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Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
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Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...
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Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal...
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Increased beta 2 defensin in recurrent aphthous ulcer.

A Al-Samadi1, A Salem, M Ainola

  • 1Department of Medicine, Institute of Clinical Medicine, University of Helsinki, Helsinki, Finland; Department of Anatomy, Institute of Biomedicine, University of Helsinki, Helsinki, Finland.

Oral Diseases
|May 24, 2014
PubMed
Summary

Beta 2 defensin (BD-2) is increased in recurrent aphthous ulceration (RAU) lesions, likely driven by TNF-α and IL-17C, to enhance antimicrobial defense, independent of oxidative stress.

Keywords:
IL-17CTNF-αbeta 2 defensinoxidative stressrecurrent aphthous ulcer

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Area of Science:

  • Immunology
  • Oral Medicine
  • Microbiology

Background:

  • Recurrent aphthous ulceration (RAU) is a common oral mucosal inflammatory condition.
  • The role of antimicrobial peptides like beta 2 defensin (BD-2) in RAU pathogenesis is not fully understood.
  • Host defense mechanisms in RAU require further elucidation.

Purpose of the Study:

  • To investigate the expression of BD-2 in RAU lesions compared to healthy controls.
  • To explore the cellular sources and regulatory factors of BD-2 in RAU.
  • To determine the influence of oxidative stress on BD-2 expression.

Main Methods:

  • Quantitative real-time PCR and immunostaining were used to analyze BD-2 expression in RAU and control mucosa.
  • Immunohistochemistry identified BD-2 positive cells (macrophages, mast cells, leukocytes).
  • In vitro studies examined the effect of tumor necrosis factor-α (TNF-α) and interleukin-17C (IL-17C) on BD-2 expression in epithelial cells.

Main Results:

  • BD-2 mRNA levels did not differ, but BD-2 protein staining was significantly higher in acute-phase RAU epithelium.
  • In RAU lesions, infiltrating leukocytes were predominantly BD-2 positive.
  • TNF-α and IL-17C synergistically upregulated BD-2 expression in epithelial cells; vitamin K3-induced reactive oxygen species did not affect BD-2.

Conclusions:

  • Antimicrobial BD-2 is significantly upregulated in epithelial and immigrant cells during acute-phase RAU.
  • This upregulation is likely mediated, in part, by synergistic effects of TNF-α and IL-17C.
  • BD-2 expression in RAU is not influenced by oxidative stress.