Delineation of the Role of Platelet-Activating Factor in the Immunoglobulin G2 Antibody Response

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Published inClinical and Diagnostic Laboratory Immunology Vol. 11; no. 4; pp. 720 - 728
Main Authors Al-Darmaki, Salma, Knightshead, Kandi, Ishihara, Yuichi, Best, Al, Schenkein, Harvey A, Tew, John G, Barbour, Suzanne E
Format Journal Article
LanguageEnglish
Published United States American Society for Microbiology 01.07.2004
Subjects
1-Alkyl-2-acetylglycerophosphocholine Esterase - metabolism
1-Alkyl-2-acetylglycerophosphocholine Esterase - pharmacology
Adult
Antibodies and Mediators of Immunity
B-Lymphocytes - immunology
Cytokines - immunology
Dendritic Cells - drug effects
Dendritic Cells - immunology
Humans
Immunoglobulin Class Switching - drug effects
Immunoglobulin Class Switching - immunology
Immunoglobulin G - immunology
In Vitro Techniques
Interferon-gamma - immunology
Interleukin-4 - immunology
Leukocytes - drug effects
Leukocytes - immunology
Lymphocyte Activation
Macrophages - drug effects
Macrophages - immunology
Periodontal Diseases - immunology
Platelet Activating Factor - immunology
Platelet Activating Factor - pharmacology
Reverse Transcriptase Polymerase Chain Reaction
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Abstract Classifications Services CVI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue CVI About CVI Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy CVI RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 1556-6811 Online ISSN: 1556-679X Copyright © 2014 by the American Society for Microbiology.   For an alternate route to CVI .asm.org, visit: CVI       
AbstractList Localized aggressive periodontitis (LAgP) is a chronic inflammatory disease characterized by severe destruction of periodontal tissues surrounding the first molars and incisors. LAgP subjects produce large amounts of immunoglobulin G2 (IgG2) antibody against oral pathogens, and this response is inversely correlated with the severity of disease. We previously demonstrated that platelet-activating factor (PAF) is required for optimal IgG2 responses. The present investigation was designed to determine the mechanism of IgG2 induction by PAF. Exogenous PAF acetylhydrolase suppressed approximately 80% of pokeweed mitogen-stimulated IgG2 production, confirming that PAF is essential for optimal responses. PAF-activated leukocytes produced gamma interferon (IFN- gamma ), a Th1 cytokine that has been associated with IgG2 responses in previous studies. The monocyte-derived cytokines interleukin-12 (IL-12) and IL-18 are upstream of IFN- gamma production, and IgG2 production was suppressed by neutralizing antibodies against these proteins. In addition, PAF induced monocyte-derived dendritic cells (DC) but not macrophages (M phi ) to secrete IL-12 and IL-18. This observation was interesting because monocyte differentiation in LAgP subjects is skewed to the DC phenotype. Although other investigators have implicated IFN- gamma in IgG2 production, its precise role in this response is controversial. Our studies suggest that IFN- gamma induces isotype switching to IgG2 but only in concert with the Th2 cytokine IL-4. Thus, it appears that the unique PAF metabolism of LAgP monocytes or DC promotes Th1 responses that are essential for optimal IgG2 antibody production. As IgG2 antibodies opsonize oral bacteria and promote their clearance and destruction, these alterations in PAF metabolism may be essential for limiting disease severity in LAgP patients.
Classifications Services CVI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue CVI About CVI Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy CVI RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 1556-6811 Online ISSN: 1556-679X Copyright © 2014 by the American Society for Microbiology.   For an alternate route to CVI .asm.org, visit: CVI       
Localized aggressive periodontitis (LAgP) is a chronic inflammatory disease characterized by severe destruction of periodontal tissues surrounding the first molars and incisors. LAgP subjects produce large amounts of immunoglobulin G2 (IgG2) antibody against oral pathogens, and this response is inversely correlated with the severity of disease. We previously demonstrated that platelet-activating factor (PAF) is required for optimal IgG2 responses. The present investigation was designed to determine the mechanism of IgG2 induction by PAF. Exogenous PAF acetylhydrolase suppressed approximately 80% of pokeweed mitogen-stimulated IgG2 production, confirming that PAF is essential for optimal responses. PAF-activated leukocytes produced gamma interferon (IFN-γ), a Th1 cytokine that has been associated with IgG2 responses in previous studies. The monocyte-derived cytokines interleukin-12 (IL-12) and IL-18 are upstream of IFN-γ production, and IgG2 production was suppressed by neutralizing antibodies against these proteins. In addition, PAF induced monocyte-derived dendritic cells (DC) but not macrophages (MΦ) to secrete IL-12 and IL-18. This observation was interesting because monocyte differentiation in LAgP subjects is skewed to the DC phenotype. Although other investigators have implicated IFN-γ in IgG2 production, its precise role in this response is controversial. Our studies suggest that IFN-γ induces isotype switching to IgG2 but only in concert with the Th2 cytokine IL-4. Thus, it appears that the unique PAF metabolism of LAgP monocytes or DC promotes Th1 responses that are essential for optimal IgG2 antibody production. As IgG2 antibodies opsonize oral bacteria and promote their clearance and destruction, these alterations in PAF metabolism may be essential for limiting disease severity in LAgP patients.
ABSTRACT Localized aggressive periodontitis (LAgP) is a chronic inflammatory disease characterized by severe destruction of periodontal tissues surrounding the first molars and incisors. LAgP subjects produce large amounts of immunoglobulin G2 (IgG2) antibody against oral pathogens, and this response is inversely correlated with the severity of disease. We previously demonstrated that platelet-activating factor (PAF) is required for optimal IgG2 responses. The present investigation was designed to determine the mechanism of IgG2 induction by PAF. Exogenous PAF acetylhydrolase suppressed approximately 80% of pokeweed mitogen-stimulated IgG2 production, confirming that PAF is essential for optimal responses. PAF-activated leukocytes produced gamma interferon (IFN-γ), a Th1 cytokine that has been associated with IgG2 responses in previous studies. The monocyte-derived cytokines interleukin-12 (IL-12) and IL-18 are upstream of IFN-γ production, and IgG2 production was suppressed by neutralizing antibodies against these proteins. In addition, PAF induced monocyte-derived dendritic cells (DC) but not macrophages (MΦ) to secrete IL-12 and IL-18. This observation was interesting because monocyte differentiation in LAgP subjects is skewed to the DC phenotype. Although other investigators have implicated IFN-γ in IgG2 production, its precise role in this response is controversial. Our studies suggest that IFN-γ induces isotype switching to IgG2 but only in concert with the Th2 cytokine IL-4. Thus, it appears that the unique PAF metabolism of LAgP monocytes or DC promotes Th1 responses that are essential for optimal IgG2 antibody production. As IgG2 antibodies opsonize oral bacteria and promote their clearance and destruction, these alterations in PAF metabolism may be essential for limiting disease severity in LAgP patients.
Localized aggressive periodontitis (LAgP) is a chronic inflammatory disease characterized by severe destruction of periodontal tissues surrounding the first molars and incisors. LAgP subjects produce large amounts of immunoglobulin G2 (IgG2) antibody against oral pathogens, and this response is inversely correlated with the severity of disease. We previously demonstrated that platelet-activating factor (PAF) is required for optimal IgG2 responses. The present investigation was designed to determine the mechanism of IgG2 induction by PAF. Exogenous PAF acetylhydrolase suppressed approximately 80% of pokeweed mitogen-stimulated IgG2 production, confirming that PAF is essential for optimal responses. PAF-activated leukocytes produced gamma interferon (IFN-gamma), a Th1 cytokine that has been associated with IgG2 responses in previous studies. The monocyte-derived cytokines interleukin-12 (IL-12) and IL-18 are upstream of IFN-gamma production, and IgG2 production was suppressed by neutralizing antibodies against these proteins. In addition, PAF induced monocyte-derived dendritic cells (DC) but not macrophages (MPhi) to secrete IL-12 and IL-18. This observation was interesting because monocyte differentiation in LAgP subjects is skewed to the DC phenotype. Although other investigators have implicated IFN-gamma in IgG2 production, its precise role in this response is controversial. Our studies suggest that IFN-gamma induces isotype switching to IgG2 but only in concert with the Th2 cytokine IL-4. Thus, it appears that the unique PAF metabolism of LAgP monocytes or DC promotes Th1 responses that are essential for optimal IgG2 antibody production. As IgG2 antibodies opsonize oral bacteria and promote their clearance and destruction, these alterations in PAF metabolism may be essential for limiting disease severity in LAgP patients.
Author Yuichi Ishihara
Suzanne E. Barbour
Al Best
John G. Tew
Salma Al-Darmaki
Harvey A. Schenkein
Kandi Knightshead
AuthorAffiliation Clinical Research Center for Periodontal Diseases, Virginia Commonwealth University, Richmond, Virginia
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S.A.-D. and K.K. contributed equally to the work described in this report.
Corresponding author. Present address: Department of Biochemistry, Virginia Commonwealth University, Box 980614, Richmond, VA 23298-0614. Phone: (804) 828-2308. Fax: (804) 828-1473. E-mail: sbarbour@hsc.vcu.edu.
Present address: Department of Periodontology, School of Dentistry, Aichi-Gakuin University, Chikusa-ku, Nagoya 464-8651, Japan.
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Localized aggressive periodontitis (LAgP) is a chronic inflammatory disease characterized by severe destruction of periodontal tissues surrounding the first...
ABSTRACT Localized aggressive periodontitis (LAgP) is a chronic inflammatory disease characterized by severe destruction of periodontal tissues surrounding the...
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StartPage 720
SubjectTerms 1-Alkyl-2-acetylglycerophosphocholine Esterase - metabolism
1-Alkyl-2-acetylglycerophosphocholine Esterase - pharmacology
Adult
Antibodies and Mediators of Immunity
B-Lymphocytes - immunology
Cytokines - immunology
Dendritic Cells - drug effects
Dendritic Cells - immunology
Humans
Immunoglobulin Class Switching - drug effects
Immunoglobulin Class Switching - immunology
Immunoglobulin G - immunology
In Vitro Techniques
Interferon-gamma - immunology
Interleukin-4 - immunology
Leukocytes - drug effects
Leukocytes - immunology
Lymphocyte Activation
Macrophages - drug effects
Macrophages - immunology
Periodontal Diseases - immunology
Platelet Activating Factor - immunology
Platelet Activating Factor - pharmacology
Reverse Transcriptase Polymerase Chain Reaction
Title Delineation of the Role of Platelet-Activating Factor in the Immunoglobulin G2 Antibody Response
URI http://cvi.asm.org/content/11/4/720.abstract
https://www.ncbi.nlm.nih.gov/pubmed/15242947
https://search.proquest.com/docview/17707644
https://search.proquest.com/docview/66687293
https://pubmed.ncbi.nlm.nih.gov/PMC440608
Volume 11
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