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Biomedical subjects

D L Archer

Publications and source records attributed to D L Archer.

At least 19 recordsLinked to original sources
PubMed1997

Chronic health effects of microbial foodborne disease.

The acute effects of foodborne disease are sometimes not the end of the illness. Several significant foodborne pathogens are capable of triggering chronic disease, and even permanent tissue or organ destruction, probably via immune mechanisms. Arthritis, septic and reactive, inflammatory bowel disease, haemolytic uraemic syndrome, Guillain-Barré syndrome, and possible several autoimmune disorders can be triggered by foodborne pathogens or their toxins. Research is needed to more fully understand the mechanisms by which the immune system is inappropriately activated by these common foodborne disease-causing agents.

Autoimmune Diseases↗
PubMed1991

Foodborne disease outbreaks in nursing homes, 1975 through 1987.

OBJECTIVE: --To describe the epidemiology of foodborne disease outbreaks in nursing homes and to identify where preventive efforts might be focused. DATA SOURCES: --Reports by state and local health departments of foodborne disease outbreaks occurring from January 1, 1975, through December 31, 1987. STUDY SELECTION: --Foodborne disease outbreaks reported to the Centers for Disease Control, Atlanta, Ga, on standard investigation forms. DATA EXTRACTION: --Each foodborne disease outbreak report was examined by an epidemiologist or statistician. Outbreaks were considered to have a known pathogen if confirmed by laboratory tests, and a known vehicle when an epidemiologic investigation implicated a specific food item. DATA SYNTHESIS: --From 1975 through 1987, 26 states reported 115 outbreaks of foodborne disease in nursing homes, causing illness in 4944 persons and death in 51. These outbreaks represented 2% of all reported foodborne disease outbreaks and 19% of outbreak-associated deaths in this period. Of 52 outbreaks with a known cause, Salmonella was the most frequently reported pathogen, accounting for 52% of outbreaks and 81% of deaths. Salmonella enteritidis outbreaks accounted for 56% of the Salmonella-associated deaths since 1981. The implicated food vehicles in S enteritidis outbreaks were made with eggs or prepared with equipment contaminated with eggs. Staphylococcal foodborne disease was the next most commonly identified cause, accounting for 23% of outbreaks. CONCLUSIONS: --Since the elderly are at high risk for serious morbidity from foodborne disease, nursing homes should practice careful food handling, preparation, and storage procedures; provide education for food handlers; and have active infection control programs to rapidly detect and control outbreaks of foodborne disease.

Aged↗
PubMed1988

Contemporary issues: diseases with a food vector.

Foodborne disease has become a contemporary issue. Several large, well-publicized outbreaks of foodborne disease have heightened public awareness that harmful microorganisms may be present in food and that chronic as well as acute disease may be caused by foodborne microbes. The field of food microbiology has likewise experienced a resurgence of interest. New tools, such as recombinant deoxyribonucleic acid technology and monoclonal antibody production, used to elucidate microbial virulence factors have facilitated identification of disease-causing microbes once thought to be harmless and demonstrated the complexity of individual virulence mechanisms previously considered to be well understood. Foodborne pathogens are also causing disease via some surprising food vectors, such as chopped, bottled garlic and sauteed onions. In addition to acute gastrointestinal disturbances, certain microorganisms may, through complex interactions with the human immune response, cause chronic diseases that affect several major organ systems. These microbes are serving as models in studies of molecular mimicry and genetic interrelatedness of procaryotes and eucaryotes. Other recently recognized attributes of foodborne microorganisms, such as the heat shock phenomenon and the possible nonculturability of some bacteria, may affect their ability to cause disease in humans. Because foodborne disease is a major cause of morbidity and mortality, the study of these diseases and their causative microorganisms presents a unique challenge to many professionals in the subdisciplines of microbiology, epidemiology, and clinical medicine.

Bacterial Toxins↗
PubMed1984

Differential effects of nordihydroguaiaretic acid (NDGA) on B-cell subsets: reversal of NDGA-induced antibody suppression by cyclic GMP is subset specific.

Nordihydroguaiaretic acid (4,4'-[2,3-dimethyl tetramethylene]-dipyrpcatechol) (NDGA), a reportedly specific lipoxygenase inhibitor, suppressed the in vitro murine plaque-forming cell (PFC) response to a thymus-dependent (TD) antigen, and the two subclasses of thymus-independent (TI) antigens, TI1 and TI2, at a final concentration of 33 microM. Suppression kinetics were inconsistent with those observed in previous experiments for other lipoxygenase inhibitors, butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT), in that BHA and BHT exert suppression early in the 5-day PFC culture system, whereas NDGA suppressed through the 96th h of the 120 h culture period. The sulfhydryl-protective agent 2-mercaptoethanol (2ME) protected both the TD and TI responses. Dibutyryl cyclic GMP (dbcGMP) failed to restore NDGA-suppressed TD and TI1 PFC responses but restored the TI2 response when added at 0-, 24-, 48-, 72-, and 96-h at concentrations of 1-2 mM. NDGA inhibited lipopolysaccharide- (LPS-) induced increases in murine splenocyte cyclic GMP (cGMP) levels, and dbcGMP failed to accelerate the onset of the TI2 PFC response appreciably. The results of these and other laboratory studies indicated that NDGA may not be a specific inhibitor of lipoxygenase. Furthermore, the B-cell subset responding to TI2 antigens may be separated from the TD- and TI1-responding subsets because of the ability of dbcGMP to restore NDGA-suppressed TI2 responses but not the TD or TI1 response. The results suggest a fundamental difference in the biochemical pathways of B-cell subsets, and that cGMP metabolism in some cells may be linked to specific protein synthesis.

Animals↗
PubMed1984

Effects of a strong and a weak carcinogen on murine alpha/beta interferon production in vivo.

A study was designed to determine whether oral doses of carcinogens would reduce an animal's ability to produce interferon. Female BCF1 mice were tested with various doses of benzo[alpha]pyrene (BP) or ethyl methanesulfonate (EMS) po (four to six mice per treatment) and challenged an hour later with the chemical interferon inducer tilorone. After 16-18 hr, mice were sacrificed and bled from the heart. Serum obtained from the blood was assayed for interferon. We found that mice treated with as little as 50 mg/kg BP or EMS had a statistically significant reduction in serum interferon titers compared with control-treated mice. Reductions in interferon titers were also noted at lower doses of the carcinogens, but due to the variability within the small sample size used, the reduction were not statistically significant. On a molar basis, BP was only two to three times more effective at reducing interferon titers than EMS. It was estimated from the data that slightly less than 10 mg/kg BP or 29 mg/kg EMS would be the doses corresponding to 50% reduction in control interferon titers. These doses are well below the reported mutations doses for these chemicals. The effect of carcinogens on in vivo interferon production reported here may be the most sensitive biologic system known for these chemicals.

Animals↗
PubMed1983

Staphylococcal enterotoxin induced mitogenesis: toxin binding and cell-cell interactions.

The binding characteristics of 125I-labelled staphylococcal enterotoxin A (125I-SEA), a T-cell mitogen, to murine lymphoid cell subpopulations were analyzed. Both T- and B-lymphocytes from murine spleens possess specific binding sites for SEA, as do T-lymphocytes from thymus. B-lymphocytes appear to have a greater capacity for binding of 125-SEA than do T-lymphocytes from either thymus or spleen. Enterotoxin did not specifically bind to thioglycollate-induced peritoneal exudate cells (PECs), used as a source of macrophages. Adherent PECs however, incorporated 125-ISEA by fluid phase endocytosis. When exposed to SEA and thoroughly washed, macrophages stimulate lymphocyte mitogenesis in spleen or thymus cell cultures not directly exposed to toxin. Maximum mitogenic stimulation took place only when both PECs and lymphocytes were exposed to SEA. The presence of splenic B-lymphocytes enhanced the mitogenic response of thymus derived T-cells to SEA. Thus, B-lymphocytes appear to contribute to SEA mitogenesis. These data suggest that mitogenic stimulation and possibly other immunological phenomena associated with SEA occur as a result of complex interactions between cellular components of the immune system.

Animals↗
PubMed1982

Disparate in vivo and in vitro immunomodulatory activities of rhodamine B.

At nontoxic concentrations (1-10 microgram/ml) rhodamine B (N-[9-(2-carboxyphenyl)-6-(diethylamino)-3H-xanthen-3-ylidene]-N- ethylethanaminium chloride; D & C Red No. 19; CAS no. 81-88-9), a low-molecular-weight dye, suppressed the primary in vitro plaque-forming-cell response of BDF1 mouse spleen cells both to the thymus-dependent antigen, sheep red blood cells and to the thymus-independent antigen, E. coli 0127: B8 lipopolysaccharide. Suppression was effective when the D & C Red No. 19 was added at any time up to 48 hr of culture. Rhodamine B at concentrations from 1 to 10 microgram/ml significantly suppressed mitogen-induced proliferation of both B- and T-lymphocytes in vitro. BDF1 mice exposed to 50 and 100 ppm dye in their drinking water for 14 days prior to splenectomy gave a depressed in vitro plaque-forming-cell response to sheep red blood cells. In contrast, a significant enhancement of antibody response resulted when mice were exposed to the dye and sheep-red-blood-cell antigen was administered in vivo. Mitogen-induced B- and T-lymphocyte proliferation was also enhanced in mice exposed to the dye for 14 days.

Adjuvants, Immunologic↗
PubMed1982

New approaches to immunotoxicity testing.

New approaches to immunotoxicity testing are reviewed and discussed. A method of activating T-cells in vivo is presented which circumvents artifacts dur to viability effects encountered with in vitro mitogen assays. The use of adoptive transfer approaches to combine the advantages of in vitro manipulation with in vivo function assays is discussed relative to natural killer cells. The need for an in vitro metabolic activation step coupled to other in vitro immunologic assays is discussed.

Animals↗
PubMed1982

The effect of lead on immune and viral interferon production.

Female BDF1 mice were exposed to lead acetate in the drinking water at concentrations ranging form 0 to 1000 micrograms/mL lead for three weeks. The mice tolerated these levels of lead exposure without exhibiting signs of clinical toxicity. Weight gains were not affected by lead exposure. The production of viral interferon induced by the oral administration of tilorone was not altered by lead exposure. The T-lymphocyte mitogens concanavalin A, phytohemagglutinin and staphylococcal enterotoxin A induced immune interferon to varying degrees, with concanavalin A and staphylococcal enterotoxin A exhibiting the most potent induction capabilities. The production of immune interferon induced by T-lymphocyte mitogens was not suppressed by lead exposure.

Animals↗
PubMed1982

Cyclic GMP as the second messenger in helper cell requirement for gamma-interferon production.

Cyclic GMP and activators (acetylcholine, E. coli heat-stable toxin) of guanylate cyclase were capable of completely replacing the helper cell or interleukin 2 requirement for gamma-interferon (IFN gamma) production by Lyt-1-,2+ cells from C57BL/6 mouse spleen cells. The cyclic GMP help was independent of DNA synthesis or proliferation in the IFN gamma-producing cells, because cyclic GMP reversed mitomycin C blockage of IFN gamma production but did not reverse the inhibition of DNA synthesis. Thus, the findings presented here are unrelated to the question of the second messenger role of cyclic GMP in the activation of lymphocytes for DNA synthesis and cellular proliferation. The cyclic GMP help for IFN gamma production was antagonized by cyclic AMP and inducers (isoproterenol) of adenylate cyclase.

Animals↗
PubMed1981

Restoration by cyclic guanosine monophosphate and extracellular calcium of butylated hydroxyanisole-suppressed primary murine thymus-dependent antibody response.

The effect of dibutyryl cyclic guanosine monophosphate (dbc-GMP) on butylated hydroxyanisole (BHA)-induced suppression of the primary in vitro thymus-dependent antibody response of BDF1 mouse spleen cultures was studied. When added at 0 hr relative to antigen addition, 1 mg of dbc-GMP (8 mM) restored by greater than 70% the BHA-inhibited primary immunoglobulin (Ig)M plaque-forming cell (PFC) response to sheep erythrocytes (SRBC). The suppression was not reversed by the addition of 50 microgram of dibutryl cyclic adenosine monophosphate (dbc-AMP), which is known to reverse suppressor T-cell activity. The addition of 10 mM extracellular calcium (Ca2+) at the same time as antigen to BHA-inhibited cultures resulted in more than 80% restoration of the anti-SRBC PFC response. Quantitation of c-GMP by radioimmunoassay demonstrated that BHA lowered by 58% the c-GMP content of splenic lymphocytes and abrogated the ability of lipopolysaccharide of E. coli (LPS) to elevate c-GMP levels in splenic lymphocytes. The data suggest that BHA exerts its immunosuppressive effect on the primary in vitro antibody response by inhibiting guanylate cyclase activity and effectively lowering c-GMP levels; exogenous dbc-GMP and Ca2+ can freely reverse the immunosuppressive effect of BHA.

Animals↗
PubMed1981

Inverse relationship between immune interferon induction and mitogen effects on the maturation of the primary antibody response.

Staphylococcal enterotoxin A (SEA) is both a potent inducer of immune interferon (IFN-gamma) and suppressor of the murine primary in vitro plaque-forming cell (PFC) response to the thymus-dependent antigen sheep erythrocytes (SRBC). Staphylococcal enterotoxin D (SED), which is structurally related to but antigenically different from SEA, is, in contrast, a poor inducer of IFN-gamma but a potent accelerator of PFC response maturation. SED added to cultures from 0.01 to 1.0 microgram/ml induced profound enhancement of the PFC response on day 3 of culture. SEA caused no acceleration of PFC maturation and suppressed the day 5 PFC response over an equivalent dose range. At the same concentration, SED only poorly induced IFN-gamma, while SEA was a potent IFN-gamma inducer. SED induced DNA synthesis in C57Bl/6 spleen cell cultures but not athymic nude (Nu/Nu) spleen cells, suggesting that SED is a T-cell mitogen. SED was most effective in accelerating PFC maturation and increasing the magnitude of the PFC response when added to cultures at the time of SRBC addition. SED was an equally effective adjuvant for SRBC of both high and low immunogenicity. Thus, two mitogens that are structurally related have diametrically opposite effects on the primary in vitro thymus-dependent antibody response that maybe related to their relative abilities to induce IFN-gamma. These effects could be related to differential activation of T-cell subpopulations.

Animals↗