Killing of Borrelia burgdorferi by macrophages is dependent on oxygen radicals and nitric oxide and can be enhanced by antibodies to outer surface proteins of the spirochete

Interaction of B. burgdorferi organisms with mouse bone marrow-derived macrophages (BMMΦ) leads to phagocytosis of microorganisms, induction of nitric oxide (NO) and superoxide radicals (O 2 − by BMMΦ and killing of spirochetes. Destruction of spirochetes by BMMΦ was quantified by a new method based...

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Veröffentlicht in:Immunology letters 1994-05, Vol.40 (2), p.139-146
Hauptverfasser: Modolell, M., Schaible, U.E., Rittig, M., Simon, M.M.
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creator Modolell, M.
Schaible, U.E.
Rittig, M.
Simon, M.M.
description Interaction of B. burgdorferi organisms with mouse bone marrow-derived macrophages (BMMΦ) leads to phagocytosis of microorganisms, induction of nitric oxide (NO) and superoxide radicals (O 2 − by BMMΦ and killing of spirochetes. Destruction of spirochetes by BMMΦ was quantified by a new method based on the release of radioactivity from spirochetes pre-labelled with [ 3H]adenine. Uptake of B. burgdorferi by BMMΦ, which mainly occurs by coiling phagocytosis, generation of NO and O 2 − radicals as well as killing of spirochetes were significantly enhanced by pre-opsonization of spirochetes with monoclonal antibodies (mAb) to the outer surface proteins A and B but not with those to the periplasmic flagellin. Addition of inhibitors specific for NO and O 2 − radical synthesis either separately or together to cultures of BMMΦ and spirochetes resulted in only partial reduction of the killing potential of effector cells. The data indicate that NO and O 2 radicals are necessary, but not sufficient, for complete elimination of B. burgdorferi by macrophages. Together with previous findings that protection against B. burgdorferi infection is conveyed by humoral immune responses the present data indicate that one of the important functions of specific antibodies is their participation in macrophage-mediated control of spirochetes.
doi_str_mv 10.1016/0165-2478(94)90185-6
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Schaible, U.E. ; Rittig, M. ; Simon, M.M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-65aa1e84af6d02f0381bffd23c91636fa962c5bbe1ed69b346bef42620486ef83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1994</creationdate><topic>Animals</topic><topic>Antibodies, Bacterial - immunology</topic><topic>Antibodies, Monoclonal</topic><topic>Antigens, Surface - immunology</topic><topic>B. burgdorferi</topic><topic>Bacterial diseases</topic><topic>Bacterial Outer Membrane Proteins - immunology</topic><topic>Bacterial Vaccines</topic><topic>Biological and medical sciences</topic><topic>Bone Marrow Cells</topic><topic>Borrelia burgdorferi</topic><topic>Borrelia burgdorferi Group - immunology</topic><topic>Borrelia burgdorferi Group - ultrastructure</topic><topic>Cells, Cultured</topic><topic>Cytotoxicity, Immunologic - immunology</topic><topic>Experimental bacterial diseases and models</topic><topic>Female</topic><topic>Infectious diseases</topic><topic>Lipoproteins</topic><topic>Lyme disease</topic><topic>Lyme Disease - immunology</topic><topic>Macrophage</topic><topic>Macrophages - immunology</topic><topic>Macrophages - ultrastructure</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred AKR</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, SCID</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - biosynthesis</topic><topic>Nitric Oxide - physiology</topic><topic>Phagocytosis</topic><topic>Spirochete</topic><topic>Superoxide</topic><topic>Superoxides - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Modolell, M.</creatorcontrib><creatorcontrib>Schaible, U.E.</creatorcontrib><creatorcontrib>Rittig, M.</creatorcontrib><creatorcontrib>Simon, M.M.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Immunology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Modolell, M.</au><au>Schaible, U.E.</au><au>Rittig, M.</au><au>Simon, M.M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Killing of Borrelia burgdorferi by macrophages is dependent on oxygen radicals and nitric oxide and can be enhanced by antibodies to outer surface proteins of the spirochete</atitle><jtitle>Immunology letters</jtitle><addtitle>Immunol Lett</addtitle><date>1994-05-01</date><risdate>1994</risdate><volume>40</volume><issue>2</issue><spage>139</spage><epage>146</epage><pages>139-146</pages><issn>0165-2478</issn><eissn>1879-0542</eissn><coden>IMLED6</coden><abstract>Interaction of B. burgdorferi organisms with mouse bone marrow-derived macrophages (BMMΦ) leads to phagocytosis of microorganisms, induction of nitric oxide (NO) and superoxide radicals (O 2 − by BMMΦ and killing of spirochetes. Destruction of spirochetes by BMMΦ was quantified by a new method based on the release of radioactivity from spirochetes pre-labelled with [ 3H]adenine. Uptake of B. burgdorferi by BMMΦ, which mainly occurs by coiling phagocytosis, generation of NO and O 2 − radicals as well as killing of spirochetes were significantly enhanced by pre-opsonization of spirochetes with monoclonal antibodies (mAb) to the outer surface proteins A and B but not with those to the periplasmic flagellin. Addition of inhibitors specific for NO and O 2 − radical synthesis either separately or together to cultures of BMMΦ and spirochetes resulted in only partial reduction of the killing potential of effector cells. The data indicate that NO and O 2 radicals are necessary, but not sufficient, for complete elimination of B. burgdorferi by macrophages. 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subjects Animals
Antibodies, Bacterial - immunology
Antibodies, Monoclonal
Antigens, Surface - immunology
B. burgdorferi
Bacterial diseases
Bacterial Outer Membrane Proteins - immunology
Bacterial Vaccines
Biological and medical sciences
Bone Marrow Cells
Borrelia burgdorferi
Borrelia burgdorferi Group - immunology
Borrelia burgdorferi Group - ultrastructure
Cells, Cultured
Cytotoxicity, Immunologic - immunology
Experimental bacterial diseases and models
Female
Infectious diseases
Lipoproteins
Lyme disease
Lyme Disease - immunology
Macrophage
Macrophages - immunology
Macrophages - ultrastructure
Medical sciences
Mice
Mice, Inbred AKR
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, SCID
Nitric oxide
Nitric Oxide - biosynthesis
Nitric Oxide - physiology
Phagocytosis
Spirochete
Superoxide
Superoxides - metabolism
title Killing of Borrelia burgdorferi by macrophages is dependent on oxygen radicals and nitric oxide and can be enhanced by antibodies to outer surface proteins of the spirochete
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