کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10941004 | 1095546 | 2013 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Neutrophil gelatinase-associated lipocalin and interleukin-10 regulate intramacrophage Chlamydia pneumoniae replication by modulating intracellular iron homeostasis
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کلمات کلیدی
LCN-2TFRDMT-1Fpn1ferroportinIL-10Chlamydia pneumoniaeHprtAtherosclerosis - آترواسکلروز(تصلب شریان)Iron - آهنInterleukin-10 - اینترلوکین 10Ferritin - فریتینdivalent metal transporter-1 - فلات دوالانت فلزی 1lipocalin-2 - لیپوکالین-2Macrophage - ماکروفاژ wildtype - نوع وحشیHAMP - هامپHepcidin - هپسیدین hypoxanthine guanine phosphoribosyl transferase - هیپوکسانتین گوانین فسفریبوسیل ترانسفرازtransferrin receptor - گیرنده انتقالین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Infection with Chlamydiae ex vivo and in vivo revealed a significantly higher bacterial growth in peritoneal macrophages of Lcn-2 â/â than of wildtype mice. These differences were significantly more pronounced upon iron challenge, which stimulated bacterial growth. Accordingly, treatment with an anti-Lnc-2 antibody increased whereas addition of recombinant Lcn-2 reduced bacterial growth in infected macrophages. When investigating the underlying mechanisms we observed partly different expression of several iron metabolism genes between Lcn-2 +/+ and Lcn-2 â/â macrophages and most strikingly an increased formation of the anti-inflammatory cytokine IL-10 by Lcn-2 â/â macrophages. Upon treatment with an anti-IL10 antibody we experienced a significant increase of Chlamydial growth within Lcn-2 â/â macrophages along with a reduction of the major iron storage protein ferritin. Herein we provide first time evidence that Lcn-2 is involved in host defence against Chlamydia presumably by limiting the availability of iron to the pathogen. In the absence of Lcn-2, increased formation of IL-10 exerts protective effects by increasing the intracellular formation of ferritin, thereby reducing the access of iron for bacteria.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Immunobiology - Volume 218, Issue 7, July 2013, Pages 969-978
Journal: Immunobiology - Volume 218, Issue 7, July 2013, Pages 969-978
نویسندگان
Rosa Bellmann-Weiler, Andrea Schroll, Sabine Engl, Manfred Nairz, Heribert Talasz, Markus Seifert, Guenter Weiss,