Background And Objective: The gingival epithelium provides the first line of defense against colonization by periodontal pathogens, both as a physical barrier and by the production of inducible innate immune mediators such as beta-defensins and pro-inflammatory cytokines. The gram-negative bacterium Aggregatibacter actinomycetemcomitans is implicated in the pathogenesis of localized aggressive periodontitis, although the bacterium is found widely in the healthy population. We hypothesized that gingival epithelial cell-derived innate immune mediators triggered in response to A. actinomycetemcomitans infection may play an important role in increased susceptibility to infection.
Material And Methods: Primary cultures of human gingival epithelial cells were cultured in the presence of A. actinomycetemcomitans. Total mRNA was examined for the presence of innate immune markers using RT-PCR.
Results: We show here that the mRNA levels of human beta-defensin 2 and interleukin-8 are elevated by live cultures of a clinical isolate of A. actinomycetemcomitans in cultured gingival epithelial cells from healthy individuals, but not by A. actinomycetemcomitans lipopolysaccharide. Cells from a patient with localized aggressive periodontitis, however, did not respond to this bacterial stimulation. In contrast, the pro-inflammatory cytokine interleukin-19 was induced in cells from both localized aggressive periodontitis and healthy subjects. Examination of Toll-like receptors and associated adapter molecules indicated lower levels of Toll-like receptor 2 mRNA in the localized aggressive periodontitis patient-derived cells compared with cells from healthy subjects.
Conclusion: These results suggest that a differential expression of innate immune response genes to A. actinomycetemcomitans in the gingival epithelium could be an underlying factor of susceptibility to localized aggressive periodontitis.
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http://dx.doi.org/10.1111/j.1600-0765.2007.00998.x | DOI Listing |
Expert Rev Respir Med
January 2025
School of Medicine and Public Health, University of Wisconsin Madison, Madison, WI, USA.
Introduction: In genetically predisposed individuals, exposure to aeroallergens and infections from RNA viruses shape epithelial barrier function, leading to Allergic Asthma (AA). Here, activated pattern recognition receptors (PRRs) in lower airway sentinel cells signal epithelial injury-repair pathways leading to cell-state changes [epithelial mesenchymal plasticity (EMP)], barrier disruption and sensitization.
Areas Covered: 1.
Endocr Connect
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Y Giwercman, Translational Medicine, Lund University, Malmö, Sweden.
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Agriculture College and Research Institute, Kudumiyanmalai, Pudukottai, Tamil Nadu, India.
Tomato is an important crop worldwide, but groundnut bud necrosis virus (GBNV) often hampers its growth. This study investigates the antiviral potential of bacterial endophytes, including CNEB54, CNEB4, CNEB26, and BAVE5 against GBNV, as well as their ability to enhance immunity and growth in tomato. All four bacterial isolates demonstrated a significant delay in GBNV symptom development 10 days post-inoculation, with disease incidence ranging from 18% to 36% compared to 84% in control.
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State Key Laboratory of Pathogen and Biosecurity, Academy of Military Medical Sciences, Beijing, China.
Emerging tick-borne orthonairovirus infections pose a growing global concern, with limited understanding of the viral ovarian tumor-like cysteine proteases (vOTUs) encoded by novel orthonairoviruses. These vOTUs, a group of deubiquinylases (DUBs), disrupt the innate immune response. Yezo virus (YEZV), a recently discovered pathogenic orthonairovirus, was first reported in Japan in 2021.
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Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, the Thoracic Diseases Research Unit, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
pneumonia (PJP) remains a significant cause of morbidity and mortality during AIDS. In AIDS, the absence of CD4 immunity results in exuberant and often fatal PJP. In addition, organism clearance requires a balanced macrophage response since excessive inflammation promotes lung injury and respiratory failure.
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