2010
DOI: 10.1074/jbc.m110.163782
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Angiotensin-converting Enzyme Overexpression in Mouse Myelomonocytic Cells Augments Resistance to Listeria and Methicillin-resistant Staphylococcus aureus

Abstract: Gene targeting in ES cells was used to substitute control of angiotensin converting enzyme (ACE) expression from the endogenous promoter to the mouse c-fms promoter. The result is an animal model called ACE 10/10 in which ACE is overexpressed by monocytes, macrophages, and other myelomonocytic lineage cells. To study the immune response of these mice to bacterial infection, we challenged them with Listeria monocytogenes or methicillin-resistant Staphylococcus aureus (MRSA). ACE 10/10 mice have a significantly … Show more

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Cited by 58 publications
(88 citation statements)
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“…The result was a very substantial reduction in tumor growth. An enhanced innate immune response was also observed when ACE 10/10 mice were challenged with L. monocytogenes or methicillin-resistant S. aureus (25). This appeared to be due to an intense monocytic/macrophagic response, and again, this resulted in reduced disease.…”
Section: Discussionmentioning
confidence: 77%
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“…The result was a very substantial reduction in tumor growth. An enhanced innate immune response was also observed when ACE 10/10 mice were challenged with L. monocytogenes or methicillin-resistant S. aureus (25). This appeared to be due to an intense monocytic/macrophagic response, and again, this resulted in reduced disease.…”
Section: Discussionmentioning
confidence: 77%
“…This is not surprising, since overexpression of catalytically active ACE is the key mechanistic feature of ACE 10/10 mice, and previous studies have shown that ACE 10/10 mice treated with ACE inhibitors exhibit the phenotype of WT mice (24,25). In WT mice and humans, ACE is normally produced by vascular endothelium, but what role this plays in the biology of Aβ, including pathogenic forms such as Aβ , is not known.…”
Section: Discussionmentioning
confidence: 97%
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“…ACE is essential in converting angiotensin I into angiotensin II, which is mainly an effector molecule in the renin-angiotensin system (RAS) and acts as pro-inflammatory modulator in the augmentation of immune responses. [12][13][14] The ACE I/D is a single nucleotide polymorphism (SNP) of ACE. The ACE I/D polymorphism is defined in the light of the presence (insertion, I) or absence (deletion, D) of a 287 bp repeat sequence within intron 16 of the ACE gene.…”
Section: Introductionmentioning
confidence: 99%