Some of the proteins of mycobacteria are preferentially associated with the cell wall and are powerful immunogens, and humoral antibody responses to these mycobacterial antigens may occur in patients with tuberculosis. In this study, Triton X-100 solubilized protein (TSP) antigen was isolated from Mycobacterium tuberculosis H37Rv by overnight shaking with 1% Triton X- 100/PMSF and 10-90% ammonium sulfate precipitation. IgG and IgM antibody levels against TSP, crude protein from the unheated cultrue filtrate (CF#) and 30 kDa antigens were determined in the sera of 80 patients with pulmonary tuberculosis and 99 healthy controls with PPD (+) and (-). High IgG reactivity to TSP and CF antigen was observed in tuberculosis patients. Mean IgG antibody titers against all of three mycobacterial antigens were differed significantly (P<0.01) between patients and controls but IgM showed no difference. By the cut-off value adding 2 standard deviation to the mean absorbance of controls, the sensitivity and specificity of the IgG antibody to TSP antigen were 93.9% and 77.5%. The specificity to TSP antigen was a litttle higher than those obtained by CF and 30 kDa antigen. From the above results, the TSP antigen may be useful for the serodiagnosis of tuberculosis.
Ammonium Sulfate ; Antibody Formation ; Cell Wall ; Humans ; Immunoglobulin G ; Immunoglobulin M ; Mycobacterium tuberculosis* ; Mycobacterium* ; Neptune* ; Octoxynol* ; Sensitivity and Specificity ; Serologic Tests ; Tuberculosis ; Tuberculosis, Pulmonary*

In response to invading pathogens, the body immune system develops an immediate defense mechanism, i.e., innate immune response, which is detected in almost all living organisms including mammals, plants, insects, etc. Recent studies have identified numerous innate immune receptors that are able to recognize pathogen-associated molecular patterns and transduce the essential intracellular signaling cascades to mount early and successful host defenses against infectious challenge. Among innate immune receptors, we will focus on two important receptors, toll-like receptors (TLRs) and nucleotide binding oligomerization domain (Nod)-like receptors, and their major intracellular signaling pathways that culminate to activate innate immune effectors and inflammatory mediators during pathogen infection. In this review, we address the recent advances of understanding intracellular signaling mechanisms by which TLRs and NLRs activate host immune defense and inflammation. The role and regulatory mechanisms by which a subet of NLRs-associated inflammasome activation induce interleukin-1beta secretion and their relevance with host defense will be also discussed. Both TLR- and NLR-mediated intracellular signaling networks serve crucial roles in mounting resistance to bacterial and viral infection through synthesis of immune mediators and antimicrobial chemicals during infection.
Immune System ; Immunity, Innate ; Inflammation ; Insects ; Interleukin-1beta ; Mammals ; Toll-Like Receptors*

Primary amenorrhea due to intrasella arachnoid cyst is a very rare disease and require careful and frequent evaluation because may produce intracranial hemorrhage, elevated intracranial pressure and rapid expansion. Surgical intervention is needed only when visual disturbance, hypopituitarism or enlarging lesion is shown. Thus, we present a case of primary amenorrhea due to intrasella arachnoid cyst which was resected through the transsphenoidal approach.
Amenorrhea ; Arachnoid* ; Female ; Hypogonadism* ; Hypopituitarism ; Intracranial Hemorrhages ; Intracranial Hypertension ; Rare Diseases

The nuclear receptor superfamily consists of the steroid and non-steroid hormone receptors and the orphan nuclear receptors. Small heterodimer partner (SHP) is an orphan family nuclear receptor that plays an essential role in the regulation of glucose and cholesterol metabolism. Recent studies reported a previously unidentified role for SHP in the regulation of innate immunity and inflammation. The innate immune system has a critical function in the initial response against a variety of microbial and danger signals. Activation of the innate immune response results in the induction of inflammatory cytokines and chemokines to promote anti-microbial effects. An excessive or uncontrolled inflammatory response is potentially harmful to the host, and can cause tissue damage or pathological threat. Therefore, the innate immune response should be tightly regulated to enhance host defense while preventing unwanted immune pathologic responses. In this review, we discuss recent studies showing that SHP is involved in the negative regulation of toll-like receptor-induced and NLRP3 (NACHT, LRR and PYD domains-containing protein 3)-mediated inflammatory responses in innate immune cells. Understanding the function of SHP in innate immune cells will allow us to prevent or modulate acute and chronic inflammation processes in cases where dysregulated innate immune activation results in damage to normal tissues.
Chemokines ; Child ; Child, Orphaned ; Cholesterol ; Cytokines ; Glucose ; Humans ; Immune System ; Immunity, Innate ; Inflammasomes ; Inflammation ; Metabolism ; Orphan Nuclear Receptors ; Social Control, Formal ; Toll-Like Receptors

No abstract available.
Humans ; Korea ; Quality-Adjusted Life Years ; Stroke

Mycobacteroides abscessus (previously Mycobacteroides abscessus; Mabc), one of rapidly growing nontuberculous mycobacteria (NTM), is an important pathogen of NTM pulmonary diseases (NTM-PDs) in both immunocompetent and immunocompromised individuals. Mabc infection is chronic and often challenging to treat due to drug resistance, motivating the development of new therapeutics. Despite this, there is a lack of understanding of the relationship between Mabc and the immune system. This review highlights recent progress in the molecular architecture of Mabc and host interactions. We discuss several microbial components that take advantage of host immune defenses, host defense pathways that can overcome Mabc pathogenesis, and how host-pathogen interactions determine the outcomes of Mabc infection. Understanding the molecular mechanisms underlying host-pathogen interactions during Mabc infection will enable the identification of biomarkers and/or drugs to control immune pathogenesis and protect against NTM infection.

Mycobacterium tuberculosis (Mtb) is an etiologic pathogen of human tuberculosis (TB), a serious infectious disease with high morbidity and mortality. In addition, the threat of drug resistance in anti-TB therapy is of global concern. Despite this, it remains urgent to research for understanding the molecular nature of dynamic interactions between host and pathogens during TB infection. While Mtb evasion from phagolysosomal acidification is a well-known virulence mechanism, the molecular events to promote intracellular parasitism remains elusive. To combat intracellular Mtb infection, several defensive processes, including autophagy and apoptosis, are activated. In addition, Mtb-ingested phagocytes trigger inflammation, and undergo necrotic cell death, potentially harmful responses in case of uncontrolled pathological condition. In this review, we focus on Mtb evasion from phagosomal acidification, and Mtb interaction with host autophagy, apoptosis, and necrosis.Elucidation of the molecular dialogue will shed light on Mtb pathogenesis, host defense, and development of new paradigms of therapeutics.

OBJECTIVE: To determine the effect of the addition of Vit. D3 (1,25-Dihydroxychole calciferol D3) to the conventional postmenopausal hormone replacement therapy on bone mineral density(BMD) DESIGN: A 2-year retrospective , randomized study Setting : Department of Obstetrics and Gynecology of Catholic university hospital Patients : 388 postmenopausal women were recruited and divided into 5 groups according to treatment regimen; A: conjugated estrogens only treated group(n=146), B : conjugated estrogens and progesterone treated group(n=103), C : conjugated estrogens and Vit.D3 treated group (n=36), D : conjugated estrogens, progesterone and Vit.D3 treated group (n=41), E : control group (n=60). METHODS: The bone mineral density of the lumbar spines and femoral neck were determined by dual-energy X-ray absorptiometry(DEXA) every 2 years. STATISTICS: The difference between before and after treatment was determined by paired t-test. The comparison among the groups were determined by one way ANOVA test and student's t-test. RESULTS: The addition of progesterone to estrogen showed insignificant increase in the lumbar and femoral neck BMD. The addition of Vit. D3 compared with conventional hormone replacement therapy insignificantly influened bone density in women with initially normal BMD, but definitely increase in women with initially osteopenic and osteoporotic BMD of femoral neck rather than lumar spine(p<0.05). CONCLUSIONS: The use of Vit. D3 combined with postmenopausal estrogen replacement effects the increase of BMD in low bone density than normal bone density, especially femoral neck.
Bone Density* ; Estrogen Replacement Therapy ; Estrogens ; Estrogens, Conjugated (USP) ; Female ; Femur Neck ; Gynecology ; Hormone Replacement Therapy ; Humans ; Obstetrics ; Progesterone ; Retrospective Studies ; Spine ; Vitamins*

Mitochondria are key organelles involved in energy production, functioning as the metabolic hubs of cells. Recent findings emphasize the emerging role of the mitochondrion as a key intracellular signaling platform regulating innate immune and inflammatory responses. Several mitochondrial proteins and mitochondrial reactive oxygen species have emerged as central players orchestrating the innate immune responses to pathogens and damaging ligands. This review explores our current understanding of the roles played by mitochondria in regulation of innate immunity and inflammatory responses. Recent advances in our understanding of the relationship between autophagy, mitochondria, and inflammasome activation are also briefly discussed. A comprehensive understanding of mitochondrial role in toll-like receptor-mediated innate immune responses and NLRP3 inflammasome complex activation, will facilitate development of novel therapeutics to treat various infectious, inflammatory, and autoimmune disorders.
Autophagy ; Immunity, Innate* ; Inflammasomes ; Inflammation* ; Ligands ; Mitochondria ; Mitochondrial Proteins ; Organelles ; Reactive Oxygen Species

OBJECTIVE : We investigated the relationship between the severity of the disease and the abnormality of some ocular movements in parkinson's disease. BACKGROUND: Disorders of eye movements have been described in diseases of the basal ganglia for over a century and ocular motor deficits of the saccadic and pursuit system have been reported in parkinsonian patients. METHOD : We studied the electro-oculography of the eye tracking and saccadic movement in 26 patients (11 males, 15 females) with Parkinson's disease. The severity of the disease was divided into two groups by Hoehn & Yahr(H-Y) staging, H-Y stage 1, 2(group A) and H-Y stage 3, 4 (Group B). Some patients antiparkinsonian drugs of L-dopa, dopamine agonist and anticholinergics. RESULT : The velocity of smooth pursuit and the velocity and latency of saccade were calculated and compared between two groups. Eye tracking test revealed decreased pursuit velocity leading to catch-up saccades, but normal phase relationship between eye and target movement, while saccadic eye movement had increased latency. These results showed more profound severity in more advanced stages of the disease. CONCLUSION : We suggest that ocular movement be often chosen as a simple but relevant example of general motor function, as well as criteria for staging of Parkinson's disease and basal ganglia play significant role in ocular movement.
Basal Ganglia ; Cholinergic Antagonists ; Dopamine Agonists ; Eye Movements ; Humans ; Levodopa ; Male ; Parkinson Disease* ; Pursuit, Smooth ; Saccades