Sökning: WFRF:(Persson Alexander 1978 )
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Mycobacterium tuber...
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Persson, Alexander,1978-Linköpings universitet,Medicinsk mikrobiologi,Hälsouniversitetet,Division of Medical Microbiology, Department of Molecular and Clinical Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden
(författare)
Mycobacterium tuberculosis-induced apoptotic neutrophils trigger a pro-inflammatory response in macrophages through release of heat shock protein 72, acting in synergy with the bacteria
- Artikel/kapitelEngelska2008
Förlag, utgivningsår, omfång ...
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elsevier,2008
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printrdacarrier
Nummerbeteckningar
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LIBRIS-ID:oai:DiVA.org:liu-20835
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https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-20835URI
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https://doi.org/10.1016/j.micinf.2007.11.007DOI
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https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-76778URI
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Språk:engelska
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Sammanfattning på:engelska
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Ämneskategori:ref swepub-contenttype
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Ämneskategori:art swepub-publicationtype
Anmärkningar
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Mycobacterium tuberculosis (Mtb) survive inside macrophages by manipulating microbicidal functions such as phago-lysosome fusion, production of reactive oxygen species and nitric oxide, and by rendering macrophages non-responsive to IFN-γ. Mtb-infected lung tissue does however not only contain macrophages, but also significant numbers of infiltrating polymorphonuclear neutrophils (PMN). These are able to phagocytose and kill ingested Mtb, but are short-lived cells that constantly need to be removed from tissues to avoid tissue damage. Phagocytosis of aged or UV-induced apoptotic PMN by macrophages induce an anti-inflammatory response in macrophages. However, in the present study, we show that engulfment of Mtb-induced apoptotic PMN by macrophages initiates secretion of TNF-α from the macrophages, reflecting a pro-inflammatory response. Moreover, Mtb-induced apoptotic PMN up-regulate heat shock proteins 60 and 72 (Hsp60, Hsp72) intracellularly and also release Hsp72 extracellularly. We found that both recombinant Hsp72 and released Hsp72 enhanced the pro-inflammatory response to both Mtb-induced apoptotic PMN and Mtb. This stimulatory effect of the supernatant was abrogated by depleting the Hsp72 with immunoprecipitation. These findings indicate that released Hsp72 from Mtb-infected PMN can trigger macrophage activation during the early stage of Mtb infections, thereby creating a link between innate and adaptive immunity.
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Biuppslag (personer, institutioner, konferenser, titlar ...)
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Blomgran-Julinder, RobertLinköpings universitet,Medicinsk mikrobiologi,Hälsouniversitetet,Division of Medical Microbiology, Department of Molecular and Clinical Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden(Swepub:liu)robbl96
(författare)
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Rahman, SaymaLinköpings universitet,Medicinsk mikrobiologi,Hälsouniversitetet,Division of Medical Microbiology, Department of Molecular and Clinical Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden(Swepub:liu)sayra72
(författare)
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Zheng, LiminDepartment of Biochemistry, College of Life Sciences, Sun Yansen (Zhongshan) University, Guangzhou, People's Republic of China
(författare)
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Stendahl, OlleLinköpings universitet,Medicinsk mikrobiologi,Hälsouniversitetet,Division of Medical Microbiology, Department of Molecular and Clinical Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden(Swepub:liu)ollst48
(författare)
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Linköpings universitetMedicinsk mikrobiologi
(creator_code:org_t)
Sammanhörande titlar
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Ingår i:Microbes and infection: elsevier10:3, s. 233-2401286-45791769-714X
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