PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Mice, Inbred CBA”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed2006

Toll-like receptor 3 agonist induces impairment of uterine vascular remodeling and fetal losses in CBA x DBA/2 mice.

The objective of this study was to examine the expression of Toll-like receptor (TLR) 3 at the maternal-fetal interface and determine whether exposure to TLR3 agonist would induce an innate immune response and trigger pregnancy loss. To address this, abortion-prone male DBA/2J mated-CBA/J female mice were given polyinosinic-polycytidylic acid (poly I:C; 10 microg/g body weight, i.p.) or PBS at gestation day (gd) 6.5. All implantation sites appeared viable at gd 7.5 when endometrium was dissected for immunohistological examination. It was noted that poly I:C treatment increased fetal losses to 40.2+/-1.7% at midgestation stage compared with control animals (11.0+/-3.0%). It was observed also that the ratio of vessel to lumen area significantly increased at gd 10.5 and gd 12.5 after poly I:C treatment, indicating that the spiral artery (SA) modification was impaired. Meanwhile, 24h after poly I:C injection, expression of TLR3 was markedly elevated within decidua basalis (DB), and endometrial TNF-alpha increased 2.7-fold but IFN-gamma remained unchanged in homogenized endometrium. These results suggest that enhanced TNF-alpha expression in endometrial stroma may play a critical role in inflammatory factor production and impairment of uterine spiral artery remodeling in the pregnancy failure of CBA x DBA/2 mating.

Animals↗
PubMed1977

The effect of Treponema pallidum on mouse survival.

Intraperitoneal infection with Treponema pallidum did not shorten the lives of inbred CBA mice. One hundred and fifty infected mice survived to a mean age of 41-24 months and 60 uninfected mice to a mean age of 41-38 months.

Animals↗
PubMed1987

Met-enkephalin levels in midbrain dopamine regions of inbred mouse strains which differ in the number of dopamine neurons.

The Met-enkephalin content in tissue micropunches of the substantia nigra zona compacta, ventral tegmental area and the caudate nucleus in BALB/c and CBA mouse strains was measured by radioimmunoassay. The CBA strain had significantly higher Met-enkephalin levels in all 3 regions than the BALB/c strain. These differences should be taken into account when relating the intensity of dopamine-induced behaviors to the number of dopamine neurons.

Animals↗
PubMed1984

Noise and the young mouse: genotype modifies the sensitive period for effects on cochlear physiology and audiogenic seizures.

A sharply defined "critical period" has been described for the young C57BL/6 mouse, during which acoustic trauma will profoundly alter subsequent auditory behavior (audiogenic seizures, acoustic startle reflex). In several genotypes and species, a broader "sensitive period" exists, during which acoustic trauma is most damaging to cochlear functions in the young ear. In order to examine the correspondence of these two events, C57BL/6 and CBA inbred mice, at eight ages ranging from 12 to 54 days, were exposed to 2 min of a 124-dB (SPL) octave band noise (8-16 kHz). A noninvasive electrocochleographic technique was used to assess cochlear microphonic (CM) and action potential (AP) thresholds in exposed mice and their nonexposed littermate controls. This allowed cochlear functional measures and behavioral tests (susceptibility to audiogenic seizures) to be made in the same animals. Noise has no observable effect on the 12-day-old CBA mouse, produced a maximal threshold elevation (47 dB for AP, 28 dB for CM) at 30-36 days, with the effect declining to nearly half of this value in 54-day-old subjects. Susceptibility to audiogenic seizures in the exposed CBA mice was greatest at the peak of this sensitive period for cochlear damage (r = .95). C57BL/6 mice also appeared unaffected when noise exposure occurred at 12 days of age; they had maximal AP (23 dB) and CM (17 dB) threshold elevations at 36 days, and 54-day-old mice had an 18-dB elevation of the AP and their CM was no longer affected. Susceptibility to audiogenic seizures was greatest in C57BL/6 mice exposed to noise at 18 days, and it did not correspond with the sensitive period for cochlear damage (r = .21). Therefore, both genotypes have a sensitive period for the effects of noise trauma on the CM and AP, the CBA has a sensitive period for acoustic priming for audiogenic seizures, and the C57BL/6 has a critical period for acoustic priming. Genetic differences in age-related losses of central nervous system auditory functions are postulated as being responsible for these behavioral differences. These data are compared with known auditory functions of the SJL and BALB/c mouse strains in order to explain genetically determined differences of the sensitive (or critical) period of acoustic priming, and for the length of time the mice subsequently remain susceptible to audiogenic seizures.

Acoustic Stimulation↗
PubMed1991

Complete Freund adjuvant treatment of pregnant females influences resorption rates in CBA/J x DBA/2 matings via progesterone-mediated immunomodulation.

Treatment of pregnant CBA/J females with CFA at day 0.5 and 7.5 of pregnancy significantly reduced the fetal resorption rates from 45% to 29% (P less than 0.05). Supernatants of progesterone-treated spleen cells from CFA treated CBA/J females pregnant of DBA/2 males significantly reduced natural cytotoxicity, while those of untreated identically pregnant mice had no effect. Supernatants of CFA-treated virgin mice blocked natural cytotoxicity to the same extent as those of CFA-treated pregnant mice. These data suggest that nonspecific immunostimulation induces progesterone receptors in spleen cells of CBA mice and that these receptors allow a progesterone dependent suppressive pathway to exert an antiresorptive effect.

Animals↗
PubMedDate not supplied

Interference between two immune responses. I.--Modification of the kinetics of the mouse response to SRBC by responses to heterologous RBC.

Influence of a preceding immunization with HoRBC on the immune response to SRBC was studied in Swiss and CBA inbred mice. In Swiss mice, a short interval (1day) between the two immunizations produced an acceleration of anti-SRBC response, while a longer interval (4-7 days) inhibited this response. This was interpreted as manifestations of nonspecific helper and suppressor activities triggered by the previous challenge. At any time of a response, there would exist a variable ratio of these two opposite activities. The helper activity was radiation-resistant while the suppressor one was radiation-sensitive at the time of its appearance and was effective on the IgG as well as on the IgM response. CBA mice response to SRBC was only influenced by the suppressor and not by the helper component of the preceding challenge with HoRBC. These CBA mice were very good responders to this antigen, and this may be the cause of their strain particularities. If we consider that each individual is permanently submitted to natural immunizations, the ratio of the resulting non-specific activities must be esentially variable with time; it can partly account for the individual amplitude variation of an engaged immune response.

Animals↗
PubMed1976

[Graft vs host reaction in reciprocal combinations of mouse strains differing by the H-2 complex of histocompatibility].

Intraperitoneal transplantation of 0.5 x 10(7), 1 x 10(7) or 2 x 10(7) spleen cells from the C57BL mice to newborn CBA recipients induced an acute form or runt disease which resulted in the death of 43%, 86% or 95% of the recipient mice, respectively, in the course of 2--3 weeks after the cell transfer. Preliminary immunization of C57BL donors with CBA isoantigens led to a marked enhancement, and immunization with foreign antigens (sheep red blood cells)--to weakening the reaction. In reverse combination of mouse strains the runt disease was 4--5 times less severe and no "preimmunization effect" occurred. In C57BL leads to CBA combination the reaction was accompanied by proliferation of pyroninophilic mononuclears and follicular destruction, while in the CBA leads to C57BL combination-by the retardation of their growth.

Animals↗
PubMed1977

H-2 mutation affecting immune response to Thy-1.1 antigen.

Mouse thymus, thymus-derived lymphocytes, and brain share an antigen determined by gene at the Thy-1 locus in chromosome 9 (1). Two alleles have been identified at this locus: Thy-1(a), coding for antigen Thy-1.1 (or theta-AKR) present in AKR and seven other strains; and Thy-1(b), coding for antigen Thy-1.2 (or{teta}-C3H) and present in C3H and all the remaining inbred strains. Injection of AKR thymocytes into inbred mice carrying the Thy-1(b) allele results in an immune response that can be measured either serologically by determining the level of antibodies in the recipients' serum (1) or by counting plaque- forming cells (PFC) detectable in spleens of the recipients by means of an assay, with AKR thymocytes as target cells(2). The magnitude of PFC and serum antibody responses after a single thymocyte injection depends on the genetic make-up of the recipient. Three genes controlling the PFC response to the Thy- 1.1 antigen have been identified: Ir-Thy-1A and Ir-Thy-1B, which are closely linked to the major histocompatibility complex (H-2) of the mouse (3-6), and Ir-5, which is located at a distance of 17 cm to the right of the H-2 complex on chromosome 17 (6). Previous genetic mapping with H-2 recombinant strains has indicated that the two Ir-Thy-1 loci are located to the left of the IC subregion (7). Further experiments strongly suggested that either one or both Ir-Thy-1 loci map to the K rather than the I region of the H-2 complex (8). In this report, the study of an H- 2 mutant, CBA-H-2(ka) (M523) (9), and its parental strain, CBA/LacStoY (CBA) provided further evidence that one of these loci apparently resides in the K region and might even be identical with the H-2K locus in that region.

Animals↗
PubMed1991

The population dynamics of acquired immunity to Heligmosomoides polygyrus in the laboratory mouse: strain, diet and exposure.

An experiment was designed to investigate aspects of the population dynamics of acquired immunity to Heligmosomoides polygyrus in laboratory mice. The influence of host strain (CBA or NIH), rate of exposure (5 or 40 L3/mouse/2 weeks) and diet (3 or 16% protein w/w) on the population dynamics of repeated infection and the response to a standard challenge infection were investigated. The time delay between the end of the period of repeated infection and the subsequent challenge (between 1 and 24 weeks) had no effect on worm recovery. The effects of both exposure and diet were significant and similar whether assessed on the basis of the dynamics of repeated infection or response to challenge: low rates of exposure and low dietary protein were both associated with low levels of acquired immunity. Mouse strain was the most important determinant of worm recovery after challenge, but had no significant effect on the degree to which parasite population growth was constrained by acquired immunity during repeated infection. It is suggested that both CBA and NIH mice raise immune responses which act on parasite survival, but that only NIH mice raise responses operative against larval establishment.

Animal Nutritional Physiological Phenomena↗
PubMed1980

[Induction of tolerance to alloantigens in adult mice].

The tolerance to allogeneic C57BL/6 cells (H--2b) was induced in adult CBA mice (H--2k). For tolerance induction three kinds of treatment were combined: thymectomy of adult CBA mice, intravenous inoculation of 1 x 10(8) spleen C57BL/6 cells and injection of 200 mg/kg of cyclophosphamide after 24 hours. Such a treatment of CBA mice resulted in long survival (up to 5 months) of allogeneic C57BL/L heart grafts. The data obtained in MLC reaction supported unresponsiveness of tolerant CBA mice to H-2 antigens of C57BL/6 mice. No lymphoid tissue chimerism was observed in tolerant mice.

Animals↗
PubMed1994

Frequency of X-Y chromosome dissociation in mouse spermatocytes from interstrain crosses, recombinant inbred strains, and chimeras: possible involvement of paternal genome imprinting.

The frequency of dissociation of the X-Y chromosome bivalent in diakinesis-metaphase I spermatocytes differs significantly between two inbred mouse strains, CBA (29%) and KE (7%), that were used to obtain reciprocal F1 hybrids, and to develop recombinant inbred (RI) strains. The level of X-Y dissociation was significantly higher in (KExCBA)F1 hybrids sired by the CBA males (24%) than in reciprocal F1 hybrids (12%), revealing the inheritance after the father. Among 14 RI strains, nine were concordant with KE, one with CBA, and four had intermediate phenotype, significantly different from both progenitor strains. This shows that at least two genes are involved, and their possible linkage with agouti and Trf loci is suggested. The linkage with agouti was confirmed by testing additional 10 CBXE incipient RI strains. There was no significant difference in the level of X-Y dissociation between EXCB RI strains derived from the original cross sired by the CBA males and CBXE RI strains derived from the reciprocal cross. The involvement of the Y chromosome-linked factors was unlikely because it was found earlier (Krzanowska, 1989: Gamete Res 23:357-365) that two congenic strains, KE and KE.CBA, differing with respect to the source of the Y chromosome, had the same level of X-Y dissociation. Thus, the difference obtained between reciprocal F1 hybrids is interpreted in terms of paternal genome imprinting imposed by CBA males and propagated only in the presence of some alleles derived from this strain.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1982

Erythroleukemia induction by Friend leukemia virus. A host gene locus controlling early anemia or polycythemia and the rate of proliferation of late erythroid cells.

This report confirms that the Fv-5 locus controls the types of erythropoiesis induced by Friend erythroleukemia virus (FLV) (21) and extends the study to investigate the mode of action of this locus. With the use of FLV obtained by a variety of procedures, we showed that the polycythemia spleen focus-forming component (SFFVp) was responsible for the contrasting changes of hematocrits observed in FV-Pp (polycythemia strain)-infected DBA/2 (Fv-5pp) or CBA (Fv-5aa) mice. These changes in hematocrits were found to be a direct result of the rise in circulating reticulocytes and erythrocytes in DBA/2 mice and a corresponding drop of these erythroid cells in CBA mice 2 wk after infection. Examination of the FV-P-induced cellular changes indicated that dramatic increase in erythropoietin (epo)-independent erythroid precursor (CFU-E*) cells was detected in the spleens and marrow of both strains of mice. The epo responsiveness of the CFU-E in the uninfected and FV-P-infected CBA and DBA/2 mice was also very similar. Similar to FLV-infected DBA/2 mice, the FV-P-infected CBA mice also developed tumorogenic cells (CFU-FV) relatively early after infection (4-6 wk). Study of the physiological and pathological changes in the marrows and spleens of these infected mice indicated that significant differences were found in the spleens of the two strains of mice. The percent of reticulocytes in the spleen cells of CBA mice remained between 10 and 20%, and level of the DBA/2 mice increased to approximately 50%. This higher rate of erythropoiesis was also reflected in the significantly higher rate of uptake of 59Fe in the spleens of the DBA/2 mice. These results suggest that the Fv-5 locus might control the hematocrit levels of these mice by regulating the rates of erythropoiesis in the spleen levels of these mice, probably by affecting the rate of proliferation of an erythroid cell or cells. The erythroid cell(s) affected is likely to be more mature than the erythroid progenitor, CFU-E, as the levels of CFU-E in these two strains of mice were similar. The hypothesis that Fv-5 may control the rates of proliferation of a late erythroid (cell(s) is also supported by the significantly higher spleen weights found in the infected DBA/2 (approximately 2.5 g/spleen) mice than in the CBA (approximately 1 g/spleen) strain.

Anemia↗
PubMed2000

Features of the genetically defined anxiety in mice.

The behaviors of male mice of the C57BL/6J (C57), CBA/Lac (CBA) and BALB/c (BALB) strains have been studied in the plus-maze and open field tests for estimation of state anxiety in the stressful novel conditions, and in the cubic box test (exploration of novel cubic box) and the partition test (behavioral reactivity to the unfamiliar partner in the neighboring compartment) for estimation of trait anxiety in the unstressful familiar conditions of the home cage. Plus-maze data suggest that C57 mice are the more anxious than CBA and BALB ones. However, it was revealed the opposite rank order in the open field. The study on the effect of pre-testing in the one of test on the behavior in the other test revealed active behavioral strategy in C57 mice in any situations. The plus-maze behavior of CBA mice was affected to a much lesser extent than in C57 ones after pre-testing in the open field, but expressed changes were observed in open field behavior of CBA mice after pre-testing in the plus-maze. BALB mice displayed low-reactive behavior after any pre-testing exposure under the state anxiety-provoking conditions. Familiar environment revealed a higher level of trait anxiety in C57 than males of other two strains: CBA and BALB mice willingly explore unfamiliar partner and cubic box while C57 mice avoid its. Mainly genetically inherent state anxiety in CBA mice and trait anxiety in C57 mice has been suggested. Lowest state and trait indices of anxiety were revealed in BALB mice in these conditions.

Animals↗
PubMed1995

Effects of endotoxin and dexamethasone on cerebral malaria in mice.

CBA/T6 and DBA/2J mice inoculated with Plasmodium berghei ANKA (PbA) develop cerebral involvement 6-8 days post-inoculation, from which the CBA mice almost invariably die and the DBA mice recover. Dexamethasone (DXM; 80 mg/kg) given to inoculated CBA mice twice, on day 3 and again within 48 h, reduced the cerebral symptoms and prevented death from cerebral malaria. Plasma tumour necrosis factor (TNF) levels, which increased at the time of the cerebral symptoms, were also reduced in these DXM-treated mice. Intravenously administered Evans Blue, a dye which binds to albumin, diffused extensively across the blood-brain barrier only during the period of cerebral symptoms, in proportion to the severity of the cerebral symptoms and the disease. In PbA-infected CBA mice, cerebral symptoms and the amounts of Evans Blue diffusing into the brain tissue were both reduced by DXM treatment, but only if the steroid was given on day 3 and again within 48 h. Endotoxin injected intravascularly into PbA-infected DBA mice after day 5 resulted in an exaggeration of cerebral symptoms and death between days 6 and 9. Plasma TNF and the amount of Evans Blue in the brain parenchyma increased above normal levels in these mice. Endotoxin injections had only minor effects on the severity of the cerebral symptoms in PbA-infected CBA mice and did not cause the animals to die sooner.

Adrenal Glands↗
PubMed1978

Maternal age related pre- and post-implantation fetal mortality: a strain survey.

Pre and post-implantation mortality were examined as a function of maternal aging in six inbred mouse strains. These strains were chosen to evaluate the effects of altered immunity (A/J and NZB/J) and premature reproductive aging (CBA). The decline in litter size observed with maternal aging does not appear to be the result of a decrease in the number of ova produced. The frequency of both pre- and post-implantation mortality increases with maternal age in all strains examined. Although the highest levels of pre- and post-implantation mortality were found in the NZB/J strain, which features altered immune responses, results from the A/J females, which also display immune dysfunction were at the other end of the spectrum. Thus, no consistant relationship was seen between altered immune function and fetal mortality. The CBA strain which is characterized by premature reproductive decline and marked maternal age-related fetal aneuploidy also demonstrated high levels of pre- and post-implantation mortality, even in the young maternal age range.

Animals↗
PubMed2003

The relative involvement of Th1 and Th2 associated immune responses in the expulsion of a primary infection of Heligmosomoides polygyrus in mice of differing response phenotype.

T helper cell (Th1 and Th2) associated responses were examined following a primary infection with the gastrointestinal nematode Heligmosomoides polygyrus in five inbred strains of mice with different resistance phenotypes. Levels of (i) mast cell protease, (ii) specific IgE, (iii) nitric oxide and (iv) specific IgG2a, as markers of Th2 and Th1 associated responses, respectively, were determined in sera and intestinal fluids and correlated with worm burdens. The "fast" responder (resistant) strains SWR and SJL produced strong Th2 and Th1 associated responses respectively in a mutually exclusive fashion. The F1 hybrid (SWRxSJL) F1, showed rapid expulsion of the parasite and expressed both intense Th1 and Th2 responses, suggesting synergism between Th1 and Th2 activity in these mice. The results indicate that both Th2 and Th1 responses operate in mice following a primary infection with H. polygyrus and that each Th response may be involved to a greater or lesser degree within certain strains. Resistance to H. polygyrus was found to correlate only to the intensity of either the gut-associated mastocytosis or nitric oxide production in these strains but not to either specific IgE or IgG2a titres. Chronic infections in the "slow" response phenotype mouse strains CBA and C57BL/10, were associated with both poor Th2 and poor Th1-associated responses attributed to a general parasite-mediated immunosuppression of the host immune response to infection.

Animals↗