Induction by immunomodulatory agents of a macrophage antigen recognized by monoclonal antibody 158.2 and correlation with macrophage function

Koestler, Thomas P.; Badger, Alison M.; Rieman, David J.; Greig, Russell; Poste, George

doi:10.1016/0008-8749(85)90344-2

Cited by 11 publications

(2 citation statements)

References 27 publications

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“…Immediately following the 2-h plastic adherence procedure, macrophages were incubated in medium containing 10 antiviral units of homogeneously pure recombinant mouse IFN-␥/ml (8.0 ϫ 10 6 U/mg of protein) for 18 to 24 h as previously reported (26,47) and then used in the bacteriocidal assays. The recombinant mouse IFN-␥ (lot 2271-54-F2) was the kind gift of Genentech, Inc. (South San Francisco, Calif.).…”

Section: Methodsmentioning

confidence: 99%

Host and Bacterial Factors Involved in the Innate Ability of Mouse Macrophages To Eliminate Internalized UnopsonizedEscherichia coli

et al. 2000

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In an effort to better understand genetic and cellular factors that influence innate immunity, we examined host and bacterial factors involved in the nonopsonic phagocytosis and killing of Escherichia coli K-12 by mouse macrophages. Unelicited (resident) peritoneal macrophages from five different mouse strains, BALB/c, C57BL/6, CD-1, C3H/HeJ, and C3H/HeN, were employed. Additional macrophage populations were obtained from CD-1 mice (bone marrow-derived macrophages). Also, for BALB/c and C57BL/6 mice, peritoneal macrophages elicited with either thioglycolate or proteose peptone, bone marrow-derived macrophages, and macrophage-like cell lines derived from the two strains were employed. Two E. coli K-12 strains that differed specifically in their abilities to produce type 1 pili containing the adhesive protein FimH were examined. The parameters used to assess macrophage bacteriocidal activity were (i) the killing of internalized (gentamicinprotected) E. coli during the approximately 4-h assay and (ii) the initial rate at which internalized E. coli were eliminated. Data on these parameters allowed the following conclusions: (i) unelicited or proteose peptoneelicited peritoneal macrophages were significantly better at eliminating internalized bacteria than thioglycolate-elicited peritoneal macrophages, bone marrow-derived macrophages, or macrophage cell lines; (ii) the host genetic background had no significant effect upon the ability of unelicited peritoneal macrophages to kill E. coli (even though the mouse strains differ widely in their in vivo susceptibilities to bacterial infection); and (iii) the FimH phenotype had no significant effect upon E. coli survival once the bacterium was inside a macrophage. Additionally, there was no correlation between the bacteriocidal effectiveness of a macrophage population and the number of bacteria bound per macrophage. However, macrophage populations that were the least bacteriocidal tended to bind higher ratios of FimH ؉ to FimH ؊ E. coli. The effect of gamma interferon, fetal calf serum, and the recombination proficiency of E. coli were examined as factors predicted to influence intracellular bacterial killing. These had no effect upon the rate of E. coli elimination by unelicited peritoneal macrophages.

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Section: Methodsmentioning

confidence: 99%

Host and Bacterial Factors Involved in the Innate Ability of Mouse Macrophages To Eliminate Internalized UnopsonizedEscherichia coli

et al. 2000

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“…IFN-y increases the expression of TNF receptors (26) and Ia on macrophages (1, 31), both of which might lead to more efficient interaction between macrophages and listeria-specific T cells. These interactions might indirectly up-regulate the T-cell activation (12) that is clearly required for release of additional IFN--y and perhaps other macrophage-activating factors that may augment the destruction of intracellular listeria by macrophages (14,23).…”

Section: Fig 3 Comparison Of Histopathological Changes In the Livermentioning

confidence: 99%

Separate and combined effects of recombinant interleukin-1 alpha and gamma interferon on antibacterial resistance

1989

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Our laboratory has previously reported that administration of murine recombinant interleukin la (rIL-la) substantially enhanced the resistance of mice to Listeria monocytogenes infection. Other investigators have reported that gamma interferon (IFN-y) plays a pivotal role in antilisteria resistance. In the present study, we have defined doses of human rIL-lac that enhanced the antilisteria resistance of mice. We then addressed the possibility that combined immunotherapy with rIL-lot and recombinant IFN-y (rIFN-y) might result in an additive or synergistic enhancement of antibacterial resistance. Simultaneous administration of rIL-la and rIFN-y enhanced antilisteria resistance (at 3 days after infection) to a greater extent than did either cytokine alone, although the results did not imply a synergistic action between the two cytokines. Experiments which examined the effects of the timing of cytokine administration indicated that maximal protection was observed when rIL-la and rIFN-y were administered together concomitantly with the L. monocytogenes challenge. When we compared the separate and combined protective effects of rIL-la and rIFN-y throughout the course of a primary L. monocytogenes infection, we observed an additive effect of the two cytokines only at 3 days after challenge, the time at which the peak bacterial burden occurs in the spleens and livers of infected mice. Histopathological comparisons of livers and spleens from cytokine-treated and control listeria-infected mice verified that cytokine treatment reduced the severity of tissue damage in cytokine-treated listeria-infected mice. In an attempt to provide a potential mechanism for the protective effects of rIL-la and rIFN-'y administration, we compared levels of colony-stimulating activity in sera from cytokine-treated and control listeria-infected mice. The highest levels of colony-stimulating activity were detected in sera from control listeria-infected mice; somewhat lower levels were found in sera from listeria-infected mice that received rIL-la and rIFN-y either alone or in combination.

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Activation of Rat Alveolar Macrophages by Gamma Interferon to Inhibit Toxoplasma gondii In Vitro

Badger¹,

Hutchman²,

Sung³

et al. 1987

Journal of Leukocyte Biology

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We have investigated the effects of murine interferons on the ability of rat alveolar macrophages (AM) to inhibit the proliferation of the intracellular protozoan Toxoplasma gondii. This activity was determined by measuring suppression of 3H-uracil uptake into the Toxoplasma and by microscopic enumeration of the intracellular organisms. Recombinant gamma interferon (rMulFN-gamma), but not alpha/beta interferon (IFN-alpha/beta) was able to activate AM for antimicrobial activity in vitro. Maximum activation was achieved by incubation with 50-200 units/ml rMulFN-gamma and the activity was lost at one unit/ml. The highest levels of activation were obtained when macrophages were incubated with interferon for 48-72 h prior to the challenge with Toxoplasma organisms. Activation could still be obtained, however, when the interferon was added to the cultures as late as 2 h after the phagocytosis of Toxoplasma. Neither MDP nor low concentrations (1-1-ng/ml) of S. typhosa lipopolysaccharide (LPS) were able to activate these cells to inhibit the growth of Toxoplasma. Phagocytosis of Toxoplasma by AM did not result in the release of O2-, in fact the spontaneous release of O2- by these cells was inhibited by Toxoplasma. This inhibition was reversed by preincubation of the cells with rMulFN-gamma.

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Induction by immunomodulatory agents of a macrophage antigen recognized by monoclonal antibody 158.2 and correlation with macrophage function

Cited by 11 publications

References 27 publications

Host and Bacterial Factors Involved in the Innate Ability of Mouse Macrophages To Eliminate Internalized UnopsonizedEscherichia coli

Host and Bacterial Factors Involved in the Innate Ability of Mouse Macrophages To Eliminate Internalized UnopsonizedEscherichia coli

Separate and combined effects of recombinant interleukin-1 alpha and gamma interferon on antibacterial resistance

Activation of Rat Alveolar Macrophages by Gamma Interferon to Inhibit Toxoplasma gondii In Vitro

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