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At least 145 records · Page 8Linked to original sources
PubMed1985

Distinction of human T-cell line (HUT-102)-derived activity stimulating granulocytic colony formation in diffusion chambers in vivo from activities stimulating erythroid and mixed-colony formation in vitro.

Medium conditioned in the presence of human HUT-102 T-cell line cells contains activities stimulating human mixed (colony-forming unit, erythroid, granulocyte, macrophage, megakaryocyte) and erythroid (burst-forming unit, erythroid) colony formation in methylcellulose in vitro and granulocyte colony formation in diffusion chambers in mice. The stimulatory effect of HUT-102-conditioned medium on colony-forming unit, granulocyte diffusion chamber was also observed in diffusion chambers implanted in nude mice. The hemopoietic activities were heat stable and could be detected from serum-free conditioned medium. Chromatographically, it was possible to separate colony-forming unit, granulocyte diffusion chamber-stimulating activity from activities stimulating burst-forming unit, erythroid and colony-forming unit, erythroid, granulocyte, macrophage, megakaryocyte. On the other hand, the latter two activities were indistinguishable by the methodology used in this study. Failure to abolish the hemopoietic activities by boiling or by human T-lymphotropic retrovirus type 1 antibody indicates that human T-lymphotropic retrovirus type 1 or its components potentially present in the conditioned medium were not responsible for the stimulatory effects.

Cell Line↗
PubMed1984

Stimulation of human and murine bone marrow cell colony formation by colony-stimulating factors obtained from the urine of mice bearing leukocytosis-inducing fibrosarcoma.

Dialyzed urine of mice bearing leukocytosis-inducing fibrosarcoma stimulated granulocyte colony formation in semisolid agar culture of human bone marrow cells. Removal of phagocytic cells prior to stimulation did not interfere with the formation of these colonies in the culture. On the other hand, macrophage colonies were predominantly produced when murine bone marrow cells were stimulated by the dialyzed mouse urine. The activity of colony-stimulating factor (CSF) in the urine of normal mice was less than 1/100 of that in the urine of tumor-bearing mice. DEAE-cellulose column chromatography separated the activity stimulating human granulocyte colony formation from that stimulating murine macrophage colony formation. Further purification showed that a sialoglycoprotein with an apparent molecular weight of 80,000 corresponded to the macrophage CSF, which was devoid of activity toward human cells. The molecular properties of the human-active granulocyte CSF could not be studied further, because it was quite unstable.

Animals↗
PubMed1996

[Effect of imidazole antifungal agents on colony formation by murine bone marrow CFUc (colony forming units in culture].

In spite of modern antifungal therapy, the prognosis of systemic mycoses in neutropenic patients is usually poor without recovery of neutrophil counts. So, even a minor myelotoxicity might be a significant disadvantage of any drug used for the treatment of neutropenic patients with fungal infections. Since "Colony Forming Units in culture" (CFUc), the common progenitors of granulocytes and macrophages, are supposed to be a major target of agents damaging bone marrow, we studied the inhibitory effect of four imidazole antifungal drugs to colony formation by murine CFUc in vitro. Clotrimazole, econazole, miconazole or ketoconazole were added to soft agar bone marrow cell cultures at final concentrations of 1 to 30 mg/l at the beginning of the 7 day culture period. A dose-dependent inhibitory effect on colony formation by CFUc was observed with all imidazole drugs studied. The 50 percent inhibitory concentrations (IC50s) were 3.54 mg/l for clotrimazole, 8.07 mg/l for econazole, 14.04 mg/l for miconazole, and 16.11 mg/l for ketoconazole. Human pharmacokinetic data available in the literature on these drugs may help to assess the potential in vivo relevance of our results. The serum levels of clotrimazole and econazole, even after oral administration, remain lower than those found to inhibit colony formation by murine bone marrow in our experiments. Taking into consideration that clotrimazole and econazole are used only topically in the clinical practice, our data do not suggest any clinically significant suppression of bone marrow by these two drugs. Intravenous administration of high doses of miconazole, however, may result in serum concentrations approaching the IC50 for colony formation by murine bone marrow cells in vitro. As for ketoconazole, it may suppress the proliferation of murine bone marrow progenitor cells in vitro at concentrations produced in vivo by high doses (12.5-18 and 30-50 mg/l after 400 or 600 mg, respectively). The serum levels produced by a daily dose of 200 mg ketoconazole (about 4 mg/l), however, did not reduce significantly the number of colonies in murine bone marrow cultures. Our present results warrant further studies of the myelotoxicity of miconazole and ketoconazole in vivo in mice with neutropenia induced by cytostatic agents.

Animals↗
PubMed1990

Divergent effects of interleukin-4 (IL-4) on the granulocyte colony-stimulating factor and IL-3-supported myeloid colony formation from normal and leukemic bone marrow cells.

Human recombinant interleukin-4 (IL-4) was studied for its effects on myeloid progenitor cells from normal and leukemic bone marrow cells in the presence and absence of additional growth factors. IL-4 itself did not support myeloid cluster or colony formation (CFU-GM). However, cultures supplied with IL-4 (300 U/mL) and IL-3 demonstrated a significant decline in myeloid colony numbers (CFU-GM) compared with the effects of IL-3 alone: (48 +/- 27 v 88 +/- 27 CFU-GM/10(5) MNC). In contrast, IL-4 augmented the G-CSF-supported CFU-GM: (80 +/- 31 v 148 +/- 52 CFU-GM/10(5) MNC). The effects of IL-4 were not mediated by accessory cells because similar results were obtained with and without T-cell, B-cell, or adherent depleted cell fractions. Morphologic analysis of clusters (day 7) and the colonies (day 14) demonstrated that IL-4 enhanced myeloid colony formation in the presence of G-CSF, whereas the cultures supplied with IL-3 and IL-4 did not show a lineage-restricted decline of CFU-GM. A heterogeneity in growth response was observed in the leukemic counterpart. With the 3H-thymidine proliferation assay, IL-4 augmented the G-CSF-induced proliferation of acute myeloid leukemic (AML) cells in 4 of the 12 cases, while the IL-3-supported proliferation was antagonized in 3 of the 12 cases. In the blast colony assay, IL-4 suppressed the IL-3-supported AML-CFU in the majority of cases, but enhanced the G-CSF stimulated AML-CFU in 3 of 6 cases. These data demonstrate divergent effects of IL-4 on the normal myeloid progenitor cell in the presence of IL-3 or G-CSF, while a variability in responsiveness is observed in the leukemic counterpart.

Bone Marrow Cells↗
PubMed1989

Effects of recombinant granulocyte colony-stimulating factor (rG-CSF) and recombinant granulocyte-macrophage colony-stimulating factor (rGM-CSF) on acute radiation hematopoietic injury in mice.

We have attempted to evaluate in vivo effects of granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) on acute radiation hematopoietic injury in mice. BDF1 mice, irradiated with 7.5-Gy x-rays, were injected i.p. twice daily for 10 days with 10(5) U recombinant human G-CSF, 3.75 x 10(5) U recombinant murine GM-CSF, or a combination of both. G-CSF significantly enhanced the recovery of not only peripheral leukocytes but also platelets and hematocrit on days 14 and 21 after irradiation. GM-CSF significantly enhanced the recovery of platelets on day 14 and peripheral leukocytes on day 21. G-CSF markedly enhanced the recovery of spleen colony-forming units (CFU-S), colony-forming units in culture (CFU-C), erythroid burst-forming units (BFU-E), and megakaryocyte colony-forming units (CFU-Meg) both in bone marrow and in the spleen. GM-CSF significantly enhanced the recovery of CFU-Meg in bone marrow on day 14. We found synergistic effects between G-CSF and GM-CSF on CFU-S, CFU-C, and CFU-Meg in the spleen on day 14, although we found antagonistic effects between G-CSF and GM-CSF on CFU-S and CFU-C in bone marrow on day 7, and on platelet counts on day 7. These results indicate that the administration of recombinant G-CSF and GM-CSF may be useful in accelerating hematopoietic recovery in patients with acute radiation hematopoietic injuries.

Acute Disease↗
PubMed1993

Regulation of granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor expression by oncostatin M.

Oncostatin M (OM) is structurally and functionally related to a subclass of hematopoietic cytokines including leukemia-inhibitory factor (LIF), ciliary neurotrophic factor (CNTF), granulocyte colony-stimulating factor (G-CSF), and interleukin-6 (IL-6). Using human endothelial cells (HEC) as a model for cytokine regulation of hematopoietic growth factor expression, we tested OM as an inducer of colony-stimulating activity. Colony-forming cell assays supplemented with culture supernatants from OM-treated HEC contained a threefold increase in colony-forming unit granulocyte-macrophage colonies. Specific immunoassay (enzyme-linked immunosorbent assay) of culture supernatants indicated that OM treatment of HEC resulted in a dose- and time-dependent increase in the accumulation of G-CSF and granulocyte-macrophage CSF (GM-CSF) (> 28-fold). The ED50 for OM induction of G-CSF and GM-CSF protein expression was 17 and 7 pmol/L, respectively. Increased protein expression was associated with a similar increase in steady-state expression of G-CSF and GM-CSF mRNA. Furthermore, a period of 12 to 24 hours elapsed before there were measurable increases in CSF expression, suggesting that OM may stimulate CSF production through a mechanism requiring the synthesis or activation of a secondary mediating factor or pathway. These findings provide the first evidence that OM may regulate myelopoiesis by inducing the cellular expression of hematopoietic growth factors.

Bone Marrow Cells↗
PubMed1975

Haematopoietic defects of W/WV mice studied with the spleen colony, agar colony, and diffusion chamber techniques.

Bone marrow progenitor cells from anaemic W/WV mice were compared with normal +/+ cells utilizing the spleen colony, the agar colony and the diffusion chamber techniques. Spleen colony formation from W/WV cells was markedly defective, and more so for erythroid than for granuloid colonies. The progenitor cell concentration was apparently normal as measured by the two other techniques. The concentration of circulating progenitor cells also seemed to be normal. On the other hand, the cell formation per progenitor cell was subnormal in all three assay systems. The initial proliferative response of W/WV spleen colony-formers and agar colony-formers to short-term diffusion chamber culturing was apparently normal. The incorporation of 3H-thymidine, related to the number of proliferative granulocytes present in the chambers, also seemed to be normal. The results indicate that the W/WV defect is not limited to the multipotent stem cells. A possible interpretation is that it is the capacity for continued self-renewal of immature cells that is defective.

Anemia↗
PubMed1975

Stability of pathogenic colony types of Neisseria gonorrhoeae in liquid culture by using the parameters of colonial morphology and deoxyribonucleic acid transformation.

This investigation describes the surveillance of the colonial stability of the pathogenic type 1 from the gonococcal strain F62 to the nonvirulent types 3 and 4 in different liquid media. The maintenance of the colony types was monitored by the parameters of colonial morphology and deoxyribonucleic acid-mediated transformation. During growth in a complex medium, Mueller-Hinton broth, only 46.7% of the gonococcal population remained as type 1 after 12 h. The greatest change in the type 1 colony-forming units correlated with the decline in viable count. The conversion process could not be prevented by the continual maintenance of the gonococcus in logarithmic growth. The frequency of transformation from PRO(minus) (proline) to PRO(plus) was proportional to this decrease in type 1 colony-forming units. In contrast to Mueller-Hinton medium, the chemically defined minimal medium Gonococcal Genetic Medium (GGM) was capable of maintaining approximately 90% of the gonococcal population in the type 1 colonial form after 16 h of growth, despite a decrease in the viable count. Although the percentage of type 1 appeared to remain constant in GGM, the apparent transformation frequency increased approximately 24-fold from 0 to 12 h of growth. GGM appears to stimulate or maintain competence, as evidenced by an eightfold increase in transformation when cells are exposed to deoxyribonucleic acid in GGM as compared to Mueller-Hinton.

Culture Media↗
PubMed1987

Stimulation of human hematopoietic colony formation by recombinant gibbon multi-colony-stimulating factor or interleukin 3.

Recently, the gene for a novel mammalian hematopoietic growth factor homologous to murine interleukin 3 was isolated from a gibbon T cell line and expressed in monkey COS cells. The factor, termed multi-colony stimulating factor (multi-CSF) or interleukin 3, is stimulatory to human target cells. We investigated the range of enriched human bone marrow and fetal liver hematopoietic progenitors responsive to multi-CSF; compared the colony types observed with those obtained in the presence of recombinant granulocyte-macrophage CSF (GM-CSF); and analyzed the effects on colony formation of combining multi-CSF with GM-CSF or granulocyte-CSF (G-CSF). The results show that multi-CSF acts as a multipoietin. Alone it stimulates the formation of colonies derived from granulocyte, macrophage, eosinophil, and megakaryocyte progenitors. In combination with erythropoietin it supports the development of both erythroid and mixed colonies. Furthermore, the data show that multi-CSF is a more potent stimulus of erythroid progenitors than GM-CSF. In combination with G-CSF multi-CSF substantially increases granulocyte colony number over the number obtained with each factor alone. We conclude that multi-CSF may prove to have important therapeutic potential in vivo as a stimulus for hematopoiesis.

Animals↗
PubMed1989

Production of colony-stimulating activity by human natural killer cells: analysis of the conditions that influence the release and detection of colony-stimulating activity.

Highly purified natural killer (NK) cell suspensions were tested for their capacity to release colony-stimulating activity (CSA) in vitro. NK cell suspensions comprised primarily CD16+ cells and were devoid of CD3+ T cells, CD15+ monocytes, and of B cells. CSA was detected in the NK cell supernatants and sustained the growth of myeloid colonies from both normal peripheral blood and bone marrow. CSA could be in part inhibited by pretreating NK cell culture supernatants with a specific goat anti-granulocyte-macrophage colony-stimulating factor (GM-CSF) antiserum. The inhibition, however, was never complete, a finding that suggests that additional factors were responsible for CSA. Incubation of NK cells with K562 cells (an NK-sensitive target) or with normal bone marrow cells resulted in the appearance of a strong colony-inhibiting activity (CIA) in the culture supernatants. Such CIA was demonstrable in an experimental system where bone marrow or peripheral blood progenitors were induced to form myeloid colonies in the presence of conditioned medium by CSA-producing giant cell tumor (GCT) cells. Stimulation of NK cells with NK-insensitive targets failed to induce CIA production. Neutralizing antitumor necrosis factor (TNF) monoclonal antibodies (MoAbs) were found capable of inhibiting CIA present in the supernatants of NK cells stimulated with K562 cells. Following treatment with anti-TNF antibodies, CSA was again detectable in the same supernatants. This finding indicates that induction of TNF production did not concomitantly switch off CSA production by NK cells. Pretreatment of NK cells with recombinant interleukin-2 (rIL-2) or gamma interferon (r gamma IFN) did not change the amount of CSA released. However, treatment with rIL-2 caused the appearance of a factor in the NK cell supernatants capable of sustaining the formation of colonies of a larger size.

Antigens, Differentiation↗
PubMed1981

Colony-forming lymphocytes in man. I. In vivo effect of hydrocortisone on phytohaemagglutinin-induced T cell colony formation.

The effect of a single dose (300 mg) of intravenous hydrocortisone on T cell colony and cluster formation was examined in healthy normal volunteers. Peripheral venous blood was drawn before and 4 and 24 hr following administration of the drug T cell colonies (greater than 50 cells/aggregate) and clusters (10-50 cells/aggregate) in response to PHA were assayed by one-stage stimulation in the microagar culture using glass capillaries. The maximum numbers of colonies and clusters were observed between days 7 and 8 of culture. At 4 hr following administration of the drug, both colony and cluster counts were significantly reduced (P less than 0.01). Colony and cluster counts returned to the initial levels 24 hr following administration of the drug. These changes in T cell clusters and colonies were accompanied with changes in the proportions of T cells with IgM (T micro) and IgG (T gamma) receptors. This study demonstrates that a single dose of i.v. hydrocortisone depresses T cell clonal expansion and suggests that this effect could be secondary to the redistribution of a subpopulation of T cells among peripheral blood and other lymphoid tissues and is perhaps not due to a direct suppression of the proliferative response. The significance of these observations is discussed.

Adult↗
PubMed1995

Detection of incorporated iododeoxyuridine in colonies by immunoperoxidase staining: a novel method to measure the proportion of cycling colony-forming cells.

In vitro suicide by tritiated thymidine (3H-TdR), hydroxyurea (HU), or cytosine arabinoside (Ara-C) is assumed to reflect the proportion of colony-forming cells in S-phase at the time of exposure. However, these techniques are not always accurate. Nonradioactive iododeoxyuridine (IdUrd) is incorporated into DNA during S-phase and can be detected by monoclonal antibodies. In the present study, a new IdUrd application was developed to investigate the kinetics of hematopoietic progenitor cells. After incubation with IdUrd, colony-forming cells were cultured in semisolid assay. An immunoperoxidase staining protocol was developed to detect IdUrd in cells of colonies in agar. Colony-forming cells in S-phase during the IdUrd exposure were postulated to give rise to IdUrd+ colonies, whereas non-S-phase cells would generate IdUrd- colonies. Toxicity, sensitivity, and IdUrd inactivation studies indicated that progenitor cells could safely be pulse-labeled for 2 hours with 40 microM IdUrd, whereas prolonged labeling with 1 microM IdUrd was at least feasible for 5 days. Molt-4 cells and normal bone marrow cells were used to compare IdUrd pulse-labeling with 3H-TdR suicide. Part of the Molt-4 cells were enriched for G1- and S-phase cells by counterflow centrifugation. The bone marrow cells were either unstimulated or stimulated with growth factors. As a result, the accuracy of both techniques could be tested in populations with different quantities of S-phase cells. Wide confidence intervals of the suicide technique contrasted with the small confidence intervals obtained with IdUrd pulse-labeling. For instance, the fraction of Molt-4 cells with 27.8% S-phase cells contained 17.7% (confidence interval -8.2 to 43.6%) clonogenic cells in S-phase when determined with 3H-TdR suicide. Of this fraction, the percentage of clonogenic cells in S-phase was 30.6% with a confidence interval of 25.5 to 36.2% when determined with IdUrd pulse-labeling. In our hands, the IdUrd pulse-labeling was more accurate than the 3H-TdR suicide technique. Thus far, kinetic studies of progenitors have been limited to the determination of the fraction of S-phase cells by suicide techniques. By prolonged IdUrd labeling, it is now possible to determine the proliferating fraction of progenitor cells.

Autoradiography↗
PubMed1988

Granulocyte-macrophage colony stimulating factor (GM-CSF) and macrophage colony stimulating factor (CSF-1) synergize to stimulate progenitor cells with high proliferative potential.

The ability to expand a population of bone marrow progenitors capable of forming macrophage colonies of high proliferative potential (HPP-CFC) was achieved using a culture system and signal requirements not previously shown to support the growth of HPP-CFC. Using bone marrow cells from untreated animals (not 5-FU-treated), culture conditions designed primarily for the detection of GM-CFC or M-CFC progenitors, and a more stringent criteria for HPP-CFC colony size (greater than or equal to 2 mm diameter), HPP-CFC progenitor expansion was demonstrated following simultaneous addition of rGM-CSF and CSF-1 to bone marrow cultures. Examination of the sequence and temporal requirements for rGM-CSF and CSF-1 addition necessary for the development of HPP-CFC-like colonies revealed that addition of the second factor could be delayed for up to 5 days and still result in the development of significant numbers of HPP-CFC colonies. Based on a comparison with human spleen cell conditioned medium (HSCM) and interleukin 1 (rIL 1), as sources of "synergistic activity" (SA) for the development of HPP-CFC-like colonies in combination with CSF-1, the combination of GM-CSF and CSF-1 appears to represent a novel pathway for stimulating the expansion of HPP-CFC progenitors with high proliferative potential.

Animals↗
PubMed1987

Serum colony stimulating activity and colony forming cells in murine brucellosis: relationship to immunopathology.

Intravenous injection of mice with Brucella abortus vaccine strain 19, results in a chronic infection, immunity to which is dependent on T cell activation of the macrophages. A major feature of the infection is splenomegaly characterized by massive numbers of macrophages. We report here investigations of the haemopoietic precursors of macrophages, the colony forming cells (CFC), and the growth factors, colony stimulating factors (CSF), controlling their production. Comparison was made amongst three mouse strains, CBA, BALB/c and C57B1/10, as well as the F1 (CBA x BALB/c), which differ in the degree of splenomegaly developed and their ability to rid themselves of infection. The proportion of colony forming cells in the spleen peaked 2 to 3 weeks after infection and was higher in those strains which developed stronger splenomegaly. On the other hand there was no relation between colony forming cells and ability to control infection. Serum CSF also peaked 2-3 weeks post infection, with similar titres in all mouse strains studied. Bone marrow exhibited an early loss of total cellularity after infection followed by recovery. There was a sharp peak in the proportion of colony forming cells in the bone marrow 2 weeks post infection. Spleen and bone marrow CFC and serum CSF all returned to normal levels before infection was resolved.

Animals↗
PubMed2000

Comparison of granulocyte-colony, stimulating factor and granulocyte macrophage-colony stimulating factor in the treatment of chemotherapy extravasation ulcers.

The results of perilesional granulocyte macrophage-colony stimulating factor and granulocyte-colony stimulating factor application in a patient with chemotherapy extravasation ulcers are reported. A 64-year-old patient with recurrent ovarian carcinoma was admitted to our department in February 1999. In June 1998, six cycles of chemotherapy were applied to the patient after surgery. At the first cycle, two ulcers appeared on both lower arms related to doxorubicin extravasation despite all interventions. When the patient was admitted to in our department, we observed an ulcer on the distal part of the right lower arm with a dimension of 1.5x2 cm and another on the proximal portion of the left lower arm with a dimension of 2.5x3 cm. Of those ulcers, the bigger and deeper one on the left was treated with weekly 400 mcg granulocyte macrophage-colony stimulating factor subcutaneously for three weeks. The lesion completely disappeared in the fourth week. The other ulcer that was left for control on the right arm was treated with weekly 48 M.U. granulocyte-colony stimulating factor for four weeks. This ulcer did not reduce in size. As a result granulocyte-colony stimulating factor did not affect the healing of chemotherapy extravasation ulcers, as did granulocyte macrophage-stimulating factor.

Antineoplastic Agents↗
PubMed2001

[Effects of recombinant human macrophage colony stimulating factor (rhM-CSF) on stromal cell derived during the time of mice colony formation unit-spleen (CFU-S) and its role on CD34+ cells expansion in vitro].

OBJECTIVE: To investigate the effects of stromal cell derived from mice spleen during in vitro expansion of CD34+ hematopoietic stem cells from umbilical cord blood. METHODS: Irradiated and non-irradiated mice at day 10, 12 and 14 were sacrificed and their spleens were taken for collecting spleen cells. The cells were stimulated with recombinant human macrophage colony stimulating factor(rhM-CSF) for collecting adherent spleen derived stroma cells. The effects of spleen derived stromal cells which treated with mitomycin served as a feeder layer, combined with different cytokines on in vitro expansion of purified cord blood CD34+ were assayed. Clonogenic assay and flow cytometry were employed to analyze phenotype of expanded cells and their ability to form different colony in vitro. RESULTS: 1) rhM-CSF efficiently stimulated spleen derived stromal cells to proliferate; 2) The mice stromal cells obtained during the time of colony formation-unit spleen (CFU-S) promoted the CD34+ cells to form colony in semisolid medium and, combined with cytokines, thereby efficiently expanded the hematopoietic cells from cord blood. After two weeks incubation, CD34 positive cells were 100 times more than original cells cultured and expanded cells still have the ability to form multi-lineage colony in vitro. CONCLUSION: rhM-CSF can stimulate the stromal cells derived from CFU-S to proliferate and support the survival and expansion of CD34+ cells separated from cord blood.

Animals↗
PubMed1978

The marrow colony forming cell and serum colony stimulating factor of the chicken.

Marrow cells of the chicken produced colonies in semisolid media. Developing colonies consisted of granulocytes, macrophages or a mixture of these two cell types. The granulocyte-macrophage CFC was nonadherent. An adherent 'CFC' was also present and it differed in several ways from the nonadherent CFC: (a) clones contained only macrophages, (b) they contained a core of nonrefractile cells, (c) their appearance was delayed 1-2 weeks, (d) they were unaffected by the presence of erythrocytes and (e) the efficiency of cloning was increased but the percentage of clones able to produce 50 or more cells was markedly decreased, i.e., the cluster/colony ratio was increased. The growth of both colony types was strictly dependent on the presence of CSF. Data obtained from dose-response studies on unfractionated marrow indicated that clusters and colonies were derived from single cells. The CSF of chicken serum yielded sigmoid dose-response curves when tested on marrow cells. Calf serum could not support cluster or colony formation when tested alone but it did have an enhancing effect on the CSF of chicken serum. Levels of serum CSF were increased by injecting chickens with bacterial endotoxin. This phenomenon occurred with five chicken lines tested, but certain chickens of the Kimber line did not respond to endotoxin with elevated levels of CSF.

Animals↗