Document Detail


Reduced expression of gamma interferon in serum and marked lymphoid depletion induced by Porphyromonas gingivalis increase murine morbidity and mortality due to cytomegalovirus infection.
MedLine Citation:
PMID:  15385479     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Porphyromonas gingivalis, a gram-negative anaerobe, is a major etiological agent of severe forms of periodontal disease. Although periodontal disease is considered a localized disease, accumulating evidence indicates that it may lead to a predisposition to a decline in immunocompetence. Human cytomegalovirus (CMV) commonly infects all human populations without producing significant clinical symptoms. Immunocompromised patients usually develop a primary or reactivated CMV infection, which is associated with high rates of morbidity and mortality. The aim of this study was to determine whether P. gingivalis increases animal susceptibility to CMV infection. Mice were inoculated with CMV and infected locally with P. gingivalis 3 days after the virus inoculation. Mortality rates were monitored, and traces of viral DNA and bacterial infection were detected systemically by using real-time PCR. Local and systemic cytokine secretion was measured, and histological sections were used to assess the pathological state of infected organs. P. gingivalis- and CMV-coinfected mice showed dramatically higher mortality rates than mice infected with P. gingivalis or CMV only. Although the organs of coinfected mice exhibited decreased viral titers, distinct necrosis and tissue damage were more evident in the livers and spleens of these mice than in those of mice infected with CMV only. Furthermore, systemic gamma interferon levels were decreased in coinfected mice, and marked lymphoid depletion was observed in their necrotic organs. In parallel control Escherichia coli-CMV coinfection experiments, the mortality and pathological results were the same as those found in mice infected with CMV only. Our results suggest a specific influence of P. gingivalis on the mouse immune response, causing increased susceptibility to CMV infection.
Authors:
Jacob Stern; Ela Shai; Batia Zaks; Amal Halabi; Yael Houri-Haddad; Lior Shapira; Aaron Palmon
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Infection and immunity     Volume:  72     ISSN:  0019-9567     ISO Abbreviation:  Infect. Immun.     Publication Date:  2004 Oct 
Date Detail:
Created Date:  2004-09-23     Completed Date:  2004-10-25     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  0246127     Medline TA:  Infect Immun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  5791-8     Citation Subset:  IM    
Affiliation:
Institute of Dental Sciences, Faculty of Dental Medicine, Hebrew University-Hadassah, Jerusalem, Israel.
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MeSH Terms
Descriptor/Qualifier:
Animals
Bacteroidaceae Infections / complications*,  immunology,  microbiology,  pathology
Cytokines / immunology,  secretion
Cytomegalovirus Infections / complications*,  immunology*,  pathology,  virology
DNA, Viral / analysis
Immunity, Cellular / immunology
Interferon-gamma / blood*,  immunology,  secretion
Liver / microbiology,  pathology,  virology
Lymphocytes / immunology*,  pathology*
Mice
Mice, Inbred BALB C
Muromegalovirus / genetics,  immunology
Porphyromonas gingivalis / genetics,  immunology,  isolation & purification,  physiology*
Spleen / microbiology,  pathology,  virology
Superinfection / complications,  immunology,  microbiology,  virology
Survival Rate
Viral Load
Chemical
Reg. No./Substance:
0/Cytokines; 0/DNA, Viral; 82115-62-6/Interferon-gamma
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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