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Biomedical subjects

K Burnham

Publications and source records attributed to K Burnham.

13 recordsLinked to original sources
PubMed2002

The effects of chromium and copper supplementation on mitogen-stimulated T cell proliferation in hypercholesterolaemic postmenopausal women.

The purpose of this study was to analyse effects of chromium and/or copper supplementation on immune function in hypercholesterolaemic postmenopausal women. A 2 x 2 factorial research design was used and 40 subjects were supplemented with 0.394 g lactose, 200 microg Cr, 3.0 mg Cu, or 200 microg Cr and 3.0 mg Cu/d for 12 weeks. A significant interactive effect of Cr and Cu supplementation on lymphocyte proliferation was observed with ConA 50 microg/ml stimulation. After 12 weeks of supplementation, ConA-stimulated (50 microg/ml) lymphocyte proliferation was significantly lower when Cu was added to the Cr supplementation group. Moreover, ConA-stimulated (100 microg/ml) lymphocyte proliferation was significantly lower in the Cu supplementation group compared to the Cr supplementation group after 12 weeks of supplementation. These results suggest that Cu blocks enhancement of lymphocyte proliferation by Cr supplementation and that Cu supplementation has potential suppressive effects on the immune function in these subjects.

Adult↗
PubMed2001

The dendritic cell populations of mouse lymph nodes.

The dendritic cells (DC) of mouse lymph nodes (LN) were isolated, analyzed for surface markers, and compared with those of spleen. Low to moderate staining of LN DC for CD4 and low staining for CD8 was shown to be attributable to pickup of these markers from T cells. Excluding this artifact, five LN DC subsets could be delineated. They included the three populations found in spleen (CD4(+)8(-)DEC-205(-), CD4(-)8(-)DEC-205(-), CD4(-)8(+)DEC-205(+)), although the CD4-expressing DC were of low incidence. LN DC included two additional populations, characterized by relatively low expression of CD8 but moderate or high expression of DEC-205. Both appeared among the DC migrating out of skin into LN, but only one was restricted to skin-draining LN and was identified as the mature form of epidermal Langerhans cells (LC). The putative LC-derived DC displayed the following properties: large size; high levels of class II MHC, which persisted to some extent even in CIITA null mice; expression of very high levels of DEC-205 and of CD40; expression of many myeloid surface markers; and no expression of CD4 and only low to moderate expression of CD8. The putative LC-derived DC among skin emigrants and in LN also showed strong intracellular staining of langerin.

Animals↗
PubMed2000

Effect of granulocyte-macrophage colony-stimulating factor on the generation of epidermal Langerhans cells.

The role of granulocyte-macrophage colony-stimulating factor (GM-CSF) and Flt3 ligand in the in vivo development of Langerhans cells (LC) was assessed, considering both the steady-state levels of LC in the epidermis and the rate of LC recovery after depletion following lipopolysaccharide (LPS) treatment. The density of LC was determined by counting following IA-specific immunofluorescent staining of epidermal sections from mouse ears. LC levels were compared in beta common chain receptor null (beta c(-/-)) mice that fail to respond to GM-CSF interleukin-5 (IL-5), in GM-CSF transgenic mice with elevated GM-CSF levels, and in mice given daily injections of Flt3 ligand. In the steady state, LC levels were increased in GM-CSF transgenic mice and present at reduced levels in beta c(-/-) mice but unchanged in Flt3 ligand-injected mice. Application of LPS to the ears of control BL/6 mice led to an approximately 70% reduction in LC 4 days later, with recovery beginning by day 8 and a return to normal levels by 2 weeks. This recovery was significantly delayed in beta c(-/-) mice and unchanged in Flt3 ligand-injected mice. These results suggest that GM-CSF (but not Flt3 ligand) enhances recruitment/maturation of LC even though GM-CSF is not essential for their formation.

Animals↗
PubMed1999

Protein-kinase-specific inhibitors block Langerhans' cell migration by inhibiting interleukin-1alpha release.

Previous studies have shown that depletion of Langerhans' cells (LC) from murine epidermis by the superantigen, staphylococcal enterotoxin A (SEA) involves interleukin-1alpha (IL-1alpha) and is inhibitable by agents that block G-protein-associated kinases. The purpose of this study was to determine whether specific kinase inhibitors block LC depletion by inhibiting IL-1alpha release and to ascertain whether LC depletion by SEA involves cell migration. These goals were addressed by measuring the IL-1alpha release within whole or LC-depleted epidermal cell suspensions in the presence of SEA and/or H-7 (an inhibitor of protein kinase C) or H-8 (an inhibitor of G-protein-associated kinases) and by examining the migration of cells with LC markers in SEA-treated skin sections. The results suggest that LC depletion by SEA involves migration and that this migration is blocked by protein kinase inhibitors, at least in part, through inhibition of SEA-induced IL-1alpha release by epidermal cells.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1996

Superantigen-induced Langerhans cell depletion is mediated by epidermal cell-derived IL-1 alpha and TNF alpha.

The purpose of this study was to examine the role of cytokines in staphylococcal enterotoxin-A (SEA)-induced epidermal Langerhans cell (LS) depletion. This was accomplished by analyzing the effect of SEA on cytokine secretion by cultured epidermal cell populations by means of ELISA and by assessing the capacity of cytokines and cytokine-specific antibodies to affect epidermal LC density (as measured by immunoperoxidase staining of epidermal cells bearing surface Ia). The results of this study indicate that SEA induces the secretion of IL-1 alpha and TNF alpha by epidermal cells, that these cytokines induce LC depletion from epidermis, and that antibodies specific for these agents inhibit the depletion of LC by SEA. Taken together, these findings suggest that IL-1 alpha and TNF alpha may play essential roles in SEA-mediated depletion of LC from murine epidermis.

Animals↗
PubMed1994

Langerhans' cell depletion by staphylococcal superantigens.

Superantigens were examined for effects on the distribution of Langerhans' cells (LC) in mouse skin. This was accomplished by analysing the expression of LC-specific markers, ATPase and IA among the epidermal portion of cultured sections of mouse skin following treatment with staphylococcal enterotoxins. In this study, treatment of skin sections with staphylococcal enterotoxin A or exfoliative toxin but not toxic shock syndrome toxin led to significant depletion of LC. This depletion was inhibited by agents which specifically block the action of GTP binding proteins or their associated kinases (cholera and pertussis toxins and H-8) as well as those which block protein or RNA synthesis. Therefore, signals which lead to LC depletion in response to staphylococcal enterotoxins appear to involve a cholera and pertussis toxin-sensitive GTP-binding protein and protein synthesis. These requirements are identical to those observed previously for LC depletion following exposure of skin to ultraviolet radiation.

Animals↗
PubMed1993

Requirements for Langerhans' cell depletion following in vitro exposure of murine skin to ultraviolet-B.

Langerhans' cells found within the skin and mucous membranes are critical regulators of antimicrobial and allergic responses. Therefore, the depletion of these cells following exposure of skin to solar ultraviolet radiation (UV) has direct functional consequences on immunity within this tissue. In order to understand how Langerhans' cell depletion is regulated following exposure of skin to medium-wave UV (UVB), the role of second messengers in these responses was investigated using a novel in vitro system. This was accomplished by analysing the expression of a specific marker associated with Langerhans' cells (ATPase) among the epidermal portion of cultured sections of mouse skin following treatment with inhibitors specific for second messenger components and subsequent exposure to UVB. In this study, inhibitors of guanosine triphosphate (GTP) binding proteins, H-8, pertussis toxin and cholera toxin as well as inhibitors of RNA and protein synthesis were all capable of blocking Langerhans' cell depletion in response to UVB treatment. In contrast, an inhibitor of protein kinase C (H-7) was incapable of specifically blocking depletion following treatment with this physical agent. These results suggest that Langerhans' cell depletion mediated by UVB may involve a pertussis and cholera toxin-sensitive G protein as well as de novo protein synthesis.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1992

Effects of petrochemicals and ultraviolet radiation on epidermal IA expression in vitro.

We previously demonstrated that combined treatment of mice with crude oil and longwave ultraviolet radiation (UVA) led to the depletion of IA-positive cells from the epidermis. In the present study, we have developed an in vitro screening assay for combined effects of purified petrochemicals and UVA on epidermal IA and Thy-1 expression. This method involves removal of skin from donor mice prior to treatment with chemicals and UVA (20,000 J/m2), followed by in vitro culture and subsequent immunoperoxidase staining. In this study, a complete correlation was observed in terms of IA-positive cell density among similarly treated cultured skin and live mice. In vivo and in vitro studies both indicated that anthracene but not phenanthrene or benzo[a]pyrene led to significant depletion of both epidermal Langerhans cells and Thy-1-positive dendritic cells when followed by UVA treatment. The in vitro assay developed for this study should prove to be a valuable tool for the screening of a wide variety of chemicals for contact photosensitizing activity.

Animals↗
PubMed1991

Tumor-associated macrophages share in vitro growth characteristics with resident but not elicited macrophages.

Recent studies have shown that tissue macrophages are capable of proliferation and that this capability is enhanced by various cytokines, including macrophage colony-stimulating factor (M-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF). Tumor-associated macrophages (TAM) have been demonstrated to proliferate in vitro, but no information is currently available on the ability of M-CSF and GM-CSF to enhance this response. To address this problem, limiting dilution analysis was utilized to examine the proliferative ability of macrophages isolated from two murine tumors of distinct origin following growth in secondary hosts. As a means of comparison, resident peritoneal macrophages (RPM) and thioglycolate-elicited macrophages (TEM) were also analyzed. Results indicate that a rare subset of TAM and RPM is capable of proliferation and that M-CSF and GM-CSF enhance the frequency of TAM and RPM which proliferate, but do not enhance the growth of TEM.

Animals↗
PubMed1991

Effects of crude oil and ultraviolet radiation on immunity within mouse skin.

Previous studies indicate that crude oil leads to increased pigmentation and erythema (sunburn) in response to sunlight in exposed individuals. However, no information is currently available concerning whether crude oil exposure might enhance the immunosuppressive effects of solar ultraviolet radiation (UVR) on the skin. In order to address this question, the back skin of shaved, female C3H/HeN mice was exposed to crude oil with or without subsequent treatment with medium-wavelength (UVB) (200 J/m2) or long-wavelength (UVA) (20,000 J/m2) UVR. Immune function was assessed in treated mice by measuring their ability to mount contact hypersensitivity responses to a hapten (2,4-dinitro-1-flyorobenzene, DNGFB) applied to the site of crude oil and UVR treatment as determined by ear swelling upon subsequent challenge. Since Langerhans cells represent an important component of immunity within the skin and because suppression of contact hypersensitivity following UVR treatment is often accompanied by disappearance of Langerhans cells from the epidermis, the impact of these agents on epidermal Langerhans cell density was also analyzed. This was accomplished by enumerating IA-positive cells within the epidermis of treated skin. In these studies, crude oil alone induced inhibition of contact hypersensitivity but had no effect on epidermal Langerhans cells. In contrast, combined treatment with crude oil and UVA led to suppression of contact hypersensitivity, which was accompanied by depletion of epidermal Langerhans cells.

Animals↗
PubMed1988

Prospective partition analysis of independently assorted sets. Accessory elements supporting clonal lymphoid activation by mitogens.

Accessory cells for mitogen-induced clonal proliferation of lymphocytes can be found after in vitro culture of murine spleen cells. Mitogenic activation of T cells (concanavalin A) depends on such accessory cells. When the cultures in which the accessory cells developed are partitioned, assortment of the accessory cells in cultures is found. When small numbers (1-10) of responder cells, T cells, are dispensed into the above cultures, clonal growth of the T cells is achieved. Neither the dose-response profile of accessory cells nor that of responding cells shows single hit kinetics. Re-categorizing the data set reveals that only cultures with over 20 adherent cells were likely to promote T cell growth and single hit kinetics for the responding cell clone and the accessory cell clone were obtained.

Animals↗
PubMedDate not supplied

High in vitro endotoxin responsiveness of macrophages from an endotoxin-resistant wild rodent species, Sigmodon hispidus.

It has been reported that macrophages primarily mediate endotoxin shock and cell death by synthesizing and releasing cytokines, largely tumor necrosis factor (TNF) and interleukin-1 (IL-1). However, macrophages from some laboratory mouse strains such as C3h/HeN are unresponsive to endotoxin both in vivo and in vitro. We found members of a wild rodent species, Sigmodon hispidus, to also be extremely resistant to bacterial endotoxin challenge. Intravenous administration of up to 100,000 micrograms/kg body mass of Escherichia coli O26:B6 endotoxin did not cause lethality in adult S. hispidus. In contrast to the endotoxin-resistant mouse strain, peritoneal macrophages derived from S. hispidus were responsive to in vitro endotoxin challenge as measured by high levels of TNF and IL-1 activity in supernatants of macrophage cultures. Thus, in vitro macrophage responsiveness to endotoxin does not always indicate high host sensitivity to endotoxin challenge.

Animals↗