OBJECTIVE: A defense mechanism is an automatic psychological process necessary for successful adaptation. It reflects adaptive capacity. The purpose of this study is to explore the relationship between the adaptation ability of individuals who face mandatory military service and the pattern of defense mechanisms. METHODS: The subjects were 69 men (21.4±2.2 years) who expressed psychological difficulties in three military service situations. Control group was 36 men (24.0±1.4 years) who had successfully completed military service. We examined psychiatric history, the pattern of defense mechanisms, and depression and anxiety levels. Defense mechanisms were compared between two groups. RESULTS: The maladjusted group used immature defenses more frequently than the control group did. There were no differences in the defense patterns according to diagnosis. The control group used more identification and rationalization, classified as immature defenses. The temporarily maladjusted group used more somatization, regression, and avoidance. CONCLUSION: Using mature defense mechanisms helped young adults to adapt to a particular situation. The maturity of the defense is more valuable than the psychiatric diagnosis. Some immature defenses are also helpful to adapt. We cautiously assume that some defenses can be protective or risk factors in adapting to stressful situations by young adults.
Anxiety ; Defense Mechanisms ; Depression ; Diagnosis ; Humans ; Korea ; Male ; Mental Disorders ; Military Personnel ; Rationalization ; Risk Factors ; Social Adjustment ; Young Adult

Interferon-gamma (IFNG) is a pleiotropic cytokine that modulates both innate and adaptive immune networks; it is the most potent activator of macrophages and a signature cytokine of activated T lymphocytes. Though IFNG is now appreciated to have a multitude of roles in immune modulation and broad-spectrum pathogen defense, it was originally discovered, and named, as a secretory factor that interferes with viral replication. In contrast to the prototypical type I interferons produced by any cells upon viral infection, only specific subsets of immune cells can produce IFNG upon infection or stimulation with antigen or mitogen. Still, virtually all cells can respond to both types of interferons. This makes IFNG a versatile anti-microbial cytokine and also gives it a unique position in the antiviral defense system. The goal of this review is to highlight the direct antiviral mechanisms of IFNG, thereby clarifying its antiviral function in the effective control of viral infections.
Antiviral Agents ; Defense Mechanisms ; Interferon Type I ; Interferon-gamma* ; Interferons ; Macrophages ; T-Lymphocytes

The concept of bipolar spectrum disorder (BSD) has developed to include affective temperaments such as cyclothymia and hyperthymia. This has greatly helped clinicians to differentiate depressed patients, who would potentially benefit from mood stabilizing treatment, from those with unipolar depression. Cyclothymia, however, has significant similarities with personality disorders, especially with borderline personality disorder (BPD). All the diagnostic items for BPD are frequently found in patients with BSD as well, which presents diagnostic challenges. There are no clear guidelines on how to differentiate BSD from BPD. Featuring borderline pathology for clinical purposes, it may be useful to rely on psychodynamic approaches to identify primitive defense mechanisms of splitting and projective identification suggesting borderline personality organization. Based on new findings on common features between BSD and BPD, some authors have proposed a renewal of the classification system of mental disorders. The dichotomy of bipolar and unipolar depression has gestated a new concept of BSD. Currently, the BSD concept forced us to formulate the border of BSD and personality disorders.
Bipolar Disorder* ; Borderline Personality Disorder ; Classification ; Defense Mechanisms ; Depressive Disorder ; Humans ; Mental Disorders ; Pathology ; Personality Disorders* ; Temperament

Periodontal diseases occur from the interplay between increased bacterial response and the response of the host immune system over time. Anxiety and depression can impair immunological defense mechanisms, causing accumulation of periodontopathogens and thus exacerbating periodontal disease. We investigated the relationship of anxiety and depression to periodontal diseases in Korean women. In this study, 3,551 women aged ≥19 years were evaluated based on data from the first year (2010) of the Fifth Korea National Health and Nutrition Examination Survey. The analysis of the factors that caused periodontal diseases revealed that dental floss or interdental toothbrush nonuse behaviors have been shown to increase the risk of periodontal disease (odds ratio [OR], 1.49; 95% confidence interval [CI], 1.14~1.95). After adjusting for conditions such as age, marital status, income, educational level, economic activity, diabetes mellitus, smoking, drinking, and frequencies of toothbrushing and interdental cleaning, we found that anxiety and depression increased the risk of developing periodontal diseases (OR, 1.47; 95% CI, 1.04~2.09). People with anxiety and depression have a higher prevalence of periodontal diseases than people without anxiety and depression. Thus, periodic periodontal care and effective self-care education are needed to manage periodontal diseases.
Anxiety* ; Defense Mechanisms ; Dental Devices, Home Care ; Depression* ; Diabetes Mellitus ; Drinking ; Education ; Female ; Humans ; Immune System ; Korea ; Marital Status ; Morinda ; Nutrition Surveys ; Oral Health ; Periodontal Diseases* ; Prevalence ; Self Care ; Smoke ; Smoking ; Toothbrushing

The gut epithelial barrier, which is composed of the mucosal layer and the intestinal epithelium, has multiple defense mechanisms and interconnected regulatory mechanisms against enteric microbial pathogens. However, many bacterial pathogens have highly evolved infectious stratagems that manipulate mucin production, epithelial cell-cell junctions, cell death, and cell turnover to promote their replication and pathogenicity in the gut epithelial barrier. In this review, we focus on current knowledge about how bacterial pathogens regulate mucin levels to circumvent the epithelial mucus barrier and target cell-cell junctions to invade deeper tissues and increase their colonization. We also describe how bacterial pathogens manipulate various modes of epithelial cell death to facilitate bacterial dissemination and virulence effects. Finally, we discuss recent investigating how bacterial pathogens regulate epithelial cell turnover and intestinal stem cell populations to modulate intestinal epithelium homeostasis.
Colon ; Defense Mechanisms ; Epithelial Cells ; Homeostasis ; Intercellular Junctions ; Intestinal Mucosa ; Mucins ; Mucus ; Stem Cells ; Tight Junctions ; Virulence

Researches on microbiota in the stomach have entered a revolutionary period in recent years due to the advanced technology that can detect culture-independent gastric microfloras. In spite of its harsh environment, stomach plays a role as an ecosystem for some microbiota. Their composition and number of colony forming units are influenced by several innate defense mechanisms such as low gastric pH, gastric mucus layer, migrating motor complex and some external factors such as gastric acid lowering medications and diet patterns. Here, we review the literatures concerning factors that influence the gastric microbiota.We believe this will be helpful for understanding the role of microbiota in the stomach.
Defense Mechanisms ; Diet ; Ecosystem ; Gastric Acid ; Gastric Juice ; Hydrogen-Ion Concentration ; Microbiota* ; Mucus ; Myoelectric Complex, Migrating ; Proton Pump Inhibitors ; Stem Cells ; Stomach

Prolonged alcohol consumption causes alcoholic liver damage due to the generation of reactive oxygen species, the accumulation of fatty acids, and an increase in inflammatory cytokines in the liver. In this study, the protective effect of a fruit extract of Paeonia anomala (FEPA) against chronic alcohol-induced liver damage was evaluated in Sprague-Dawley rats fed an ethanol or a control Lieber-DeCarli diet for 5 weeks to induce alcoholic liver damage. FEPA (50, 25, and 10 mg/kg body weight/day) as well as the reference control silymarin (25 mg/kg body weight/day) were administered along with the ethanol diet. FEPA protected against increases in alanine aminotransferase and aspartate aminotransferase in serum and attenuated alcohol-induced increases in triglycerides, tumor necrosis factor alpha, thiobarbituric acid-reactive substances, and cytochrome P450 2E1 enzyme activity in the liver compared with the group treated with ethanol only. Anti-oxidative defenses such as the total glutathione level and glutathione peroxidase activity were increased by FEPA treatment. These results suggest that FEPA exerts protective effects against chronic alcohol-induced liver damage by attenuating hepatosteatosis and pro-inflammatory cytokine production and enhancing anti-oxidative defense mechanisms in the liver.
Alanine Transaminase ; Alcohol Drinking ; Alcoholics ; Animals ; Aspartate Aminotransferases ; Cytochrome P-450 CYP2E1 ; Cytokines ; Defense Mechanisms ; Diet ; Ethanol ; Fatty Acids ; Fruit* ; Glutathione ; Glutathione Peroxidase ; Humans ; Liver* ; Paeonia* ; Rats* ; Rats, Sprague-Dawley ; Reactive Oxygen Species ; Silymarin ; Triglycerides ; Tumor Necrosis Factor-alpha

Human mast cells are potent effector cells in host defense mechanisms of innate and acquired immunity, including inflammatory diseases such as asthma and atherosclerosis. Mast cells originate from pluripotent hematopoietic progenitors in the bone marrow. Activation of mast cells by different stimuli triggers the release of a large range of mediators, including de novo synthesized eicosanoids which are highly biologically active lipid mediators. For the generation of lipid mediators, cytoplasmic lipid droplets have been shown to function as a major intracellular pool of arachidonic acid, the precursor for eicosanoids biosynthesis. The article summarizes current knowledge on mast cell biosynthesis of lipid mediator and the role in inflammation.
Adaptive Immunity ; Arachidonic Acid ; Asthma ; Atherosclerosis ; Bone Marrow ; Cytoplasm ; Defense Mechanisms ; Eicosanoids ; Humans ; Inflammation ; Mast Cells*

OBJECTIVE: The imbalance between pro-inflammatory and anti-inflammatory cytokines may underlie different pain states. Although ascorbic acid is the most important physiological antioxidant that affects host defense mechanisms and immune homeostasis, there is limited information on the effects of ascorbic acid on the production of cytokines. METHODS: In this study, we investigated the in vitro effect of L-ascorbic acid (AA) on the production of pro-inflammatory and anti-inflammatory cytokines by stimulating C57BL/6 mouse splenocytes with the polyclonal activators lipopolysaccharide or concanavalin A. RESULTS: AA significantly downregulated the expression of IL-6, IL-12, and TNF-alpha at 48 h and 72 h in mouse splenocytes treated with a combination of polyclonal activators and AA. AA treatment also resulted in upregulation of IL-4 and IL-10 at 72 h. These findings demonstrated that AA significantly potentiated production of anti-inflammatory cytokines whereas there was an inverse association between AA and expression of pro-inflammatory cytokines in mouse splenocytes. CONCLUSION: AA may have potential applications in the reduction of inflammatory pain because of its function in modulating the production of cytokines. However, further in vivo investigations are necessary to elucidate the mechanisms involved.
Animals ; Ascorbic Acid* ; Concanavalin A ; Cytokines* ; Defense Mechanisms ; Homeostasis ; Interleukin-10 ; Interleukin-12 ; Interleukin-4 ; Interleukin-6 ; Interleukins ; Mice* ; Tumor Necrosis Factor-alpha ; Up-Regulation

BACKGROUND: Reactive oxygen species (ROS) play an important role in the induction of apoptosis under pathological conditions. Recently, a significant increase in ROS production and disrupted apoptosis mechanisms in keloids have been reported. Nuclear factor erythroid 2-related factor 2 (Nrf2) represents one of the most important cellular defense mechanisms against oxidative stress and is implicated in the regulation of apoptosis. Recently, it has been reported that Nrf2 upregulates Bcl-2, an anti-apoptotic protein. OBJECTIVE: To compare Nrf2 protein expression in normal skin tissues to keloid tissues. METHODS: ROS generation in keloid tissues was evaluated with OxyBlot analysis. Western blotting and/or immunohistochemical staining approaches were used to study expression of Nrf2 or Bcl-2 in keloid and normal skin tissues. Cellular fractionation was performed to examine subcellular distribution of Nrf2. Transfection of fibroblasts with Nrf2-specific small interfering RNA (siRNA) was conducted to understand the relationship between Nrf2 expression and apoptosis induction. RESULTS: Protein oxidation, a marker of oxidative stress, is increased in keloid tissues. Western blot analysis clearly showed that Nrf2 and Bcl-2 are downregulated in keloid tissues. Immunohistochemical staining of Nrf2 confirmed the results of the western blot analysis. Transfection of fibroblasts with the Nrf2-specific siRNA results in increased apoptosis and decreased cell viability. CONCLUSION: Collectively, our data indicate that Nrf2 expression is downregulated in keloid tissues, and that Nrf2 is involved in the development of apoptosis in Nrf2 siRNA-transfected fibroblasts. We propose that a defective antioxidant system and apoptotic dysregulation may participate in keloid pathogenesis.
Apoptosis ; Blotting, Western ; Cell Survival ; Defense Mechanisms ; Fibroblasts ; Keloid* ; NF-E2-Related Factor 2 ; Oxidative Stress ; Reactive Oxygen Species ; RNA, Small Interfering ; Skin* ; Transfection