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PubMed1978

Experimental amyloidosis in mice of different ages. Effects of neonatal thymectomy and amyloidogenic stimulation of pregnant mice.

Murine amyloidosis, induced by repeated injections of sodium caseinate, was compared in young and adult Swiss albino mice and in young thymectomized and nonthymectomized mice. Thymectomized mice developed amyloidosis earlier and more severely than intact mice. Mothers of young mice were injected with sodium caseinate during pregnancy and after birth sodium caseinate injections were given to the offspring, but this treatment did not seem to induce amyloidosis in the young mice. A much shorter latent period before development of amyloidosis was seen in the adult group than in the young mice. This may be the result of a depletion of cellular and humoral immunity with aging. The shorter latent period and more severe development of amyloidosis in the thymectomized groups supports the view that an impaired immunological state may constitute a basis for the development of amyloidosis.

Aging↗
PubMed1979

Genetics of xenotropic virus expression in mice. I. Evidence for a single locus regulating spontaneous production of infectious virus in crosses involving NZB/B1NJ and 129/J strains of mice.

The extent of infectious xenotropic virus expression in homogenized splenic tissues from the high-virus-expressing NZB/BINJ mice and the non-virus-expressing 129/J mice and their crosses has been examined. The data suggest that a single autosomal "dominant-like" gene controls the spontaneous production and release of infectious xenotropic virus in NZB mice. Analysis of infectious virus production in second-backcross families [(F1 X 129) X 129] confirmed this conclusion. Variations in the amount of X-tropic virus released were evident in all genetic crosses. Virus titers (expressed as focus-forming units per milliliter) of supernatant fluid ranged from high levels in the NZB mice to somewhat lower levels in crosses involving the 129 mice. In the absence of a definite pattern in the titers observed in the genetic crosses studied, the term dominant-like is proposed for the single gene regulating the expression of X-tropic virus in NZB mice.

Animals↗
PubMed1976

Immunity to Plasmodium Berghei yoelii in mice. I. The course of infection in T cell and B cell deficient mice.

The course of infection with 17X nonlethal Plasmodium berghei yoelii was examined in BALB/c mice which were deficient in either T cells or B cells. Markedly increased parasitemia and mortality were observed in athymic (nude) mice which had been backcrossed on a BALB/c background (T cell deficient) compared to similar mice which had been grafted with neonatal BALB/c thymus, and were also observed in BALB/c mice suppressed from birth with goat antiserum to mouse mu-chain (B cell deficient) compared to age- and sex-matched BALB/c controls. These results establish the requirement for the presence of both T cells and B cells for effective resistance to an intercurrent infection with 17XNL P.b. yoelii in adult BALB/c mice. Mechanisms by which the requirement for both T cells and B cells could be explained were discussed. The model of mu suppression was shown to be a valuable tool for an evaluation of the cellular basis of immunity to an infectious disease.

Animals↗
PubMed1979

Studies of congenitally immunologic mutant New Zealand mice. II. Absence of T cell progenitor populations and B cell defects of congenitally athymic (nude) New Zealand Black (NZB) mice.

Congenitally athymic (nude) mice on an NZB, NZW, and BALB/c background were produced by repetitive selective backcrossing. F'12 generation nude mice of these three strains were compared to their littermate nu/+ controls with respect to survival, histology, blood counts, splenic surface markers, response to mitogens, spontaneous plaque-forming cells, and appearance of naturally occurring thymocytotoxic antibodies (NTA). Under specific pathogen-free conditions, NZB nude mice survive less than 3 weeks, dying of a runting-like disease with infection by local normally noninvasive organisms. A contributing factor to his premature death is the relative absence of T cell progenitor populations in the NZB nude vs NZW nude or BALB/c nude groups. Furthermore, NZB nude mice have a significantly earlier appearance of NTA than nu/+ littermates and likewise appear to have heightened spontaneous polyclonal B cell responses against the haptens dansyl, nitroiodophenyl, trinitrophenyl,2,4 dinitrophenyl, and sulfonate. It is suggested that NZB mice have several critical immunologic defects, including abnormalities of thymic epithelial cells, T cell differentiation pathways, and chronically polyclonal activated B cell populations. These defects interact to produce the clinical expression of autoimmunity.

Animals↗
PubMed1977

Differences in the mechanism of tolerance to dinitrophenylated bovine gamma globulin when induced in normal adult mice or in reconstituted irradiated mice: dependence of the mechanism of tolerance on the structural organization of the lymphoid system.

Tolerance can be induced in adult mice by a single intravenous injection of 0.5 mg dinitrophenylated bovine gamma globulin. The cellular mechanism of the unresponsive state is different depending upon whether the tolerance is induced in normal intact adult mice or in reconstituted, irradiated mice. The tolerant state induced in intact mice is characterized by a high avidity of the residual antibody-forming cells in partially tolerant animals and a prompt reversibility on cell transfer. The overall properties of this unresponsive state are consistent with the hypothesis that it is mediated by the production of small amounts of high affinity antibody in response to the tolerance-inducing injection of antigen. In contrast, the unresponsiveness induced in reconstituted, irradiated mice by the same procedure was characterized by a low avidity of the residual antibody-forming cells in partially tolerant animals and stability on transfer of spleen cells from unresponsive into irradiated recipients. No suppressor cell activity was detected and mixed cell transfer studies were consitent with the view that this unresponsive state represented a B-lymphocyte clonal deletion. The presence or absence of T lymphocytes in the population of cells used for reconstituting the irradiated recipients did not effect the ease of tolernace induction or the cellular mechanism of the tolerant state which was produced. If irradiated mice reconstituted with B and T lymphocytes were rested for 2 wk before tolerance induction then a reversible "high affinity"-type tolerance is obtained such as is typical of normal intact animals. Restorationof a "normal" response to the tolerance-inducing injection of antigen is dependent upon the presence of thymus cells in the population of cells used for reconstitution. It is suggested that the structural integrity of the lymphoid tissue is critical in determining whether B cell will be rendered tolerant after exposure to antigen in vivo.

Age Factors↗
PubMed1976

Effect of capsular polysaccharide of Klebsiella pneumoniae on Host resistance to bacterial infections. II. Effects on peritoneal leukocytes of normal mice and mice infected with virulent Salmonella enteritidis.

In normal mice, the total count of peritoneal leukocytes was markedly decreased after intraperitoneal (i.p.) injection of the capsular polysaccharide of Klebsiella pneumoniae (CPS-K) depending on the dosage injected. This decrease was mainly due to the depletion of macrophages, and a decrease in the number of lymphocytes occurred to a lesser extent. CPS-K in relatively smaller doses mobilized polymorphonuclear neutrophilic leukocytes (PMN) into the peritoneal fluid but it decreased them transiently in larger doses. In mice infected i.p. with a virulent strain of Salmonella enteritidis, there was an abundant emigration of PMN into the peritoneal fluid. When 200 mug of CPS-K was injected i.p. immediately before bacterial challenge, emigration of PMN was markedly delayed for 48 hr after infection. Associated with this suppressed emigration of PMN, the numbers of macrophages and lymphocytes in the peritoneal fluid were significantly less in mice treated with CPS-K than those in untreated control mice for 48 hr after infection. The numbers of both cell-associated and extracellular bacteria in the peritoneal fluid were markedly greater in mice treated with CPS-K than those in untreated control mice. In both in vivo and in vitro experiments, ingestion of bacteria by macrophages and PMN was not blocked by CPS-K or neutral CPS-K, the active substance responsible for the infection-promoting effect of CPS-K. It appeared that CPS-K somehow impaired the intraphagocytic bactericidal activity.

Animals↗
PubMed1977

Immunity to sporozoite-induced malaria infeciton in mice. I. The effect of immunization of T and B cell-deficient mice.

The cellular basis of immunity to sporozoites was investigated by examing the effect of immunization of T and B cell-deficient C57BL/6N X BALB/c AnN F1 (BLCF1) mice compared to immunocompetent controls. Immunization of T cell-deficient (ATX-BM-ATS) BLCF1 mice with x-irradiated sporozoites did not result in the generation of protective immunity. The same immunization protocols protected all immunocompetent controls. In contrast, B cell-deficient (micron-suppressed) BLCF1 mice were protected by immunization in the majority of cases. The absence of detectable serum circumsporozoite precipitins or sporozoite neutralizing activity in the micron-suppressed mice that resisted a sporozoite challenge suggests a minor role for these humoral factors in protection. These data demonstrate a preeminent role for T cells in the induction of protective immunity in BLCF 1 mice against a P. berghei sporozoite infection.

Animals↗
PubMed1977

Immunosuppressive factor(s) extracted from lymphoid cells of nonresponder mice primed with L-glutamic acid60-L-alanine30-L-tyrosine10 (GAT) II. Cellular source and effect on responder and nonresponder mice.

The synthetic terpolymer of L-glutamic acid60-L-alanine30-L-tyrosine10 (GAT) fails to stimulate development of GAT-specific antibody responses in nonresponder strains of mice, but does stimulate the development of GAT-specific suppressor T cells that inhibit the development of normal anti-GAT antibody responses to GAT complexed to methylated bovine serum albumin (GAT-MBSA). Furthermore, extracts prepared from lymphoid cells of GAT-primed, but not control, nonresponder mice inhibit the development of antibody responses to GAT-MBSA by normal nonresponder mice. This suppression is specific, dose-dependent, and can be readily analyzed in vitro. The suppressive factor is a T-cell product. An extract from GAT-primed DBA/1 mice inhibits the response to GAT-MBSA by spleen cells from histoincompatible strains of mice that are nonresponders to GAT, but not strains that are responders to GAT.

Animals↗
PubMed1976

A comparison of mice in rebound-thrombocytosis with platelet-hypertransfused mice for the assay of thrombopoietin.

Rebound-thrombocytosis and platelet hypertransfusions were compared as methods of preparing assay animals for the measurement of thrombopoietin (TSF). In immunothrombocythaemic mice, the amount of 35S incorporation into the platelet mass after injections of a standard dose of TSF was related to the length of time after rabbit anti-mouse platelet serum (RAMPS) injection. After 2 platelet transfusions, however, there was no decrease in 35S incorporation values of mice with time after injections of control or TSF-containing substances. When platelet counts were made 3 days after the last platelet transfusion, the counts decreased with the number of transfusions. Mice in rebound-thrombocytosis were responsive to TSF as evidenced by higher platelet counts (P less than 0.05) and increased 35S incorporation into platelets (P less than 0.005), whereas mice made thrombocytotic by platelet transfusions were not. Assuming that increased platelet counts induced by the different techniques affect assay mice only by inhibiting blood cell production by haematopoietic cells, these data are consistent with the hypothesis that sensitivity to TSF depends upon the proliferative state of the megakaryocytic precursor population.

Animals↗
PubMed1976

Tuberculin shock in red mice and CF1 mice immunized with strains of BCG or Mycobacterium tuberculosis.

Groups of red mice and CF1 mice immunized intravenously with varying doses of a weak and a strong strain of BCG and a strain of M. tuberculosis were challenged 3-4 weeks later with 2 or 0.5 mg of purified tuberculin injected intravenously. The shock sensitivity of the animals in the individual groups was evaluated on the basis of the number of deaths and the survival times after challenge. In the red mice, the strain of M. tuberculosis induced a significantly greater sensitivity than the BCG strains. The strong strain of BCG induced a slightly greater sensitivity than the weak strain, but the difference was not significant. The CF1 mice were more sensitive to tuberculin shock than the red mice, but any difference in the sensitivity of the animals in the individual groups immunized with the three strains could not be demonstrated.

Animals↗
PubMed1978

Histocompatibility difference between C3HfeB/HeN and C3H/HeN mice: tumour induced in C3HfeB/HeN mice expresses C3H/HeN-associated alloantigen.

A transplacentally induced lung tumour of C3HfeB/HeN mouse origin expresses, as a tumour-associated antigen, a normal tissue component of strain A mice. The genetic locus coding for this alloantigen has been shown to be linked to the H-2 major histocompatibility complex. In the present study we demonstrate that this antigen is also expressed on normal tissues of C3H/HeN mice. Skin grafts exchanged between C3HfeB/HeN and C3H/HeN mice are reciprocally rejected at approximately 3 weeks after grafting. C3HfeB/HeN mice were derived from C3H/HeN mice in 1945. These strains have apparently deviated since then in their genetic regulation of the expression of the MHC-linked genetic locus. The finding of the C3H/HeN-associated antigen on a C3HfeB/HeN mouse-derived lung tumour indicates that this deviation is reversible.

Animals↗
PubMed1975

Specific unresponsiveness to skin allografts in mice. IV. Immunological reactivity of mice treated with liver extracts, Bordetella pertussis, and antilymphocyte serum.

The strain-specific unresponsiveness to H-2 incompatible skin allografts induced by treatment of adult mice with single inoculations of donor strain liver extract and Bordetella pertussis vaccine, as well as three doses of antilymphocyte serum, has been investigated by several in vivo and in vitro methods, with a view to elucidating it mechanism. Lymphoid cells from mice with long surviving skin grafts were found to be reactive in graft-versus-host assays (as measured by splenomegaly or popliteal lymph node enlargement), and mixed lymphocyte culture tests gave positive results. Attempts to cause lethal runting of F1 hybrid mice injected at birth with spleen cells from unresponsive mice gave variable results. However, the injection of F1 hybrid cells into the footpads of unresponsive animals failed to elicit a significant host-versus-graft response. Although lymphoid cells from unresponsive animals did not include detectable numbers of cytotoxic cells, such cells could be generated by previous in vitro mixed lymphocyte culture stimulation or, to some degree, by the injection of the animals with F1 hybrid cells. Attempts to prevent mixed lymphocyte culture stimulation or cytotoxicity with serum from unresponsive mice failed at the serum concentrations used. The data indicate that long-term unresponsiveness in this system is maintained by the production in the hosts of factors that interfere with the cell-mediated response.

Animals↗
PubMed1979

Pathogenicity of cultivated murine leprosy bacilli of Hawaiian-Ogawa strain in mice. 4) Visceral lesions in mice produced by intraperitoneal infection.

The pathogenicity of two substrains (HO-R and HO-S) of cultivated murine leprosy bacilli was examined by intraperitoneal inoculation to various strains of mice (C3H, KK, BALA/c, DDD and C57BL/6). HO-R (Rough Form) was first isolated on 1% Ogawa's egg yolk medium from the leprous lesions produced by original Hawaiian strain (H bacilli). HO-S (Smooth Form) was dissociated in vitro during the 9th to 15th subculture of HO-R on the same kind of medium. In all the mice tested, intraperitoneal inoculation with HO-R bacilli produced progressively severe visceral lesions in the manner similar to H bacilli harvested from subcutaneous leproma. The only exception was, however in DDD strain of mice H bacilli produced only slight visceral lesions even in the later stage of infection. HO-S was much lower in the pathogenicity than the above two strains of murine leprosy bacilli. Visceral lesions produced by intraperitoneal inoculation with HO-S used to be very slight in all the strains of mice except BALB/c. BALB/c strain mice were highly susceptible to intraperitoneal as well as subcutaneous infection with HO-S. From the above observations, it is concluded that the characteristic features of pathogenicity of cultivated murine leprosy bacilli, such as mouse strain differences, are all the same regardless of infection route.

Animals↗
PubMed1977

Antigen-induced arthritis in mice. I. Induction of arthritis in various strains of mice.

Antigen-induced arthritis was established in the mouse by immunizaiton with methylated bovine serum albumin (mBSA) in complete Freund's adjuvant with B pertusis vaccine. The knee joint was injected after 21 days with mBSA in saline. The arthritis was chronic, antigen-specific, and T-cell dependent in hypothmic nu/nu mice. C57BL and balb/c mice were susceptible, whereas CBA mice were relatively resistant. Susceptibility was dominant; one gene was loosely linked to the "b" allele of the H-2 complex of C57BL mice.

Animals↗
PubMed1977

Comparative study of macrophage migration in different strains of mice: absence of migration in C3H mice.

In the course of studying the susceptibility of mice to Salmonella infection, we discovered that C3H/HeJ mice differ from other strains in both their susceptibility to infection and their response to prior vaccination. Others have noted the absence of the usual B cell stimulation by LPS in these mice. To investigate the status of delayed hypersensitivity in C3H/HeJ mice, we tried to use the technique of macrophage migration. Under conditions of normal migration for other strains, C3H/HeJ peritoneal and splenic macrophages failed to migrate, thus establishing another differentiating immunological trait for this strain.

Animals↗
PubMed1979

Recognition among mice. Evidence from the use of a Y-maze differentially scented by congenic mice of different major histocompatibility types.

Previous studies of mating preference signified that mice can sense one another's major histocompatibility complex (MHC) types, probably by olfaction. This conclusion has now been substantiated by the use of a Y-maze whose two arms were differentially scented with currents of air conducted through boxes occupied by B6 (H-2b) males and by B6-H-2k congenic males. Four B6 mice, two males and two females, were successfully trained, by water deprivation and reward, to enter the arm scented by B6 or B6-H-2k males. One of the males and one of the females were trained to select the B6-scented arm; the other male and female were trained to select the B6-H-2k-scented arm. Untrained mice showed no MHC discrimination in the maze. The performance of the trained mice in distinguishing between MHC congenic homozygous F2 segregants derived from a cross of B6-H-2k with B6 was as good as their performance in distinguishing the respective inbred strains, thus essentially eliminating alternative and significant additional explanations of MHC-associated sensory discrimination. The data further indicate that chemosensory discrimination of MHC types can be entirely dissociated from sex differences and from the circumstances of mating.

Animal Communication↗
PubMed1978

Studies on brain lesion by administration of monosodium L-glutamate to mice. I. Brain lesions in infant mice caused by administration of monosodium L-glutamate.

Light-microscopic examination was performed on the brain lesions induced by monosodium L-glutamate (MSG) in neonatal and infant mice of ICR strain. Lesions characterized as cytoplasmic balooning, chromatin clumping, pyknosis and karyorrhexis of neurons were recognized in the arcuate nucleus (AN), subfornical organ, preoptic area, area postrema and cerebral cortex. The most vulnerable region was the AN in which the region near the root of the median eminence was easily damaged. The changes in the AN were severest in 7-day-old mice, but only slight in 20-day-old mice. Thresholds of inducing AN lesions in 10-day-old mice after intraperitoneal injection and force-tube feeding were 0.4 and 0.7-0.8 g/kg body weight, respectively. The threshold of retinal changes was about 2.5-fold that of AN in force-tube feeding. In neonatal mice injected daily with 4 g MSG/kg body weight, the neurons of the AN disappeared almost completely by the 4th day of intraperitoneal administration.

Age Factors↗
PubMed1979

The production of contact sensitivity by the injection into the footpads of recipients of the lymph node cells from mice 1 day after painting the skin with contact sensitizing agent: requirement for matching at the major histocompatibility complex between donor and recipient mice.

Donor mice were painted on the skin of the abdomen with the contact sensitizing agent, oxazolone. One day later 2-5 x 10(6) cells from the regional lymph nodes were injected into the footpads of recipient mice. Contact sensitivity was detected 6 days later by challenging the ears of the recipients and measuring the increase of thickness at 24 h. Good contact sensitivity was obtained when CBA cells were injected into CBA mice and BALB/c cells injected into BALB/c mice; the injection of BALB/c (H-2d) cells into CBA (H-2k) mice and vice versa failed to give rise to contact sensitivity. Hybrid F1 cells gave intermediate responses. The contact sensitivity caused by the injection of small numbers of lymph node cells into the footpad is interpreted as a mode of active immunization and the present results show that this only occurs when there is genetic matching at the major histocompatibility complex between the donor and the recipient mouse.

Animals↗