ABSTRACT
BACKGROUND: Bronchial asthma is a clinical syndrome characterized by reversibility of airway obstruction. However, many asthmatics have evidence of residual airway obstruction. It has become evident that the repair of the chronic inflammatory process can lead to various irreversible changes. It is generally accepted that the most common cause for the change is cigarette smoking but it is controversial whether asthma progresses to emphysema. High resolution computed tomography (HRCT) is more sensitive and more accurate than chest plain films in determining the type and extent of emphysema. This study was carried out to determine whether asthma can be a cause of emphysema without the effect of cigarette smoking and to evaluate clinical characteristics in asthmatics with emphysema. METHODS: We studied 58 asthmatic patients with reversible airway obstruction and evaluated the presence of emphysema using HRCT and pulmonary function test. According to HRCT findings, they were divided into 2 groups : Asthmatics with emphysema and the ones without emphysema. REWSULTS: Of the 58 patients, 7 were revealed to have emphysema. (1) 6 asthmatics with emphysema were smokers, but one patient was a nonsmoker. (2) Highly significant differences between asthmatics with and without emphysema were found in cigarette smoking (p< 0.01) and smoking consumption (p< 0.01). (3) There were no significant differences in the duration of asthma, age or sex between patients with and without emphysema. (4) There were no significant differences in FEV1(%), FEV1/FVC (%), diffusing capacity for carbon monoxide (DLco) (%) and DLco/alveolar volume between patients with and without emphysema (5) Differences between asthma patients without emphysema and those with emphysema were found to be significant in bronchial wall thickeness (p< 0.05) and in total Ig E levels (p=0.07). CONCLUSION: These results indicate that smoking is a main factor in causing emphysema in asthmatics.
Subject(s)
Adolescent , Adult , Aged , Female , Humans , Male , Asthma/complications , Comparative Study , Middle Aged , Pulmonary Emphysema/etiology , Respiratory Function Tests/statistics & numerical data , Smoking/adverse effects , Tomography, X-Ray Computed/methodsABSTRACT
No abstract available.
Subject(s)
Animals , Mice , Capsaicin , Colon , Cytokines , Lung , Melanoma, Experimental , RNA, MessengerABSTRACT
Vibrio vulnificus, a halophilic vibrio is an estuarine gram-negative bacteria that is associated with severe and frequently fatal wound infections and life-threatening septicemia. Bacteriocins are defined as antibacterial substance produced by various species of bacteria which are usually active against closely related organisms. Bacteriocins have found widespread application in epidemiological studies as specific markers of bacteria. It was proposed by Ha et al. (1990. J. Korean. Soc. Microbiol. 25: 586.) to give the bacteriocins produced by V. vulnificus the name "vulnificins". In the present study, a total of 72 strains of V. vulnificus isolated from patients and oysters were subjected to screen potential producers and indicators of vulnificin, applying ultraviolet induction method. Sensitivity of several strains of Serratia marcesans, Pseudomonas aeruginosa, Shigella flexneri, Salmonella typhi and Yersinia enterocolitica to vulnificins were also examined out. All the tested strains of V. vulnificus produced vulnificins active against indicator strains with various different inhibitory patterns. The spectrum of vulnificin activity and sensitive spectrum of indicator strains were considerably broad. Interestingly, almost all strains of S. marcescens, P. aeruginosa, Salmonella sp., Shigella sp. and Y. enterocolitica tested were sensitive to 1-7 vulnificin(s). Taken together, the present study demonstrated that all of the isolates of V. vulnificus produced vulnificins and that 8 good vulnificin producers and 10 good indicators were detected. These strains can be employed efficiently for establishing vulnificin typing scheme of V. vulnificus and for the detection of bacteriocinogeny and sensitivity in V. vulnificus. Biological role of vulnificin remains to be further elucidated.
Subject(s)
Humans , Bacteria , Bacteriocins , Gram-Negative Bacteria , Ostreidae , Pseudomonas aeruginosa , Salmonella , Salmonella typhi , Sepsis , Serratia , Shigella , Shigella flexneri , Vibrio vulnificus , Vibrio , Wound Infection , Yersinia enterocoliticaABSTRACT
Capsaicin, the pungent principle of hot peppers, is a neurotoxin that depletes unmyelinated primary sensory neurons (polymodal nociceptors) of neuropeptides like tachykinins. However, the role of capsaicin-sensitive sensory nerve in the production of cytokines, penicillin V (PEV)-induced active fatal anaphylaxis and other immune responses is not yet fully established. Neonatal mice were pretreated s.c. with a single injection of 10 ug of capsaicin per mouse in volume of 20 ul within 5 days of age. Using 5-8 week old mice pretreated as neonates with capsaicin, the capsaicin- pretreated and vehicle-treated control mice were examined for various parameters of immune responses described above. For the induction of active fatal anaphylaxis with PEV, 8 week old mice pretreated as neonates and age-matched capsaicin- untreated control mice were sensitized i.p. with 500 ug of PEV-ovalbumin conjugate plus 2*10(9) B. pertussis and 1.0 mg alum and challenged i.v. with PEV-bovine serum albumin conjugate 14 days later. It was found that neonatal capsaicin-pretreatment significantly enhanced contact hypersensitivity to TNCB and hemagglutination response to SRBC, but significantly inhibited the proliferation response of rnurine splenocyte to Con A and LPS. Interestingly, neonatal capsaicin pretreatment significantly inhibited the intensity of PEV-induced active fatal anaphylaxis and decreased the mortality due to anaphylactic shock. It also significantly inhibited LPS- induced production of cytokines such as TNF-a, IL-1B, IL-6, IL-10, and IL-12. The capsaicin-pretreatment also resulted in an inhibition of the activation of NF-kB. Taken together, these data showed for the first time that neonatal capsaicin-pretreatment significantly inhibited an antibiotic (PEV)-induced anaphylaxis and production of various cytokines, and suggest that capsaicin-sensitive primary sensory nerve may play an important regulatory role in active fatal anaphylaxis and cytokine production, thus potentially presenting tools for immune intervention. In particular, the data presented also indicated the possibility to selectively down-modulate cytokine production and NF-kB activation may offer a broad application for therapeutic intervention in neuroimmunological diseases and other pathological situations.
Subject(s)
Animals , Humans , Infant, Newborn , Mice , Anaphylaxis , Capsaicin , Cytokines , Denervation , Dermatitis, Contact , Hemagglutination , Interleukin-10 , Interleukin-12 , Interleukin-6 , Mortality , Neuropeptides , NF-kappa B , Penicillin V , Sensory Receptor Cells , Serum Albumin , Tachykinins , Whooping CoughABSTRACT
Human seminal plasrna (HSP) is mixture of secretion derived from various glands associated with male reproductive tract which comprises approximately 80-90% of the volume of normal ejaculate. The present study was undertaken in an effort to explore the effect of HSP pretreatment on the production of IL-1B, TNF-a and IL-12, in mice, and to investigate if HSP may cause to induce active systemic anaphylaxis (ASA) in mice. In addition, effects of HSP pretreatment on contact hypersensitivity to trinitrochlorobenzene (TNCB), antibody response to polyvinylpyrroridone (PVP), a thymus-independent antigen and on ASA induced by egg albumin (OVA) were also studied in this study. For the experiments of contact hypersensitivity, antibody response and cytokine production, mice were pretreated i.p. daily with 0.3ml of HSP or sterile saline alone (control) for 3 consecutive days before antigen sensitization or lipopolysaccharide injection for the cytokine induction. For the experiments of OVA- induced anaphylaxis, mice were pretreated by a single s.c. injection of HSP 0.3ml per mouse before sensitization. For induction of ASA in mice by HSP, a group of mice were sensitized i.p. 2 consecutive days with 0.3ml of HSP and one day with 0.3 ml of HSP plus 2x10(9) B. pertussis and 1.0 mg of alum (schedule A) or another group of mice were sensitized i.p. with a single i.p. injection of 0.3 ml of HSP with 2x10' B. pertussis and 1.0 mg of alum (schedule B). All sensitized and unsensitized control mice were challenged i.v. with 0.2ml of HSP 14 days after HSP sensitization, and mortality were observed. It was found that HSP pretreatment inhibited the production of IL-lB, TNF-a and IL-12, and also inhibited OVA-induced ASA, contact hypersensitivity to TNCB and anti-PVP antibody production. Interestingly, ASA was induced by HSP irrespective of the applied sensitization schedule. Taken together, this study may provide the direct evidences that HSP may inhibit the production of IL-1B, TNF-a and IL-12 and this may be the first to show the induction of ASA by HSP in mice.
Subject(s)
Animals , Humans , Male , Mice , Anaphylaxis , Antibody Formation , Appointments and Schedules , Dermatitis, Contact , Interleukin-12 , Mortality , Ovum , Picryl Chloride , Semen , Whooping CoughABSTRACT
Normal human B cells produce autocrine growth factor in response to Staphylococcus aureus Cowan I strain (SAC). However, the functional role and molecular nature of the B cell derived-B cell growth factor (B-BCGF) are largely unknown. We have tried to investigate the nature of B-BCGF using mAb for several years. We report here that B- BCGF is capable of binding to hemoglobin (Hb). The concentrated culture supernatant from tonsillar B cells stimulated with SAC for 24 h was loaded into the fast protein liquid chromatography and ion-exchange chromatography. The peak with BCGF activity was shown to have a M.W. of 16-18 Kda in polyacrylamide gel electrophoresis followed by silver stain. Amino acid sequence of the fraction was found to identical to human hemoglobin (Hb) by more than 85%. However, Hb itself had no BCGF activity. The presence of Hb in culture supernatant was due to the contamination of SRBC during B cell purification. SRSC were completely removed from B cells by percoll-gradient centrifugation and B cells were stimulated with SAC and exogenous Hb was added to the cultures. The Hb fraction from FPLC again showed a BCGF activity. These data strongly suggested that BCGF binds to Hb. We confirmed this in dot blot as well as Western blot. The M.W of Hb-binding BCGF was 20 Kda. This information may provide a rapid progress in research of BCGF.
Subject(s)
Humans , Amino Acid Sequence , B-Lymphocytes , Blotting, Western , Centrifugation , Chromatography, Ion Exchange , Chromatography, Liquid , Electrophoresis, Polyacrylamide Gel , Silver , Staphylococcus aureusABSTRACT
The present study was undertaken to investigate the effect of acute administration of ethanol on production of cytokines such as IL-1j3, IL-2, IL-6, IL-10 and TNF-a, induction of penicillin V-induced active fatal anaphylaxis, and resistence to Salmonel/a typhimurium infection in mice. Ethanol administration into mice was performed by intraperitoneal injection of 0.5 ml of 20 % ethanol for 3 consecutive days before induction of cytokines with lipopolysaccharide (LPS), Con A or Salmone/la injection. Serum levels of cytokines were measured by ELISA. It was found that ethanol administration significantly inhibited both the serum levels of all cytokines examined and the resistance of mice to S. typhimurium. However, ethanol administration failed to prevent penicillin-induced fatal anaphylaxis. Taken together, the present results may need new insights in the diagnosis and treatment of various immunologically-mediated diseases.
Subject(s)
Animals , Mice , Anaphylaxis , Cytokines , Diagnosis , Enzyme-Linked Immunosorbent Assay , Ethanol , Injections, Intraperitoneal , Interleukin-10 , Interleukin-2 , Interleukin-6 , Interleukins , Penicillin V , Penicillins , Salmonella Infections , SalmonellaABSTRACT
"Capsaicin, the pungent principle of hot peppers, is a neurotoxin that depletes primary sensory neurons of neuropeptides like tachykinin. The objectives of these experiment was to examine the effects of capsaicin on Salmonel/a typhimurium-induced production of cytokines such as TNF-a, IL-1B, IL-6, IL-10 and IL-12 and on production of nitric oxide in peritoneal macrophages. In addition, the effects of capsaicin on survival rates of S. typhimurium-infected mice and on nuclear transcription factor (NF-kB) activation were also investigated. Mice were pretreated with a single s.c. injection of 100 ug of capsaicin and were infected i.v. with S. typhimurium (5xO5/mouse) in 0.2 ml volume after capsaicin pretreatment. The serum cytokine levels were measured 30, 60, 120, 180 and 240 min after Salmonella infection, using ELISA kits. The activation of NF-B was also examined by gel shift assay in spleens, thymuses and brains of mice that had been pretreated with a single s.c. injection of 100 ug of capsaicin. It was found that Sa/mone/la infection induced the production of TNF-a, IL-1B, IL-6, IL-10 and IL-12, but capsaicin pretreatment inhibited the production of TNF-a, IL-1B, IL-10 and IL-12, but enhanced IL-6 production 120 min after Salmonella infection. Interestingly, the capsaicin pretreatment inhibited the activation of NF-kB in spleens and thymuses. There were no differences in the numbers of bacteria in livers, brains, spleens, kidneys and lungs between capsaicin- pretreated mice and the control animals in applied experimental conditions. Suprisingly, however, capsaicin pretreatment increased both the survival rates of Sa/mone//a-infected mice and production of nitric oxide by peritoneal macrophages compared with capsaicin-untreated control mice. Taken together, these results indicate that the capsaicin-sensitive primary sensory neurons may play an important modulatory role in the production of cytokine, nitric oxide and NF-B activation and the pathogenesis of salmonellosis."
Subject(s)
Animals , Mice , Bacteria , Brain , Capsaicin , Cytokines , Enzyme-Linked Immunosorbent Assay , Interleukin-10 , Interleukin-12 , Interleukin-6 , Kidney , Liver , Lung , Macrophages, Peritoneal , Neuropeptides , NF-kappa B , Nitric Oxide , Salmonella Infections , Salmonella typhimurium , Salmonella , Sensory Receptor Cells , Spleen , Survival Rate , Tachykinins , Thymus Gland , Transcription FactorsABSTRACT
It has been known that the interconnection between the gervous, endocrine and immune system are largely mediated through regulatory soluble factors such as neruopeptides, cytokines and hormones. Capsaicin, the pungent principle of hot peppers, is a neurotoxin that affects primary sensory neurons of the C and A-b type and depletes primary sensory neurons (polymodal nociceptors) of neuropeptides like tachykinin. In this study capsaicin was used to explore the possible role of the neruons on the expression of cellular and humoral immune responses and TNF-a prodcution. Mice were pretreated with s.c. injections in the neck region with a single dose of 100 u,g of capsaicin per mouse before immunization. ...continue...