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Biomedical subjects

F Gervais

Publications and source records attributed to F Gervais.

At least 55 records · Page 3Linked to original sources
PubMed1988

Increased natural resistance to Listeria monocytogenes in senescent mice correlates with enhanced macrophage bactericidal activity.

Natural resistance to Listeria monocytogenes is increased in aging (18-22-month-old) AB6F1 mice when compared to their younger counterparts. We have investigated several parameters of macrophage function of old AB6F1 mice to establish what macrophage characteristics determine their enhanced resistance to Listeria. Senescent mice had an increased number of macrophages present in unstimulated peritoneal cavity. These macrophages exhibited enhanced bactericidal activity and H2O2 production. Old mice showed a diminished subcutaneous inflammatory response. Kupffer cells obtained from normal uninfected old mice had good levels of listericidal activity, but Kupffer cells obtained from normal young mice could not kill Listeria. The increased natural resistance to Listeria monocytogenes seen in old AB6F1 mice could be the result of enhanced macrophage bactericidal activities in the liver prior to the infection.

Aging↗
PubMed1987

Genetic regulation of lipopolysaccharide-induced interleukin 1 production by murine peritoneal macrophages.

The production of IL 1 by LPS-stimulated peritoneal macrophages from inbred mouse strains was studied. Macrophages from A/J (A) mice were deficient in IL 1 production, when compared with high IL 1-producing strains, including C57BL/6J (B). The difference between A and B macrophages was maintained over a wide LPS concentration range and throughout a 72-hr incubation period. Because of these differences, it was possible to investigate the mechanisms regulating IL 1 production by applying techniques of genetic analysis by using recombinant inbred (RI) strains derived from the A and B progenitors. A strain distribution pattern (SDP) of IL 1 production (low/high response) was obtained with the use of 15 AXB/BXA RI strains. This suggested the presence of a major gene locus controlling the production of IL 1 in response to LPS stimulation, with allelic differences presumably resulting in deficient or efficient IL 1 production. In addition, there appeared to be one or more other loci involved in determining the magnitude of the IL 1 response to LPS in the responder mice. The IL 1 response did not appear to be linked to the major histocompatibility complex, since B10.A mice (which share the same H-2a haplotype as A/J) were efficient IL 1 producers. There did not appear to be any correlation between the degree of IL 1 production and the magnitude of the peritoneal macrophage inflammatory response, or between IL 1 production and LPS responsiveness (as determined by splenocyte proliferation). SDP analysis also indicated that the IL 1 response was not linked to macrophage tumoricidal activity. A comparison of the SDP for IL 1 production with a library of SDP for other known genetic waits suggested linkage with at least four loci on chromosome 1.

Animals↗
PubMed1986

Bee venom melittin blocks neutrophil O2- production.

Bee venom (BV) is used in folk medicine to treat arthritis. It has antiinflammatory effects in animal models of rheumatic disease. We have studied the effects of BV on human neutrophil production of superoxide (O2-) and hydrogen peroxide, finding potent, nontoxic, dose-dependent production inhibition. Melittin, the major fraction of BV (50-70%) shows high-affinity calmodulin binding (Kd 3 nM). Drugs which bind calmodulin, such as trifluoperazine, inhibit O2- production by human neutrophils. For these reasons we have investigated the effect of melittin and other BV peptides on O2- production by human peripheral blood leukocytes. We show that melittin inhibited O2- production both pre- and poststimulation in contrast to other BV fractions which were without effect. Oxygen radicals and their derivatives from inflammatory cells are implicated in the tissue damage occurring during inflammation. The inhibition is due to a direct effect on cells, and not indicator medium, dismutation, toxic or scavenging effects. We propose that melittin may serve as a prototype small (mol wt 1280), cationic, amphipathic, calmodulin-binding, membrane-active, superoxide-production-inhibiting peptide, providing a model for peptides which could have a role in in vivo regulation of radical production.

Anti-Inflammatory Agents↗
PubMed1986

Serum amyloid P-component-induced enhancement of macrophage listericidal activity.

Purified serum amyloid P component (SAP), the major acute-phase reactant of mice, augmented the in vitro listericidal activity of inflammatory (elicited) macrophages, bone marrow-derived monocytes, and macrophages from a subcutaneous site of inflammation. Monocytes and macrophages from C57BL/B6 mice, which are relatively resistant to Listeria monocytogenes, exhibited a significantly greater enhanced killing capacity for listeria than macrophages from listeria-susceptible A/J mice. SAP did not alter the extent of phagocytosis by macrophages of opsonized L. monocytogenes, nor was SAP opsonic for listeria. Mannose-derived simple sugars inhibited the binding of SAP to macrophages and consequently prevented the enhanced SAP-dependent listericidal activity. Macrophages from lipopolysaccharide-hyporesponsive mice also had increased microbicidal activity following incubation with SAP. SAP activated macrophages independently of lymphokine. Therefore, SAP may serve as a mediator of the heightened nonspecific host defense response that is associated with the acute phase of the systemic inflammatory response.

Amyloid↗
PubMed1986

Analysis of macrophage bactericidal function in genetically resistant and susceptible mice by using the temperature-sensitive mutant of Listeria monocytogenes.

Innate resistance to infection by Listeria monocytogenes is genetically controlled and is critically dependent on prompt macrophage recruitment to the sites of infection. Experiments reported here were designed to examine whether there was an additional, qualitative difference between the intrinsic bactericidal activity of the inflammatory macrophages of genetically resistant (C57BL/6J) and susceptible (A/J) hosts. To critically evaluate the bactericidal (rather than bacteriostatic) function of the macrophage, a temperature-sensitive (ts) mutant of L. monocytogenes was developed. Mutagenesis was induced with nitrosoguanidine, and the ts mutants were isolated following enrichment with penicillin-gentamicin combinations. The ts mutants were found to carry the cell surface and biochemical characteristics of the original wild-type strain of L. monocytogenes. Inflammatory peritoneal macrophages from resistant C57BL/6J mice were found to have enhanced listericidal activity when compared with inflammatory macrophages from susceptible A/J mice. However, further analysis of the macrophage populations revealed that this seemingly qualitative advantage was due to the relatively greater proportion of inflammatory macrophages present in the inflammatory exudates of resistant C57BL/6J mice. When homogeneous populations of pure inflammatory macrophages were compared, no interstrain differences in their listericidal activity in vitro were seen. These results suggest that the susceptibility of A/J strain mice to L. monocytogenes is not due to an intrinsic deficiency of the listericidal activity of the inflammatory macrophage. The slight increase in bactericidal activity of macrophages from resistant mice that was reported by others (C. J. Czuprynski, B. P. Canono, P. M. Henson, and P. A. Campbell, Immunology 55:511-518, 1985) is caused by the difference in the relative percentage of resident cells present in the peritoneal exudates from resistant and susceptible mice.

Animals↗
PubMed1984

Bee venom inhibits superoxide production by human neutrophils.

Investigation of the antiinflammatory properties of bee venom demonstrates that it inhibits production of superoxide anion by human neutrophils in a potent, selective, nontoxic, dose-dependent fashion, both pre- and poststimulation by particulate and soluble activators of the neutrophil oxidative metabolism burst. The effect is not due to receptor competition, superoxide dismutase, and/or catalase activity, scavenging, or indicator media effects. These findings may explain the antiinflammatory effects of whole bee venom in experimental systems, its widespread use in folk medicine, and lead to the development of potent, new antiinflammatory substances for therapeutic use in man.

Bee Venoms↗
PubMed1984

The effect of the non-steroidal anti-inflammatory drug Etodolac on macrophage migration in vitro and in vivo.

The possible mode of action of Etodolac, a potent anti-inflammatory drug, has been investigated. The effect of Etodolac on macrophage inflammatory depressed the influx of inflammatory macrophages into peritoneal cavity following stimulation with a sterile irritant. This decrease in macrophage accumulation in vivo correlated with the effect of Etodolac on the macrophage chemotaxis in vitro. Etodolac was also capable of reducing the macrophage ability to migrate towards a chemoattractant. In vivo Etodolac should reduce the amount of damage produced at the site of chronic inflammation since fewer macrophages would migrate to the inflammatory sites.

Acetates↗
PubMed1984

Natural resistance to listeriosis: role of host inflammatory responsiveness.

The accumulation of inflammatory macrophages at the infective foci appears to represent the major host defense mechanism during the early or innate phase of resistance to infection with Listeria monocytogenes. Certain inbred strains of mice, such as A/J [A] have genetically-determined defects in macrophage mobilization in vivo in response to intraperitoneal (IP) treatment with the nonspecific inflammatory stimulus, thioglycollate. These strains of mice are also genetically-susceptible to infection with Listeria. In contrast, other strains (C57BL/6J or B10.A/SgSn [B]) are high responders for both genetically-determined traits. Linkage analysis of the two traits in backcross progeny showed that the trait of a high macrophage inflammatory response segregates with the trait of resistance to Listeria. These observations suggested that the gene(s) controlling the level of the macrophage inflammatory response is identical with or linked to the gene(s) controlling resistance to Listeria. We have found additional evidence to support this hypothesis by analyzing the expression of the two traits in 12 AXB/BXA recombinant inbred [RI] mouse strains derived from progenitor B (high macrophage response, Listeria-resistant) and A (low macrophage response, Listeria-susceptible) mice. Furthermore, those AXB/BXA strains, which like progenitor A mice, are susceptible to infection with Listeria exhibit a defect in the number of polymorphonuclear leukocytes recovered from peritoneal exudates 18 h after IP injection with thioglycollate. The strain distribution pattern of both the resistance/susceptibility to Listeria and the leukocyte inflammatory response in RI strains is concordant with that of Hc allele coding for effective/defective levels of C5 complement protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Genetic control of resistance to Listeria monocytogenes: regulation of leukocyte inflammatory responses by the Hc locus.

The control mechanisms responsible for the innate resistance of C57BL/6J (B) mice and for the innate susceptibility of A/J (A) mice to infection with Listeria monocytogenes were studied by typing the recombinant inbred (RI) strains derived from these two progenitors for the trait of Listeria resistance/susceptibility. The strain distribution pattern (SDP) of this trait obtained in the 13 AXB/BXA RI strains studied suggests that an allelic difference at a major locus (Lr-1) is responsible for the trait of resistance/susceptibility to Listeria. In addition, another putative gene (Lr-2) unlinked to Lr-1 is postulated to control the level of bacterial load within the group of susceptible strains. The SDP of A and B alleles at the Lr-1 locus was fully concordant with that observed for the Hc locus (controlling the level of the C5 component of complement). This suggests that the genetic susceptibility of A strains of mice to Listeria infection is either directly due to or related to the C5 deficiency found in that strain. This conclusion is enhanced by the observation of a significant protection of A mice from listeriosis by the infusion of C5-rich serum. A survey of RI strains for the magnitude of PMN and macrophage inflammatory responses showed that the expression of both traits co-segregated and that the C5 deficiency was the major factor responsible for the defective inflammatory response of A strain mice. We conclude that a defect in the phagocyte inflammatory responses caused by C5 deficiency is the major reason for the extreme susceptibility of A mice to Listeria.

Animals↗
PubMed1983

Immunologic dysfunction in patients with classic hemophilia receiving lyophilized factor VIII concentrates and cryoprecipitate.

The occurrence of the acquired immune deficiency syndrome (AIDS) in patients with hemophilia has suggested that an infectious agent transmitted through the frequent use of pooled blood products could be responsible. To determine if the amount or type of factor VIII preparation alters the risk of acquiring immune defects, three groups of asymptomatic heterosexual men were studied: 34 with severe classic hemophilia who were receiving lyophilized factor VIII concentrate, 10 with either mild classic hemophilia or moderately severe von Willebrand's disease who were receiving cryoprecipitate and 22 normal men who served as controls. Anergy was noted in 68%, 57% and 5% respectively of the three groups. In comparison with the control group, the group treated with lyophilized factor VIII concentrate had a significantly decreased mean ratio of helper to suppressor T lymphocytes, poor responses of the lymphocytes to mitogens, high unstimulated background activity of these cells and significantly elevated serum IgG levels. Although some of the patients with classic hemophilia who were treated with cryoprecipitate were also anergic, they did not manifest these in-vitro abnormalities. The data indicate that a majority of apparently immunocompetent individuals with classic hemophilia show in-vivo and in-vitro evidence of impaired cellular immunity and may be at risk for the development of opportunistic infections and neoplasms.

Acquired Immunodeficiency Syndrome↗
PubMed1981

Relative lack of Epstein Barr virus (EBV) receptors on B cells from persistently EBV seronegative adults.

Viral receptors are essential for the entry of the virus into the cell. EBV receptors can be detected on fresh lymphocytes by a technique that uses EBV-coupled tanned red blood cells that form rosettes with lymphocyte-bearing receptors. This technique was found to detect viral receptors only and not surface immunoglobulins. T cell depletion of the lymphocyte population showed that these receptors were present on B lymphocytes. Study of the presence of these EBV receptors on the surface of fresh lymphocytes from 66 subjects (age 2 to 66), selected out of a group of over 2000 individuals, showed that the majority of these donors had receptors for the virus. However, a few of these adults persistently failed to develop anti-EBV antibodies, even if they were in close contact with the infectious agent. The lymphocytes of 11 such individuals were found to be lacking EBV receptors. Transformation assay of these lymphocytes did not give rise to lymphoblastoid cell lines whereas lymphocytes from 4 individuals, who were EBV seropositive or seronegative but receptor positive, yielded permanent lymphoblastoid cell lines. This would suggest that a few EBV seronegative adults (less than 0.5%) display natural resistance to EBV transformation of their lymphoid cells as a result of absolute or relative lack of EBV receptors on these cells.

Adolescent↗