S. E. Mergenhagen

National Institute of Dental and Craniofacial Research

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H Gewurz

Rush University Medical Center

Sharon M. Wahl

Johns Hopkins All Children's Hospital

David L. Rosenstreich

Albert Einstein College of Medicine

Ralph Snyderman

Duke University

Ann L. Sandberg

National Institute of Dental and Craniofacial Research

L M Wahl

Goethe University Frankfurt

Jeremy Farrar

World Health Organization

A. Rizzo

Ospedale Vincenzo Cervello

Joost J. Oppenheim

Frederick National Laboratory for Cancer Research

Henry W. Scherp

National Institute of Dental and Craniofacial Research

Cooperative Institutions

National Institutes of Health

National Institute of Dental and Craniofacial Research

National Cancer Institute

Johns Hopkins University

United States Public Health Service

National Institute of Allergy and Infectious Diseases

University of Minnesota

University of California, San Francisco

University of Alabama

University of Michigan–Ann Arbor

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Importance of Actinomyces and certain gram-negative anaerobic organisms in the transformation of lymphocytes from patients with periodontal disease

Infection and Immunity (1976)

John J. Baker S. P. Chan S. S. Socransky Joost J. Oppenheim S. E. Mergenhagen

Dental plaque deposits are known to be potent stimulants of lymphocyte transformation in patients with periodontal disease but not in normal subjects. Since plaque deposits consist mainly of whole bacteria, the cell walls of the most commonly found organisms in plaque were tested for their capacity to induce lymphocyte transformation. There was a direct correlation between the severity of peridontal disease and the amount of transformation induced by the cell walls of oral bacteria and by solubilized dental plaque. Cord blood leukocytes and lymphocytes from clinically normal people did not respond, which indicates that these stimulants are antigens rather than mitogens. Of the eleven bacteria tested, four members of the family Actinomycetaceae (Actinomyces viscosus, A. israelii, A. naeslundii, and Arachnia propionica), the related Propionibacterium acnes, and an anaerobic gram-negative anaerobic rod (27N). The high prevalence of the former organisms in the mature dental plaque that forms around the gingival crevice area and the potent efficacy with which they stimulate lymphocytes indicates that Actinomyces and certain gram-negative anaerobes may be important etiological agents in chronic periodontal inflammation in man.

Propionibacterium Acnes

Actinomyces naeslundii

Dental plaque

Actinomycetaceae

Anaerobic infection

10.1128/iai.13.5.1363-1368.1976

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Citations (99)

Interactions of the Complement System with Native and Chemically Modified Endotoxins

Journal of Bacteriology (1968)

H Gewurz S. E. Mergenhagen A. Nowotny J. K. Phillips

Endotoxic lipopolysaccharides (LPS) isolated from Serratia marcescens, Veillonella alcalescens , and Salmonella typhosa were potent in their ability to induce fixation of complement (C′) in normal guinea pig, rabbit, mouse, and human serum. The C′-fixing ability of LPS was pronounced even when assays were performed in undiluted serum, and was lost after each of four chemical modifications which resulted in loss of biological toxicities. The detoxification procedures had in common the cleavage of ester-bound, long-chain carboxylic acids. The ability of biologically active LPS to fix C′ in normal guinea pig serum was reflected chiefly in dramatic uptake of classical C′3 (C′3t); fixation of C′1, C′4, and C′2 was virtually undetectable. Hence, it was the capacity for fixation of C′3t which was lost most overtly during detoxification. Addition of immune serum to the assay mixtures resulted in detectable fixation of C′1 and C′4. Biologically active LPS also fixed more of these components than did detoxified LPS. Immune serum restored the ability of detoxified LPS to fix C′3t, but whether this is by the original pathway is not yet clear. We concluded that the loss of certain biological activities and the loss of ability to fix C′3t in normal serum after LPS detoxification involved loss or rearrangement of substrates on LPS which either initiated or supported, or both, its interaction with the complement system. It was apparent that the ability to fix C′ can serve as a valuable in vitro indicator of the integrity of the toxic conformation of biologically active LPS membrane fragments. These experiments supported the hypothesis that certain of the biological activities induced by endotoxins are mediated via the complement system.

Veillonella

Complement fixation test

Detoxification

10.1128/jb.95.2.397-405.1968

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Enhanced Humoral Immunity in Mice Infected with Attenuated Venezuelan Equine Encephalitis Virus

The Journal of Immunology (1969)

R J Howard Charles P. Craig G. S. Treviño Suanne F. Dougherty S. E. Mergenhagen

Abstract Attenuated Venezuelan equine encephalitis virus (VEE) infection increased the antibody response to human γ globulin (HGG) in adult Balb/c mice. Mice infected 1 or 11 days before but not 29 days before immunization with 1 mg HGG showed increased rates of elimination of 131I-HGG and elevated hemagglutination titers to HGG. In addition, VEE infection prevented the induction of tolerance to HGG and converted a tolerance-inducing stimulus into an immunizing stimulus. However, VEE infection did not prolong the survival of skin allografts across weak or strong histocompatibility barriers. Two to 6 days after infection, mice showed increased rates of clearance of colloidal carbon. This may have been related to the proliferation of reticuloendothelial cells, since VEE infection caused a proliferation of these cells in germfree mice. In addition, germfree mice infected with VEE had increased spleen weights, and germinal centers appeared in histologic sections of spleens. Increased γ globulin concentrations were seen in the sera of infected germfree mice, which could be attributed only partially to antivirus antibody. Thus, VEE behaves as an adjuvant for humoral antibody responses.

Hemagglutination assay

10.4049/jimmunol.103.4.699

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Preparation and Biological Activities of Endotoxins from Oral Bacteria

The Journal of Infectious Diseases (1961)

S. E. Mergenhagen Edward G. Hampp Henry W. Scherp

Journal Article Preparation and Biological Activities of Endotoxins from Oral Bacteria Get access Stephan E. Mergenhagen, Stephan E. Mergenhagen From the National Institute of Dental Research, National Institutes of Health, Bethesda 14, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar Edward G. Hampp, Edward G. Hampp From the National Institute of Dental Research, National Institutes of Health, Bethesda 14, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar Henry W. Scherp Henry W. Scherp From the National Institute of Dental Research, National Institutes of Health, Bethesda 14, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar The Journal of Infectious Diseases, Volume 108, Issue 3, May 1961, Pages 304–310, https://doi.org/10.1093/infdis/108.3.304 Published: 01 May 1961 Article history Received: 04 November 1960 Published: 01 May 1961

National library

10.1093/infdis/108.3.304

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LPS REGULATION OF THE IMMUNE RESPONSE: CELLULAR AND MOLECULAR BASIS OF ADJUVANTICITY AND THE ROLE OF SUPPRESSOR T CELLS ON HOST RESPONSES

Elsevier eBooks (1980)

Jerry R. McGhee Suzanne M. Michalek Hiroshi Kiyono Jeremy Farrar David L. Rosenstreich

Heterologous

Splenocyte

10.1016/b978-0-08-024952-0.50036-3

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Macrophage Activation by Mycobacterial Water Soluble Compounds and Synthetic Muramyl Dipeptide

The Journal of Immunology (1979)

Sharon M. Wahl L M Wahl J B McCarthy L Chedid S. E. Mergenhagen

The adjuvant effects of mycobacteria can be replaced by more chemically defined isolates of the cell walls including a water soluble fraction (WSA) and by the synthetic analog N-acetyl-muramyl-L-alanyl-D-isoglutamine (MDP), which is the minimal structure required for adjuvanticity. These compounds can directly activate macrophages as determined by an increase in spreading and adherence and by an elevated synthesis of the enzyme collagenase. Moreover, this increase in collagenase production is modulated by enhanced production of prostaglandins that influences intracellular levels of cyclic AMP. In addition, both MDP and WSA induced macrophages to produce a biologically active mediator that triggers quiescent fibroblasts into active proliferation. It thus appears that a mechanism for mycobacterial adjuvant action as determined with MDP and WSA is via activation of macrophages, which may then precipitate a multiplicity of other reactions resulting in enhanced immune phenomena. Furthermore, the granulomatous and fibrotic reactions associated with mycobacterial infection may be a consequence of this direct activation of macrophages.

Muramyl dipeptide

10.4049/jimmunol.122.6.2226

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The rat mast cell antigen AD1 (homologue to human CD63 or melanoma antigen ME491) is expressed in other cells in culture.

The Journal of Immunology (1992)

H Nishikata C Oliver S. E. Mergenhagen R P Siraganian

Previously we reported that the mAb AD1 recognized a heavily glycosylated 50- to 60-kDa protein (AD1 Ag) sterically close to the high-affinity IgE receptor on rat basophilic leukemia (RBL-2H3) cells. The N-terminal amino acid sequence of the AD1 Ag was nearly identical to that of human CD63 (melanoma-associated Ag ME491). In this study we cloned the cDNA of AD1 Ag from a rat basophilic leukemia 2H3 cDNA library. An open reading frame of 238 amino acids was identified that contained the N-terminal 43 amino acid sequence. No evidence of a signal peptide was found. However, four predominantly hydrophobic stretches of sequence were predicted to form membrane-spanning helices, and three putative N-glycosylation sites were identified. The AD1 Ag and CD63 were highly conserved between rat and human, suggesting that the sequence of this protein is important for its function. By immunostaining various rat tissues, the AD1 Ag was found localized to mast cells. However, it was located to lysosomes, secretory granules and the plasma membrane of RBL-2H3 cells and to lysosomes and plasma membrane of many other cultured cell lines. The AD1 Ag could be induced by placing cells in culture. Fibroblasts and hepatocytes freshly isolated from rat embryos stained very weakly for AD1 Ag; however, after 24 to 48 h in culture they were strongly positive. This increase in the expression of the AD1 Ag was accompanied by an increase in detectable RNA message. Therefore, AD1/ME491/CD63 Ag is a mast cell marker in tissue, but is also associated with other cells in culture.

10.4049/jimmunol.149.3.862

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Citations (47)

Nature and Significance of Somatic Antigens of Oral Bacteria

Journal of Dental Research (1967)

S. E. Mergenhagen

Somatic antigen

10.1177/00220345670460013901

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Citations (40)

VIRUS-MACROPHAGE-LYMPHOCYTE INTERACTIONS

Elsevier eBooks (1977)

Holger Kirchner G. Darai K. Keyssner K. Münk S. E. Mergenhagen

10.1016/b978-0-12-458050-3.50109-0

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Macrophage- and astrocyte-derived transforming growth factor beta as a mediator of central nervous system dysfunction in acquired immune deficiency syndrome.

The Journal of Experimental Medicine (1991)

Sharon M. Wahl J B Allen Nancy McCartney‐Francis Maria Cristina Morganti-Kossmann Thomas Kossmann

The multifunctional cytokine, transforming growth factor beta (TGF-beta), was identified by immunocytochemistry in the brain tissues of four patients with acquired immune deficiency syndrome (AIDS), but not in control brain tissue. The TGF-beta staining was localized to cells of monocytic lineage as well as astrocytes, especially in areas of brain pathology. In addition, the brain tissues from the AIDS patients contained transcripts for human immunodeficiency virus 1 (HIV-1) by in situ hybridization, suggesting a correlation between the presence of HIV-1 in the brain and the expression of TGF-beta. However, the expression of TGF-beta was not limited to HIV-1-positive cells, raising the possibility of alternative mechanisms for the induction of TGF-beta in these AIDS patients' brains. To investigate these mechanisms, purified human monocytes were infected in vitro with HIV-1 and were shown to secrete increased levels of TGF-beta. In addition, HIV-1-infected monocytes released a factor(s) capable of triggering cultured astrocytes that are not infected with HIV-1 to secrete TGF-beta. The release of TGF-beta, which is an extremely potent chemotactic factor, may contribute to the recruitment of HIV-1-infected monocytic cells, enabling viral spread to and within the central nervous system (CNS). Moreover, TGF-beta augments cytokine production, including cytokines known to be neurotoxic. The identification of TGF-beta within the CNS implicates this cytokine in the immunopathologic processes responsible for AIDS-related CNS dysfunction.

TGF beta 1

Monocyte

10.1084/jem.173.4.981

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Citations (296)