MLA) and alpha-bungarotoxin, which affect a nicotinic cholinergic (nACh) receptor with an alpha7 subunit, had similar actions on responses to nicotine from individual medial septal cells and cerebellar interneurons. When MLA was tested against responses to nicotine from neurons in the two brain regions, MLA antagonized responses to nicotine from only 27% of the neurons rather than the 90% found for ethanol. This latter observation provided evidence that ethanol was affecting neurons with MLA-insensitive receptors. When the actions of ethanol on responses to nicotine were compared directly with the action of MLA on the same medial septal neurons, both ethanol and MLA caused a greater than 50% antagonism of the response to nicotine, indicative that nACh receptors with the alpha7 subunit were sensitive to ethanol. CONCLUSIONS: Collectively, these data provide evidence that ethanol affects responses to nicotine not only from nACh receptors on medial septal cells and cerebellar interneurons containing an alpha7 subunit (i.e., MLA-sensitive receptors), but also from nACh receptor subtypes without this specific nACh receptor subunit (i.e., MLA-insensitive receptors).

Aconitine↗
PubMed2000

Separate proliferation kinetics of fibroblast growth factor-responsive and epidermal growth factor-responsive neural stem cells within the embryonic forebrain germinal zone.

The embryonic forebrain germinal zone contains two separate and additive populations of epidermal growth factor (EGF)- and fibroblast growth factor (FGF)-responsive stem cells that both exhibit self-renewal and multipotentiality. Although cumulative S phase labeling studies have investigated the proliferation kinetics of the overall population of precursor cells within the forebrain germinal zone through brain development, little is known about when and how (symmetrically or asymmetrically) the small subpopulations of stem cells are proliferating in vivo. This has been determined by injecting timed-pregnant mice with high doses of tritiated thymidine ((3)H-thy) to kill any stem cells proliferating within the striatal germinal zone in vivo and then by assaying for neurosphere formation in vitro. Injections of 0.8 mCi of (3)H-thy given every 2 hr for 12 hr to timed-pregnant mice at E11, E14, and E17 resulted in significant depletions in the number of neurospheres generated by FGF-responsive stem cells at E11 and by EGF-responsive and FGF-responsive stem cells at E14 and E17. With increasing embryonic age, the depletions observed in the number of neurospheres generated in vitro in response to FGF2 after exposure to (3)H-thy in vivo decreased, suggesting there is an increase in the length of the cell cycle of FGF-responsive neural stem cells through embryonic development. The results suggest that the FGF-responsive stem cell population expands between E11 and E14 by dividing symmetrically, but switches to primarily asymmetric division between E14 and E17. The EGF-responsive stem cells arise after E11, and their population expands through symmetric divisions and through asymmetric divisions of FGF-responsive stem cells.

Animals↗
PubMed1975

Drugs and punished responding. V. Effects of drugs on responding suppressed by response-dependent and response-independent electric shock.

A procedure was used where responses by a pigeon produced electric shock both to that pigeon (response-dependent shock) and to another pigeon (response-independent shock) working under the same schedule of food presentation. Both response-dependent and response-independent shock partially suppressed responding. Pentobarbital, chlordiazepoxide and ethanol increased responding suppressed by response-dependent shock, but only pentobarbital increased responding suppressed by response-independent shock. Morphine, d-amphetamine, chlorpromazine, doxepin, and pentazocine either had no effect, or further decreased rates of responding suppressed by response-dependent or response-independent shock.

Animals↗
PubMed1976

Regulation of antibody response in vitro. X. Biphasic effect of cyclic AMP on the secondary anti-hapten antibody response to anti-immunoglobulin and enhancing soluble factor.

The effect of elevation of an intracellular cyclic AMP level on in vitro anti-hapten antibody response was studied, by using mesenteric lymph node cells of rabbits which were primed with dinitrophenylated Ascaris antigen (DNP-Asc) or DNP-ragweed antigen (DNP-Rag). The anti-hapten antibody response was induced by stimulation of the primed B cells by either DNP-heterologous carrier conjugate or anti-immunoglobulin (anti-Ig) for 24 hr (first stage), followed by 6-day culture of the activated cells in the presence of nonspecific enhancing factor (second stage). The stimulation with anti-Ig induced IgG anti-hapten antibody response and enhanced the formation of total IgG. Addition of dibutyryl cyclic AMP or aminophylline with anti-Ig or DNP-heterologous carrier during the first stage enhanced IgG anti-hapten antibody response. The optimal concentration of these reagents for the enhancement was 5 x 10(-4) M to 10(-3) M. The presence of 5 x 10(-6) M prostaglandin E1 during the first stage also enhanced the antibody response. Similarly, the presence of dibutyryl cyclic AMP or aminophylline during the stimulation of DNP-Rag-primed cells with homologous antigen (first stage) enhanced the antibody response. If the same concentration of dibutyryl cyclic AMP or aminophylline was added together with enhancing soluble factor during the second stage after the stimulation of the primed cells with anti-Ig, both the antibody response and the formation of IgG were suppressed. The antibody response of DNP-Rag-primed cells stimulated with homologous antigen was also suppressed if dibutyryl cyclic AMP or aminophylline was added during the subsequent culture (second stage). Evidence was obtained that suppression of antibody response by cyclic AMP during the second stage is probably due to inhibition of the proliferation of B cells. Neither of these drugs suppressed the formation of enhancing soluble factor from the carrier-specific cells stimulated with the homologous carrier. The results obtained in the present experiments suggested that stimulation of hapten-primed B cells with anti-gamma chain in the presence of an optimal concentration of dibutyryl cyclic AMP resulted in the formation of a significant amount of IgG anti-DNP antibody without participation of T cells.

Animals↗
PubMed1991

GH response to GH-releasing factor in dementia and its relation with TSH response to TSH-releasing factor.

We have studied the GH response to GH-releasing factor (GRF) and the TSH response to TSH-releasing factor (TRH) in two groups or patients with dementia. A group of 28 patients with Alzheimer's disease (AD) and another group of 28 patients with dementia of vascular origin (VD). The GH response to GRF exhibited no difference between AD and VD patients (12.2 +/- 10.85 micrograms/L vs. 9.96 +/- 9.9) and there was no correlation with GH response to GRF and sex, stage of the disease and cerebral atrophy. The number of cases with exaggerated, normal or without response were similar in AD or VD patients. The TSH response to TRH exhibited no difference between AD and VD patients (9.18 +/- 4.93 mU/ml vs. 10.35 +/- 8.81). There was no correlation with TSH response to TRH and sex, stage of the disease, cerebral atrophy and response of GH to GRF. The number of cases with exaggerated, normal or without response was similar in AD or VD patients.

Aged↗
PubMed1985

Genetic regulation of the immune response to hepatitis B surface antigen (HBsAg). V. T cell proliferative response and cellular interactions.

We previously demonstrated that in vivo antibody production to HBsAg in the mouse is regulated by at least two immune response (Ir) genes mapping in the I-A (HBs-Ir-1) and I-C (HBs-Ir-2) subregions of the H-2 locus. To confirm that H-2-linked Ir genes regulate the immune response to HBsAg at the T cell level and to determine if the same Ir genes function in T cell activation as in B cell activation, the HBsAg-specific T cell responses of H-2 congenic and intra-H-2 recombinant strains were analyzed. HBsAg-specific T cell proliferation, IL 2 production, and the surface marker phenotype of the proliferating T cells were evaluated. Additionally, T cell-antigen-presenting cell (APC) interactions were examined with respect to genetic restriction and the role of Ia molecules in HBsAg presentation. The HBsAg-specific T cell proliferative responses of H-2 congenic and intra-H-2 recombinant strains generally paralleled in vivo anti-HBs production in terms of the Ir genes involved, the hierarchy of responses status among H-2 haplotypes, antigen specificity, and kinetics. However, the correlation was not absolute in that several strains capable of producing group-specific anti-HBs in vivo did not demonstrate a group-specific T cell proliferative response to HBsAg. The proliferative responses to subtype- and group-specific determinants of HBsAg were mediated by Thy-1+, Lyt-1+2- T cells, and a possible suppressive role for Lyt-1-2+ T cells was observed. In addition to T cell proliferation, HBsAg-specific T cell activation could be measured in terms of IL 2 production, because anti-HBs responder but not nonresponder HBs-Ag-primed T cells quantitatively produced Il 2 in vitro. Finally, the T cell proliferative response to HBsAg was APC dependent and genetically restricted in that responder but not nonresponder parental APC could reconstitute the T cell response of (responder X nonresponder)F1 mice, and Ia molecules encoded in both the I-A and I-E subregion are involved in HBsAg-presenting cell function.

Animals↗
PubMed1981

Lymphoid cell responses to bacterial cell wall components: mitogenic responses of murine B cells to Streptococcus mutans carbohydrate antigens.

The mitogenic activity of various purified serotype carbohydrate and cell wall lysate fractions of Streptococcus mutans for murine lymphocytes has been determined. The highest mitogenic responses occurred after 48 hr of stimulation with these carbohydrate preparations when tested on splenic cultures derived from C3H/HeJ and BALB/c mice. The response pattern obtained with optimum concentrations of these preparations was very similar to that seen with the B cell mitogen, LPS. A purified serotype g carbohydrate (M1 g) prepared by mutanolysin enzyme treatment of S. mutans 6715 cell walls stimulated good mitogenic responses in BALB/c nude and nu/+ splenic cultures, suggesting an effect on mouse B cells. This was further substantiated by studies showing that this antigen also induced responses in cultures of B cells purified by nylon wool fractionation, whereas purified T cells did not respond. Mitogenic responses were due to the carbohydrate moiety and not to possible LPS contamination, since alkaline treatment or mixture with polymyxin B greatly reduced responses to LPS; however, no alteration of mitogenic responses to M1 g occurred. Further, LPS nonresponsive C3H/HeJ spleen cells yielded good mitogenic responses to M1 g. On the other hand, periodate treatment, which is known to decompose carbohydrate moieties completely abrogated the mitogenic activity of M1 g antigen. Additional studies with serotypes c and e carbohydrate, which also induced mitogenic responses, suggested that this activity for lymphoid cells may be a common property of S. mutans cell wall carbohydrate.

Animals↗
PubMed1976

Regulation of antibody response in different immunoglobulin classes. I. Selective suppression of anti-DNP IgE antibody response by preadministration of DNP-coupled mycobacterium.

Selective suppression of IgE antibody response was demonstrated. Preadministration of DNP-coupled mycobacterium (DNP-Tbc) inhibited the formation of anti-DNP IgE antibody induced by DNP-OA without any suppressive effect on anti-DNP IgG antibody response. Secondary anti-DNP IgE antibody response by DNP-OA was also significantly depressed by the preadministration of DNP-Tbc. Anti-OA IgE antibody response induced by DNP-OA was also depressed by DNP-Tbc, whereas anti-OA IgE antibody response induced by PAB-OA was not affected by the preadministration of DNP-Tbc. Preimmunization with DNP-MGG induced much higher anti-DNP IgG antibody response than DNP-Tbc, but DNP-MGG did not suppress the induction of anti-DNP IgE antibody. The transfer of DNP-Tbc-primed spleen cells into normal mice depressed anti-DNP IgE antibody response. B cell-depleted cell populations also showed a comparable inhibitory effect to that of unfractionated DNP-Tbc primed cells. In the adoptive cell transfer experiment, DNP-Tbc-primed cells depressed anti-DNP IgE antibody response of DNP-OA-primed cells when these cells were stimulated with DNP-OA. These results suggested that DNP-specific T cells induced with DNP-Tbc selectively inhibited IgE antibody response.

Animals↗
PubMed1993

Fever and the immune response. The effects of physiological temperatures on primary murine splenic T-cell responses in vitro.

Fever is a common sign of clinical disease but its biological purpose is unclear. Several cytokines mediate fever as well as the regulation of immune responses, and it was previously shown that murine thymocyte proliferative responses to IL-1 and IL-2 are exquisitely temperature-sensitive. The present studies were performed to determine whether such a high degree of temperature sensitivity was also a property of the primary in vitro immune responses of mature, murine splenic T cells. Using a physiological range of temperatures spanning those of normal skin (29 degrees C) to those of febrile core tissues (39 degrees C), primary murine spleen cell proliferative responses to either Con A, solid-phase anti-CD3 antibody, specific Ag, or allogenic cells were all found to display a high degree of temperature sensitivity. A similar pattern of strong temperature sensitivity was found for the capacity of primary MLR cultures to generate allospecific effector CTL. All of these forms of T-cell temperature sensitivity are expressed both in terms of the absolute degree of the response and in terms of its kinetics, the warmer temperatures up to 35 degrees C to 37 degrees C giving larger responses sooner than the lower physiological temperatures of 29 degrees C to 33 degrees C, at which these responses are markedly inhibited relative to those at 37 degrees C. In contrast, the effector cytolytic activity of a previously formed population of CTL is remarkably insensitive to the same temperature changes that strongly regulate the generation of those effector cells. The temperatures that usually define fever are those appropriate to the core tissues of a febrile animal, yet temperature changes in this range (37 degrees C-39 degrees C) had little stimulatory effect upon the T-cell responses studied, and were, in some cases, actually inhibitory. Temperature changes appropriate to the peripheral tissue temperatures in an animal becoming febrile (29 degrees C-37 degrees C) appear to be the ones that strongly regulate mature primary T-cell responses. These results suggest that one purpose of either fever or local tissue inflammation may be to temporarily ablate the cooler portions of normal thermal gradients, thereby selectively amplifying the emergence of T-cell immunity in peripheral tissues.

Animals↗
PubMed1996

Bias in the gamma delta T cell response to Listeria monocytogenes. V delta 6.3+ cells are a major component of the gamma delta T cell response to Listeria monocytogenes.

Despite extensive research, the role that gamma delta T cells play in the immune response to infectious disease has yet to be established. Here we report the generation of a mAb specific for the V delta 6.3 TCR and investigate the gamma delta+ and V delta 6.3+ T cell responses to the intracellular bacterium Listeria monocytogenes in BALB/c mice. By infecting animals with various doses of Listeria and analyzing the components of the cellular immune response at the two primary sites of infection, the liver and spleen, we have shown that the kinetics, composition, and magnitude of the gamma delta and V delta 6.3 T cell responses are dependent upon the injected dose of bacteria and the organ in which the infection is established. At low doses of infection, the gamma delta T cell response occurs late in the disease course, while at high doses, the response is earlier and of greater magnitude, particularly in the liver. At all infectious doses and in both tissues, the V delta 6.3+ population predominates and together with V delta 4+ cells composes the bulk of the gamma delta T cell response. Changes in the morphology of gamma delta+ and V delta 6.3+ cells at the site of infection are consistent with cellular activation and suggest that these cells are active participants in the Listeria-induced immune response. The results of our study suggest that many features of the gamma delta T cell response to Listeria are dose and tissue related.

Animals↗
PubMedDate not supplied

Divergent antibody responses to vaccines and divergent body weights of chicken lines selected for high and low humoral responsiveness to sheep red blood cells.

Primary and secondary antibody responses to intramuscularly administered proteins of Eschericia coli (F11), Newcastle disease virus (NCD), infectious bronchitis virus (IB), and infectious bursal disease virus (IBD), respectively, were measured at weekly intervals in two chicken lines. The latter had been divergently selected for high and low antibody responses to sheep red blood cells (SRBC), and in a random-bred control line. An oil-based adjuvant was required to induce primary and secondary antibody responses to NCD, IB, and IBD. With respect to F11, elevated antibody responses were found in birds sensitized and boosted to F11 with and without adjuvant. The humoral response to F11 and to all viral antigens was significantly higher in the high (H) line than in the low (L) line, whereas the control (C) line showed intermediate titers. At 5 and 17 weeks of age, L line birds were significantly heavier than birds of the H and the C lines. A negative phenotypic correlation within lines between body weight at 17 weeks of age and antibody titers at 1 week after sensitization was found, but no further correlations between humoral responses and body weight or growth could be established. The present results suggest that selection for enhanced humoral responsiveness to SRBC resulted in enhanced responsiveness to components of several vaccines. Mechanisms underlying the relationship between divergent selection for immune responsiveness and body weight are discussed.

Animals↗