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Titolo:
Impairment of endotoxin-induced macrophage inflammatory protein 2 gene expression in alveolar macrophages in Streptozotocin-induced diabetes in mice
Autore:
Amano, H; Yamamoto, H; Senba, M; Oishi, K; Suzuki, S; Fukushima, K; Mukaida, N; Matsushima, K; Eguchi, K; Nagatake, T;
Indirizzi:
Nagasaki Univ, Inst Trop Med, Dept Internal Med, Nagasaki 8528523, Japan Nagasaki Univ Nagasaki Japan 8528523 ternal Med, Nagasaki 8528523, Japan Nagasaki Univ, Inst Trop Med, Dept Pathol, Nagasaki 8528523, Japan Nagasaki Univ Nagasaki Japan 8528523 ept Pathol, Nagasaki 8528523, Japan Nagasaki Univ, Inst Trop Med, Dept Biochem, Nagasaki 8528523, Japan Nagasaki Univ Nagasaki Japan 8528523 pt Biochem, Nagasaki 8528523, Japan Nagasaki Univ, Sch Med, Dept Internal Med 1, Nagasaki 8528523, Japan Nagasaki Univ Nagasaki Japan 8528523 rnal Med 1, Nagasaki 8528523, Japan Nijigaoka Hosp, Dept Metab Dis, Nagasaki, Japan Nijigaoka Hosp Nagasaki Japan oka Hosp, Dept Metab Dis, Nagasaki, Japan Kanazawa Univ, Sch Med, Canc Res Inst, Dept Mol Oncol, Kanazawa, Ishikawa 920, Japan Kanazawa Univ Kanazawa Ishikawa Japan 920 , Kanazawa, Ishikawa 920, Japan Univ Tokyo, Sch Med, Dept Mol Prevent Med, Tokyo 113, Japan Univ Tokyo Tokyo Japan 113 h Med, Dept Mol Prevent Med, Tokyo 113, Japan
Titolo Testata:
INFECTION AND IMMUNITY
fascicolo: 5, volume: 68, anno: 2000,
pagine: 2925 - 2929
SICI:
0019-9567(200005)68:5<2925:IOEMIP>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; NEUTROPHIL RECRUITMENT; BACTERIAL CLEARANCE; CYTOKINES; INTERLEUKIN-8; DEFENSE; CELLS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
30
Recensione:
Indirizzi per estratti:
Indirizzo: Amano, H Nagasaki Univ, Inst Trop Med, Dept Internal Med, 1-12-4 Sakamoto,Nagasaki8528523, Japan Nagasaki Univ 1-12-4 Sakamoto Nagasaki Japan 8528523 8523, Japan
Citazione:
H. Amano et al., "Impairment of endotoxin-induced macrophage inflammatory protein 2 gene expression in alveolar macrophages in Streptozotocin-induced diabetes in mice", INFEC IMMUN, 68(5), 2000, pp. 2925-2929

Abstract

To elucidate the mechanism of the high incidence of lower respiratory tract infections in patients with diabetes mellitus, we investigated the kinetics of production of macrophage inflammatory protein 2 (MIP-2), an importantmediator of lung neutrophil recruitment, using mice with streptozotocin-induced diabetes. Intratracheal challenge with 1 mg of lipopolysaccharide (LPS), an endotoxin, per kg of body weight resulted in a time-dependent increase in the levels of MIP-2 protein in bronchoalveolar lavage (BAL) fluid, with the peak concentration (49.4 +/- 13 ng/ml) occurring at 3 h and significant neutrophil accumulation becoming apparent by 3 h in normal mice. In diabetic mice, the peak level of MIP-2 protein in BAL fluid did not occur until 6 h and was reduced to 21.9 +/- 10 ng/ml. Immunohistochemical studies using anti-MIP-2 antibody confirmed that the main cellular source of MIP-2, inthe lung after LPS challenge was alveolar macrophages (AMs) in normal mice. The lungs in diabetic mice, however, showed no AR ls staining for MIP-2 within 3 h after LPS challenge. PCR analysis using whole-lung RNA showed a time-dependent increase in MIP-2 mRNA levels after LPS instillation. The level of MIP-2 mRNA in diabetic mice was markedly decreased compared to that in normal mice. Our results indicate that impairment of MIP-2 mRNA expression in the AMs in diabetic mice resulted in delayed neutrophil recruitment inthe lungs, and this may explain the development and progression of pulmonary infection in diabetes mellitus.

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Documento generato il 13/07/20 alle ore 17:23:50