No abstract available.
Child* ; Humans ; Mycoplasma pneumoniae ; Mycoplasma* ; Pneumonia, Mycoplasma*

No abstract available.
Fracture Healing* ; Hematoma*

Thl cloned cell line 28-4 which is an I-A + KLH - specific Th1 type clone of (C57BU6xC 3H) F1 origin was kindly provided by professor Tomio Tada. In these studies, employing these cloned cells, the author investigated both proliferation responses of Thl cells in the presence of various concentrations of cytokines, such as IL-2, IL-4 or IL-6 and proliferation of Thl cells to various concentration of mitogens such as PHA, ConA or PWM. In addition, the author also investigated the proliferation response of Th1 cells to the optimal dose of PHA, ConA or PWM in the presence or absence of above mentioned cytokines. It was found that IL-2, IL-4 or IL-6 alone their growth stimulation degree was dependent on cytokine concentration and that PHA, ConA or PWM stimulated Thl cell proliferation and optimal dose of PHA ConA and PWM was 3 g, 4 g and 2 g per ml, respectively. In addition, proliferation response of Th1 cells to ConA or PWM in the presence of IL-2 was significantly enhanced, but the proliferation response to PHA was not increased significantly. However, IL-4 did not significantly modulate mitogen-activated Thl cell proliferation response. Interestingly, IL-6 decreased PHA- or ConA-activated proliferation of Thl cells, but did not change PWM-activated proliferation. Taken together, these studies strongly suggested that IL-2, IL-4 or IL-6 itself clone stimulated the Thl cell proliferation and that PHA, ConA or PWM also stimulated Thl cell proliferation. In addition, these studies also indicated that IL-2 increased ConA- or PWM-activated Thl cell proliferation, but IL6 inhibited PHA- or ConA-activated Th1 cell proliferation and that IL-4 did not significantly change the mitogen-activated Th1 cell proliferation.
Cell Line ; Cell Proliferation ; Clone Cells ; Cytokines* ; Interleukin-2 ; Interleukin-4 ; Interleukin-6 ; Mitogens ; Th1 Cells*

No abstract available.
Animals ; Capsaicin* ; Macrophages, Peritoneal* ; Mice*

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.
Anaphylaxis* ; Animals ; Cytokines* ; Diagnosis ; Enzyme-Linked Immunosorbent Assay ; Ethanol ; Injections, Intraperitoneal ; Interleukin-10 ; Interleukin-2 ; Interleukin-6 ; Interleukins ; Mice* ; Penicillin V* ; Penicillins* ; Salmonella Infections* ; Salmonella*

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.
Anaphylaxis ; Animals ; Capsaicin* ; Cytokines ; Denervation* ; Dermatitis, Contact ; Hemagglutination ; Humans ; Infant, Newborn ; Interleukin-10 ; Interleukin-12 ; Interleukin-6 ; Mice ; Mortality ; Neuropeptides ; NF-kappa B ; Penicillin V ; Sensory Receptor Cells ; Serum Albumin ; Tachykinins ; Whooping Cough

PURPOSE: To report a case with proptosis associated with orbital panniculitis. METHODS: A 34-old-year man with unilateral proptosis for 1 month presented with diffuse swelling and redness in the eyelid and conjunctiva. His systemic symptoms were high fever, headache, nausea, diarrhea, dizziness, weight loss, malaise and hepatosplenomegaly. He had subcutaneous nodules on the inguinal region, the pubis, and the upper abdomen. Ophthalmic examinations, orbit magnetic resonance imaging(MRI), and biopsy from orbital tissue were performed. RESULTS: The right eye revealed proptosis(22/14/102, Hertel's exophthalmometer), but other ocular findings including the fundus were normal. Diffuse infilterative lesions and definite proptosis were shown on orbit MRI. Biopsy specimen of orbital tissue revealed histiocytes containing nuclei and nuclear debris, mononuclear cells infiltration, and the characteristic 'bean-bag' cell i.e., macrophage exhibiting hemophagocytosis, which is histopathological characteristic of cytophagic histiocytic panniculitis. Proptosis, swelling and redness of the eyelid improved gradually following systemic corticosteroid therapy to control the disease. CONCLUSION: This report describes a rare finding of proptosis as the manifesting sign of orbital panniculitis.
Abdomen ; Biopsy ; Conjunctiva ; Diarrhea ; Dizziness ; Exophthalmos* ; Eyelids ; Fever ; Headache ; Histiocytes ; Macrophages ; Magnetic Resonance Imaging ; Nausea ; Orbit* ; Panniculitis* ; Weight Loss

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.
Anaphylaxis* ; Animals ; Antibody Formation ; Appointments and Schedules ; Dermatitis, Contact ; Humans* ; Interleukin-12 ; Male ; Mice* ; Mortality ; Ovum ; Picryl Chloride ; Semen* ; Whooping Cough

No abstract available.
Nevus, Pigmented*

No abstract available.
Child* ; Humans ; Hypercalciuria*