دورية أكاديمية
أعرض في EDS

Effects of IL-34 on Macrophage Immunological Profile in Response to Alzheimer's-Related Aβ 42 Assemblies.

التفاصيل البيبلوغرافية
العنوان: Effects of IL-34 on Macrophage Immunological Profile in Response to Alzheimer's-Related Aβ 42 Assemblies.
المؤلفون: Zuroff LR; Neurosurgery Department, Cedars-Sinai Medical Center, Los Angeles, CA, United States.; Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States., Torbati T; Neurosurgery Department, Cedars-Sinai Medical Center, Los Angeles, CA, United States.; Department of Neurology, David Geffen School of Medicine, UCLA, Los Angeles, CA, United States.; Western University of Health Sciences College of Osteopathic Medicine of the Pacific, Pomona, CA, United States., Hart NJ; Neurosurgery Department, Cedars-Sinai Medical Center, Los Angeles, CA, United States.; Keck School of Medicine, University of Southern California, Los Angeles, CA, United States., Fuchs DT; Neurosurgery Department, Cedars-Sinai Medical Center, Los Angeles, CA, United States., Sheyn J; Neurosurgery Department, Cedars-Sinai Medical Center, Los Angeles, CA, United States., Rentsendorj A; Neurosurgery Department, Cedars-Sinai Medical Center, Los Angeles, CA, United States., Koronyo Y; Neurosurgery Department, Cedars-Sinai Medical Center, Los Angeles, CA, United States., Hayden EY; Department of Neurology, David Geffen School of Medicine, UCLA, Los Angeles, CA, United States., Teplow DB; Department of Neurology, David Geffen School of Medicine, UCLA, Los Angeles, CA, United States., Black KL; Neurosurgery Department, Cedars-Sinai Medical Center, Los Angeles, CA, United States., Koronyo-Hamaoui M; Neurosurgery Department, Cedars-Sinai Medical Center, Los Angeles, CA, United States.; Department of Biomedical Sciences, Applied Cellular Biology and Physiology, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
المصدر: Frontiers in immunology [Front Immunol] 2020 Jul 16; Vol. 11, pp. 1449. Date of Electronic Publication: 2020 Jul 16 (Print Publication: 2020).
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Frontiers Research Foundation] Country of Publication: Switzerland NLM ID: 101560960 Publication Model: eCollection Cited Medium: Internet ISSN: 1664-3224 (Electronic) Linking ISSN: 16643224 NLM ISO Abbreviation: Front Immunol Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [Lausanne : Frontiers Research Foundation]
مواضيع طبية MeSH: Alzheimer Disease/*immunology , Amyloid beta-Peptides/*metabolism , Interleukins/*metabolism , Macrophages/*physiology , Peptide Fragments/*metabolism, Animals ; CD36 Antigens/metabolism ; Cells, Cultured ; Humans ; Interleukins/immunology ; Macrophage Colony-Stimulating Factor/metabolism ; Matrix Metalloproteinase 9/metabolism ; Mice ; Mice, Inbred C57BL ; Phagocytosis ; Protein Multimerization
مستخلص: Interleukin-34 (IL-34) is a recently discovered cytokine that acts as a second ligand of the colony stimulating factor 1 receptor (CSF1R) in addition to macrophage colony-stimulating factor (M-CSF). Similar to M-CSF, IL-34 also stimulates bone marrow (BM)-derived monocyte survival and differentiation into macrophages. Growing evidence suggests that peripheral BM-derived monocyte/macrophages (BMMO) play a key role in the physiological clearance of cerebral amyloid β-protein (Aβ). Aβ 42 forms are especially neurotoxic and highly associated with Alzheimer's disease (AD). As a ligand of CSF1R, IL-34 may be relevant to innate immune responses in AD. To investigate how IL-34 affects macrophage phenotype in response to structurally defined and stabilized Aβ 42 oligomers and preformed fibrils, we characterized murine BMMO cultured in media containing M-CSF, IL-34, or regimens involving both cytokines. We found that the immunological profile and activation phenotype of IL-34-stimulated BMMO differed significantly from those cultured with M-CSF alone. Specifically, macrophage uptake of fibrillar or oligomeric Aβ 42 was markedly reduced following exposure to IL-34 compared to M-CSF. Surface expression of type B scavenger receptor CD36, known to facilitate Aβ recognition and uptake, was modified following treatment with IL-34. Similarly, IL-34 macrophages expressed lower levels of proteins involved in both Aβ uptake (triggering receptor expressed on myeloid cells 2, TREM2) as well as Aβ-degradation (matrix metallopeptidase 9, MMP-9). Interestingly, intracellular compartmentalization of Aβ visualized by staining of early endosome antigen 1 (EEA1) was not affected by IL-34. Macrophage characteristics associated with an anti-inflammatory and pro-wound healing phenotype, including processes length and morphology, were also quantified, and macrophages stimulated with IL-34 alone displayed less process elongation in response to Aβ 42 compared to those cultured with M-CSF. Further, monocytes treated with IL-34 alone yielded fewer mature macrophages than those treated with M-CSF alone or in combination with IL-34. Our data indicate that IL-34 impairs monocyte differentiation into macrophages and reduces their ability to uptake pathological forms of Aβ. Given the critical role of macrophage-mediated Aβ clearance in both murine models and patients with AD, future work should investigate the therapeutic potential of modulating IL-34 in vivo to increase macrophage-mediated Aβ clearance and prevent disease development.
(Copyright © 2020 Zuroff, Torbati, Hart, Fuchs, Sheyn, Rentsendorj, Koronyo, Hayden, Teplow, Black and Koronyo-Hamaoui.)
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معلومات مُعتمدة: R01 AG055865 United States AG NIA NIH HHS
فهرسة مساهمة: Keywords: Alzheimer's disease; IL34; MCSF; amyloid-beta; macrophage; myeloid cells; phagocytosis; scavenger receptors
المشرفين على المادة: 0 (Amyloid beta-Peptides)
0 (CD36 Antigens)
0 (IL34 protein, human)
0 (Interleukins)
0 (Peptide Fragments)
0 (amyloid beta-protein (1-42))
81627-83-0 (Macrophage Colony-Stimulating Factor)
EC 3.4.24.35 (Matrix Metalloproteinase 9)
تواريخ الأحداث: Date Created: 20200809 Date Completed: 20210419 Latest Revision: 20211119
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC7378440
DOI: 10.3389/fimmu.2020.01449
PMID: 32765504
قاعدة البيانات: MEDLINE
الوصف
تدمد:1664-3224
DOI:10.3389/fimmu.2020.01449