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ABSTRACT: To investigate whether tachykinins are released in the airways by stimulating the esophagus, airway plasma extravasation induced by intraesophageal hydrochloric acid (HCl) in the presence or absence of the neutral endopeptidase (NEP) inhibitor phosphoramidon and the neurokinin-1-receptor antagonist FK888 was studied in anesthetized guinea pigs. Airway plasma extravasation also was studied in the presence of the NEP inhibitor in guinea pigs pretreated with capsaicin or bilateral vagotomy. Propranolol and atropine were used in all animals to block adrenergic and cholinergic nerve effects. Airway plasma leakage was evaluated by measuring extravasated Evans blue dye. One normal HCl infusion into the esophagus significantly increased plasma extravasation in the trachea. Phosphoramidon significantly potentiated plasma extravasation induced by HCl infusion into the esophagus in the trachea and main bronchi, and FK888 significantly inhibited extravasation in a dose-related manner. In capsaicin-treated animals, airway plasma extravasation was completely inhibited even in the presence of phosphoramidon. Tracheal plasma extravasation potentiated by phosphoramidon was significantly inhibited in the bilaterally vagotomized animals. These results suggest that locally acting substances are released by intraesophageal HCl stimulation that cause airway plasma extravasation. These substances are generated through activation of neural pathways, including some that traffic through the vagus nerves that link the esophagus or airways.
The American Journal of Medicine 01/2002; 111 Suppl 8A:25S-30S. · 5.43 Impact Factor
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ABSTRACT: To determine prognostic factors of nosocomial pneumonia in general wards, we performed prospective clinical study using multivariate statistical analysis. Eighty patients with nosocomial pneumonia in our units were enrolled in the study between December, 1996 and January 1998. Clinical setting and severity of pneumonia were evaluated, and laboratory data were collected at the occurrence of nosocomial pneumonia. Death due to nosocomial pneumonia occurred in 29 of 80 patients (mortality rate 36%). Univariate analysis showed the following factors associated with mortality: the presence of an ultimately or rapidly fatal underlying condition, prior antibiotics use, use of antacids, presence of 'high-risk' micro-organisms, sepsis, respiratory failure, multiple organ failure, bilateral chest X-ray infiltrates, a Simplified Acute Physiology Score (SAPS) index > or = 11, albumin < 3.0 g dl(-1), and lactate dehydrogenase (LDH) > or = 796 IUI(-1). Furthermore, multivariate analysis identified three factors significantly associated with mortality: the presence of an ultimately or rapidly fatal underlying condition [odds ratio (OR)=7.0; 95% confidence interval (CI)=1.2-41.1; P=0.03]; SAPS index > or = 11 (OR=7.6; 95% CI=1.1-51.9, P=0.04); LDH > or = 796 IUI(-1) (OR=28.2; 95% CI=2.0-406, P=0.01). Our study indicates that host factors and disease severity factors are important prognostic factors of nosocomial pneumonia in general wards.
Respiratory Medicine 01/2002; 96(1):18-23. · 2.47 Impact Factor
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ABSTRACT: The aim of this study was to determine the role of matrix metalloproteinases (MMPs) in the pathogenesis of acute lung injury induced by hyperoxia. Twenty-three pigs were exposed in sealed cages to >80% oxygen (for 24-120 h) or room air. Correlation between MMP-2/MMP-9 activity, measured by gelatin zymography in bronchoalveolar lavage fluid (BALF), and the histological findings and pathological parameters were examined in detail. Sources of these MMPs in the hyperoxic lung were analysed by immunohistochemistry. The histological progression of acute lung injury in this model ranged from the early exudative to the early proliferative phase of diffuse alveolar damage (DAD). MMP-2 and -9 activities were elevated under prolonged hyperoxic exposure. MMP-9 activity correlated significantly with the oxygen tension in arterial blood/inspiratory oxygen fraction, the lung wet-to-dry weight ratio, and the number of neutrophils in BALF, whereas MMP-2 activity did not correlate at all with these factors. MMP-9 activity correlated more closely with the pathological findings of DAD than did MMP-2 activity. Strong MMP-9 expression was observed in neutrophils, alveolar macrophages as well as alveolar lining epithelial cells. These results suggest that matrix metalloproteinase. which may derive from neutrophils recruited into airspaces, plays an important role in the pathogenesis of hyperoxic diffuse alveolar damage
European Respiratory Journal 12/2001; 18(5):827-37. · 5.89 Impact Factor
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S Hirayama,
H Kohrogi,
A Ueda,
C Kiyofuji,
N Hirata,
K Fujii,
E Goto,
K Fujita,
K Tsumori,
S Hirosako,
D Noguchi,
O Kawano, M Ando
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ABSTRACT: Several reports have suggested that the prevalence of asthma in adults is currently increasing. However, recent prevalence of asthma has not reported in Japan, especially in rural-mountain areas. To investigate the prevalence of asthma in adults in Japan, we conducted clinical epidemiological research on 5066 inhabitants of Menda town, in a rural-mountain area of Japan. The study population comprised 98.7% of adults in the town, including senior high school students whose age were more than 15 years old. The prevalence of asthma among adults was 3.6%. The ratio of prevalence in males to prevalence in females was 1.44. Peaks prevalences were observed in the age ranges of 15-19 and > 70 years old in males, and 15-19, 40-49 and > 70 years old in females.
Arerugī = [Allergy] 12/2001; 50(12):1163-70.
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ABSTRACT: We describe a 74-year-old patient with dyspnoea and tachypnoea induced by chlorpromadinone acetate, a synthetic progesterone used to treat prostatic hyperplasia. The dyspnoea, tachypnoea and hypocapnia improved after discontinuing the chlorpromadinone acetate. It is important to recognize that synthetic progesterones can cause dyspnoea and hyperventilation.
Respirology 10/2001; 6(3):265-7. · 2.42 Impact Factor
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ABSTRACT: Cigarette smoking is the primary preventable cause of various diseases and death. Smoking has been causally related to lung cancer, other malignancies, atherosclerosis, coronary heart disease, and chronic obstructive pulmonary disease. There have been few studies, however, of whether the ordinary citizen in Japan understand the risks of serious diseases caused by smoking. Four hundred and thirty six people attended a seminar of respiratory diseases entitled "Cigarette smoking and lung cancer; prevention and treatment of asthma; senile care and prevention of pneumonia". After the seminar, unsigned questionnaires were filled out by 403 of those in attendance. Three hundred eighty nine (165 males and 224 females) respondents correctly answered the questionnaires, and these were analyzed in the study. Attendants comprised 243 who had never smoked (63%), 99 former smokers (25%), and 39 current smokers (10%). Three hundred forty seven attendants (89%) answered that smoking is harmful to the health, and 371 (95%) that it is causally related to lung cancer. In contrast, lower numbers of attendants answered that smoking is causally related to other diseases: pulmonary emphysema, 65% of the responses; chronic bronchitis, 68%; laryngeal cancer, 77%; myocardial infarction, 53%; and atherosclerosis, 49%. Of the 39 current smokers, 27 answered that they would stop smoking after the seminar. Although many people partly understand the risks of smoking, they do not have a clear knowledge of the risks of diseases besides lung cancer. Education about the risks of smoking and about smoking cessation is required.
Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society. 07/2001; 39(6):389-93.
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ABSTRACT: Discoidin domain receptor 1 (DDR1) tyrosine kinases constitute a novel family of receptors characterized by a unique structure in the ectodomain (discoidin-I domain). The DDR1 ligand is the extracellular matrix protein collagen. To identify receptor tyrosine kinases (RTKs) involved in control of growth and differentiation of human bronchial epithelial (HBE) cells, a polymerase chain reaction-based search for RTKs in HBE cells was performed. DDR1 was the most abundant clone identified. Northern analysis detected a 3.6 kb DDR1 messenger ribonucleic acid (mRNA) expressed in HBE cells and transformed HBE lines, BET-1A and BEAS-2B. In addition, fluorescence-activated cell sorter (FACS) analyses using an anti-DDR1 antibody showed that DDR1 was expressed on HBE cells and two HBE lines. Immunohistochemical staining using human bronchial tissue demonstrated that DDR1 was mainly expressed at the basolateral cell surface of the bronchial epithelium. Furthermore, immunostaining of type IV collagen, a major component of the basement membrane, clearly showed that the basement membrane was closely attached to the basal surface of the bronchial epithelium. Since collagen binds to and activates discoidin domain receptor 1 tyrosine kinase, colocalization of discoidin domain receptor 1 and its ligand type IV collagen demonstrates a potential interaction of discoidin domain receptor 1 on the bronchial epithelium with type IV collagen. Further study of this interaction may define the functional significance of the collagen-discoidin domain receptor 1 signalling pathway in health and in disease.
European Respiratory Journal 06/2001; 17(5):969-74. · 5.89 Impact Factor
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ABSTRACT: The inflammatory process in granulomatous disorders such as sarcoidosis is mainly the consequence of delayed hypersensitivity induced by causative antigens. Propionibacterial DNA was isolated recently by PCR from human sarcoidosis tissue. Hence, we developed a model using sensitized rabbits for T cell-mediated pulmonary granulomatosis induced by Propionibacterium acnes (P. acnes) and investigated the role of monocyte chemoattractant protein-1 (MCP-1) in the pathogenesis of the granuloma formation in vivo. Intravenous injection of P. acnes into sensitized rabbits induced massive pulmonary granulomas on day 3. Maximum levels of MCP-1 in sera and bronchoalveolar lavage fluid (BALF) were detected on day 1 and preceded recruitment of monocyte/macrophages and T cells. In BALF, monocyte chemotaxis peaked 1 day after P. acnes challenge, and T cell chemotaxis peaked 3 days after P. acnes challenge. Anti-MCP-1 IgG inhibited monocyte chemotaxis by 80.2% and T cell chemotaxis by 35.7%. Phenotypic analysis of migrating T cells revealed that activated and memory T cells (CD26(+)/CD45RO(+)) but not naive cells were preferentially attracted to BALF. Administration of MCP-1 antiserum in vivo inhibited the development of granulomas in both size 59.9% reduction and number 28.6% reduction, the number of infiltrating leukocytes in BALF, and the expression of adhesion molecules on leukocytes in peripheral blood and BALF. Our data indicate that MCP-1 plays important roles in granuloma formation by attracting and activating specific types of cells in this model. Furthermore, results suggest that the rabbit model resembles human angiocentric granulomatosis and would be useful for investigating the immunopathogenesis of human pulmonary granulomatosis.
Microscopy Research and Technique 06/2001; 53(4):288-97. · 1.79 Impact Factor
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ABSTRACT: The mechanisms underlying the therapeutic efficacy of erythromycin (EM) in diffuse panbronchiolitis (DPB) was investigated. For this purpose, an experimental rabbit model of DPB induced by Pseudomonas aeruginosa inoculation was employed. Daily administration of EM (3 mg x kg x day(-1)) led to an increase in the number of macrophages in bronchoalveolar lavage fluid (BALF) at an early phase, while reducing the size of granulomatous lesions at the late phase without affecting the number of viable bacteria recovered from the infected lung. Reverse transcriptase polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA) and immunohistochemical studies showed that monocyte chemoattractant protein (MCP)-1 was produced in both BALF and infected lung. EM treatment resulted in a significant increase in the level of MCP-1 in BALF, while reducing that of tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta and IL-8. EM also increased MCP-1 messenger ribonucleic acid (mRNA) and protein expression in the infected lung. MCP-1 blockade abolished the protective effect of EM, as neutralization of MCP-1 with anti-MCP-1 antibodies reduced the EM-induced increase in the number of macrophages in BALF, and augmented size of the granulomatous lesions, as compared to control. The results of the present study suggest that erythromycin attenuates the pulmonary granuloma formation, at least in part, by increasing the production of monocyte chemoattractant protein-1.
European Respiratory Journal 04/2001; 17(3):360-7. · 5.89 Impact Factor
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The Japanese journal of antibiotics 03/2001; 54 Suppl A:125-9.
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ABSTRACT: To clarify the pathogenesis of chronic eosinophilic pneumonia (CEP), the apoptosis of eosinophils from bronchoalveolar lavage (BAL-Eos) was compared with that of eosinophils from peripheral blood (PB-Eos) in six cases of CEP. The survival rate of eosinophils and the percentage of apoptotic cells of both types of eosinophils were examined, and the effects of interleukin 5 (IL-5) were evaluated. The role of Fas expression in apoptosis of these eosinophils was also studied. The survival rate of BAL-Eos on the third day of culture was significantly higher than that of PB-Eos (p < 0.01). This was associated with a lower proportion of apoptotic cells in BAL-Eos than in PB-Eos; the percentages of apoptotic cells in PB-Eos and BAL-Eos after 24 h of incubation were 21.7 +/- 3.4% and 10.6 +/- 1.7% respectively. IL-5 suppressed apoptosis and increased the survival rate of both PB-Eos and BAL-Eos. It was found that the apoptotic character of BAL-Eos differed from that of PB-Eos in at least three ways. Firstly, the positive rate of Fas expression on PB-Eos was increased after 24 h of incubation, whereas that on BAL-Eos did not change. Secondly, the expression of Fas on PB-Eos was suppressed by IL-5 (18.5 +/- 4.2% - 8.3 +/- 3.2%, p < 0.05), whereas IL-5 failed to suppress Fas expression on BAL-Eos (3.3 +/- 1.6% - 3.6 +/- 1.0%). Lastly, binding of antibody to Fas antigen induced apoptosis of PB-Eos, but not of BAL-Eos. These data suggested that Fas seemed to be involved in the apoptosis of PB-Eos, whereas BAL-Eos were Fas-resistant in chronic eosinophilic pneumonia. In conclusion, apoptosis of eosinophils might be suppressed by proinflammatory cytokines such as IL-5 leading to their accumulation in the lung. Chronic stimulation of eosinophils in the alveolar space with IL-5 may play a crucial role chronic eosinophilic disorders.
European Respiratory Journal 03/2001; 17(2):190-4. · 5.89 Impact Factor
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ABSTRACT: Destruction of subepithelial basement membrane is a key event in the pathogenesis of idiopathic pulmonary fibrosis (IPF). To evaluate the role of matrix metalloproteinases (MMPs) in parenchymal remodeling in idiopathic interstitial pneumonia (IIP), we studied MMP-2 and -9 activity, in bronchoalveolar lavage fluid (BALF) by zymography and the expression of MMP-2 and -9 and TIMP-2 in lung tissue by immunohistochemistry. BALF and lung tissues were collected from 26 patients with usual interstitial pneumonia (IPF-UIP), 11 with nonspecific interstitial pneumonia (NSIP), and 6 with bronchiolitis obliterans organizing pneumonia (BOOP). IPF-UIP cases showed predominant expression of MMP-9, whereas NSIP and BOOP cases showed predominant MMP-2 expression in BALF and in tissues. In BALF samples from rapidly progressive IPF-UIP cases, neutrophil-derived MMP-9 activity, as well as MMP-9 active form were characteristically detected. Furthermore, the MMP-9 activity correlated significantly with an increase of neutrophils in BALF, whereas the MMP-2 activity associated with NSIP and BOOP correlated with an increase of lymphocytes. These results indicate that MMP-9 in IPF-UIP and MMP-2 in NSIP and BOOP may contribute to pulmonary structural remodeling through type IV collagenolytic activity. The characteristic contributions of matrix-degrading proteins may relate to the distinct prognostic features of these diseases.
American Journal of Respiratory and Critical Care Medicine 12/2000; 162(5):1949-56. · 11.08 Impact Factor
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T Johkoh,
N L Müller,
M Akira,
K Ichikado,
M Suga, M Ando,
T Yoshinaga,
T Kiyama,
N Mihara,
O Honda,
N Tomiyama,
H Nakamura
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ABSTRACT: To determine whether various eosinophilic lung diseases can be differentiated by means of thin-section computed tomography (CT).
Thin-section CT scans in 111 patients with eosinophilic lung diseases-40 with chronic eosinophilic pneumonia, 16 with Churg-Strauss syndrome, 16 with allergic bronchopulmonary aspergillosis (ABPA), 13 with acute eosinophilic pneumonia, 12 with simple pulmonary eosinophilia, 11 with drug-induced eosinophilic pneumonia, and three with hypereosinophilic syndrome-were assessed independently by two observers. The observers recorded the abnormalities, diagnosis, and degree of confidence in the diagnosis.
The two observers made a correct first-choice diagnosis on average in 61% of readings. The correct diagnosis was made in 78% of cases of chronic eosinophilic pneumonia; 81%, acute eosinophilic pneumonia; 44%, Churg-Strauss syndrome; 84%, ABPA; 17%, simple pulmonary eosinophilia; 27%, drug-induced eosinophilic pneumonia; and 33%, hypereosinophilic syndrome. The two observers made a correct diagnosis with a high degree of confidence in 36% of readings. There was moderate agreement between the observers for the correct diagnosis (kappa, 0.47) and for the correct diagnosis with a high degree of confidence (kappa, 0.59).
Although eosinophilic lung diseases often can be differentiated by means of thin-section CT, correlation between CT findings and careful clinical evaluation are required for a definitive diagnosis.
Radiology 10/2000; 216(3):773-80. · 5.73 Impact Factor
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ABSTRACT: The aim of this study was to elucidate the mechanism of anemia associated with autonomic dysfunction in rats. Using 6-hydroxydopamine (6-OHDA)-treated sympathectomized rats, changes in systolic blood pressure, plasma catecholamine levels, hemograms, erythropoietin (EPO) secretion, and beta-adrenergic receptors on erythrocytes were monitored, and compared with desipramine- and 6-OHDA-treated, and control rats. In 6-OHDA-treated rats, systolic blood pressure and plasma catecholamine levels significantly decreased from 7 days after 6-OHDA administration, returning to the control values on day 28. Hemoglobin (Hb), hematocrit (Hct) and red blood cell (RBC) levels significantly decreased from day 14 to day 28, and reached normal values after day 35, but neither corpuscular constants nor white blood cell (WBC) levels changed after anemia occurred. Administration of desipramine 1 day before 6-OHDA injection prevented anemia. EPO levels did not elevate, even after bloodletting to load anemia, and the EPO circadian rhythm was irregular in 6-OHDA-treated rats. beta-adrenergic receptors measured using 125I-cyanopindolol (CYP) significantly decreased from day 7 to day 28, and reached normal values after day 35. These results suggest that irregular EPO secretion via disordered autonomic nerves may induce anemia in patients with autonomic disorders.
Autonomic Neuroscience 09/2000; 82(3):123-9. · 1.86 Impact Factor
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ABSTRACT: We examined endothelium-dependent vasodilatation in 15 familial amyloidotic polyneuropathy (FAP) amyloidogenic transthyretin (ATTR) Valine30Methionine (Val30Met) patients and 12 healthy volunteers. Using ultrasonography, we measured the radial artery diameters under both baseline and hyperemic conditions. Endothelium-dependent vasodilatation was expressed as a percent increase in the diameters of the radial artery after induced hyperemia. Endothelium-dependent vasodilatation tended to decrease in the patients, compared with healthy volunteers. Responses were not elicited at all in patients with disease of more than 9 years' duration. Linear negative correlation was observed between endothelium-dependent vasodilatation and disease duration (P < 0.01). Correlation between endothelium-dependent vasodilatation and degree of autonomic dysfunction was significant (P = 0.0524) and for age was close to significance (P = 0.051). These results suggest that the peripheral vasomotor dysfunction in FAP patients may predominantly depend on the amount of amyloid deposition around the vessels through the course of illness.
Muscle & Nerve 08/2000; 23(7):1084-8. · 2.37 Impact Factor
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ABSTRACT: We recently showed that macrophage-stimulating protein (MSP), a serum protein homologous to hepatocyte growth factor, promotes ciliary motility by activating its receptor, RON, on the airway ciliated epithelium. To investigate the functional involvement of MSP and RON in bronchiectasis, in which mucociliary clearance (MCC) is impaired, first we examined RON expression on the bronchial ciliated epithelium of patients with bronchiectasis. We confirmed RON expression at the apical surface of bronchial ciliated epithelium of patients with bronchiectasis as well as those of normal human bronchus. Next, we examined whether MSP is present in sputum of patients with bronchiectasis and normal control subjects. By Western blotting, we found that half of the MSP in sputum is present as a biologically active alpha/beta chain heterodimer (mature MSP). In addition, we found that the MSP concentrations in sputum were significantly elevated in patients with bronchiectasis (n=8; 16.8+/-3.0 ng ml(-1)) compared with normal controls (n=9; 8.4+/-2.4 ng ml(-1); P<0.05). In contrast, the difference in concentrations of serum MSP (pro-MSP) was not significant between the two groups. These results indicate that (i) MSP is supplied to the airways and converted to a biologically active form, (ii) MSP is increased in patients with bronchiectasis compared with normal controls. Taken together, our findings suggest that increased MSP may be involved in compensation for impaired MCC in bronchiectasis.
Respiratory Medicine 08/2000; 94(8):784-90. · 2.47 Impact Factor
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ABSTRACT: To investigate whether superantigens induce interstitial pneumonia associated with collagen vascular disease (CVD), staphylococcal enterotoxin B (SEB) was intratracheally administered to SCID mice reconstituted with peripheral blood mononuclear cells (PBMCs) from CVD patients that suffered lung complications. Although a slight accumulation of inflammatory cells into the perivascular area was seen in the lungs of SCID mice injected with PBMCs from CVD patients or healthy donors, SEB administration significantly increased the severity of inflammation in the lungs of SCID mice that received CVD patient PBMCs. Furthermore, human leukocytes were detected by immunohistochemistry in the lungs of SCID mice that received SEB after reconstitution with PBMCs from CVD patients but not in other groups of SCID mice. CD45RO(+) memory T cells comprised the majority of infiltrating human leukocytes. These results suggest the possibility that external superantigens may induce the development of interstitial pneumonia in patients that have a genetic background predisposition to autoimmune disease.
Clinical Immunology 08/2000; 96(1):38-43. · 4.05 Impact Factor
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K Ichikado,
M Suga,
Y Gushima,
T Johkoh,
K Iyonaga,
T Yokoyama,
O Honda,
Y Shigeto,
S Tomiguchi,
M Takahashi,
H Itoh,
J Ikezoe,
N L Müller, M Ando
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ABSTRACT: To determine whether lung abnormalities at thin-section computed tomography (CT) in experimental hyperoxic lung injury correlate with the pathologic phases of diffuse alveolar damage (DAD).
Eighteen juvenile pigs were exposed to more than 80% oxygen-for 24, 48, 72, 96, or 120 hours-or room air in sealed cages. Their removed lungs were inflated with air infused through the trachea and examined with thin-section CT. Two independent observers, without knowledge of the exposure times, compared 63 areas selected on the CT scans with the corresponding pathologic and histologic findings, which were evaluated independently by two pathologists.
CT findings correlated well with histologic findings (rho = 0.86, P <.001), which corresponded to the pathologic phases of DAD. All areas of normal CT attenuation, eight of nine spared regions within areas of opacity, and two of 15 areas of ground-glass opacity corresponded to the early exudative pathologic phase of DAD. All areas that showed traction bronchiolectasis at CT corresponded to the early proliferative pathologic phase. There was good observer agreement regarding the interpretation of CT findings (kappa statistic, >0.60) and histologic results (>/=0.70).
Thin-section CT findings reflect the pathologic phases of DAD, although the early exudative phase cannot be specifically depicted by thin-section CT. Traction bronchiolectasis on a CT scan suggests progression to the proliferative phase.
Radiology 08/2000; 216(2):531-8. · 5.73 Impact Factor
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Y Ando,
Y Ohtsu,
H Terazaki,
K Kibayashi,
M Nakamura,
E Ando,
N Matsunaga,
K Obayashi,
M Uchino, M Ando,
S Tsunenari
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ABSTRACT: Twenty-nine-year-old twin brothers having the amyloidogenic transthyretin (ATTR) Val30Met gene developed the clinical symptoms of familial amyloidotic polyneuropathy (FAP) in 1995. The twins had the same educational background and lived in the same district. FAP manifestations were similar in both cases, although electromyographic examinations revealed sensorimotor polyneuropathy in No. 1 and sensory polyneuropathy in No. 2. DNA analysis revealed that they were monozygotic twins. In addition to environmental factors, genetic factors may play an important role in determining the onset of FAP.
Amyloid 07/2000; 7(2):133-6. · 2.66 Impact Factor
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ABSTRACT: We established a T cell line, STO-5, which constitutively produced monocyte/macrophage chemotactic activity via human T cell lymphoma-leukemia-virus-induced transformation of normal human T cells.
We isolated and purified a lactose-binding protein, MCF-pl5-L (MW of about 50 kD, pl of about 5) from a conditioned medium of STO-5. By using highly purified MCF-pl5-L, its biological and physicochemical properties were elucidated in comparison with C5a and MCP-1.
MCF-pl5-L exhibited an evident dose-dependent monocyte chemotactic activity (MCA). MCF-pl5-L had no or little affinity for heparin unlike chemokines such as MCP-1. We further found that MCF-pl5-L exhibited potent chemotactic activity not only for monocytes but also for alveolar macrophages. In contrast, C5a and MCP-1 failed to show evident chemotactic activity for alveolar macrophages though they did show MCA. MCF-pl5-L failed to exhibit evident eosinophil and neutrophil chemotactic activities, indicating its chemotactic activity is selective for monocytes/macrophages. Regarding the biological functions of MCF-pl5-L other than MCA and chemotactic activity for alveolar macrophages, we found that MCF-pl5-L but not C5a and MCP-1 could prolong the life span of alveolar macrophages, probably by inhibiting apoptosis of macrophages, and stimulate the production of TNF-alpha from macrophages.
These results suggest that MCF-pl5-L plays a role as an immune modulator for monocytes/macrophages in the site.
International Archives of Allergy and Immunology 06/2000; 122(1):66-75. · 2.40 Impact Factor
