Browsing by Subject "Macrophage polarization"

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    M1- and M2-macrophage polarization in thioacetamide (TAA)-induced rat liver lesions; a possible analysis for hepato-pathology
    (F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2014) Wijesundera, Kavindra Kumara; Izawa, Takeshi; Murakami, Hiroshi; Tennakoon, Anusha Hemamali; Golbar, Hossain M.; Katou-Ichikawa, Chisa; Tanaka, Miyuu; Kuwamura, Mitsuru; Yamate, Jyoji
    “Classically activated macrophages (M1)” and “alternatively activated macrophages (M2)”, which appear in injured tissues, control either inflammation or remodeling. The mechanism remains unclear. To clarify the M1-/M2-macrophage polarization in acute liver injury, M1- and M2-related factors were analysed in F344 rats by a single injection of TAA (300 mg/kg BW), and liver samples were collected on post injection (PI) hour 10 and days 1 to 10. Macrophage immunopheno-types were analyzed by single and double immuno-labeling. M1-/M2-related factors were analyzed by real-time RT-PCR. On PI hour 10 (when centrilobular lesions were not still developed), expressions of IFN-γ, TNF-α, IL-1ß, and IL-6 for M1, and IL-4 for M2 were already increased, followed by increased expressions of IL-10 and TGF-ß1 for M2 on PI days 1-3 with development of centrilobular lesions and subsequent reparative fibrosis. On PI hour 10, CD204+ and MHC class II+ macrophages already increased in the intact periportal/Glisson’s sheath regions, accompanied by an increased number of granzyme B+ NK cells. Reactive cells at PI hour 10 might produce M1-related factors. In addition to these macrophages, CD68+ and CD163+ macrophages, and CD3+ T cells appeared in the injured centrilobular region on PI days 1-3; there were macrophages reacting simultaneously to CD68/MHC class II, CD163/MHC class II, CD68/CD204, CD163/CD204, and MHC class II/CD204 in varying degrees. Although CD68+ and CD163+ macrophages are regarded as M1- and M2-types, respectively, the double labeling indicated that macrophage immunophenotypes are interchangeable in injured regions and subsequent fibrosis. An M1-/M2-macrophage paradigm would be useful to analyze hepatotoxicity and to understand the pathogenesis. Histol Histopathol 29, 497-511 (2014)
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    Oroxin B prevented sepsis-evoked acute lung injury by promoting M2 macrophage polarization through the TLR4/NF-κB axis
    (2025) Jianhua Liu; Changhong Zhang; Feng Li; Nana Duan; Zhihua Zhang; Chen Li; Biología Celular e Histología
    Acute lung injury (ALI) is a frequent complication of sepsis that aggravates sepsis mortality and morbidity, which is tightly related to the inflammatory process. Oroxin B (OB), a flavonoid from Oroxylum indicum (L.) Vent, has exhibited anti-inflammatory properties in several illnesses. Nevertheless, it is still unclear how OB affects sepsis-induced ALI and how it works. RAW264.7 cells were challenged with lipopolysaccharide (LPS, 10 μg/mL), and mice received cecal ligation and puncture (CLP) to produce sepsis-evoked ALI in in vitro and in vivo models. The action of OB on sepsis-elicited ALI was probed through cell counting kit-8, pathological staining, enzyme-linked immunosorbent assay, reverse transcription-quantitative polymerase chain reaction, and western blot. The results showed that OB improved pathological damage and pulmonary fibrosis in CLP-challenged mice. OB also reduced the concentration of MPO, the protein content in BALF, and macrophage and neutrophil numbers in BALF from CLP-challenged mice. Molecularly, OB decreased the levels of IL-1β, IL-6, TNF-α, CD86, and iNOS but increased the level of Arg1 and CD206 in both LPS-evoked RAW264.7 cells and CLP-treated mice. Mechanistically, OB downregulated the level of the TLR4/NF-κB axis in both LPS-challenged RAW264.7 cells and CLP-treated mice. Overexpression of TLR4 abrogated the effect of OB on the above-mentioned indicators in LPS-elicited RAW264.7 cells. Therefore, OB improved sepsis-elicited ALI by attenuating inflammation and promoting M2 macrophage polarization through the TLR4/NF-KB signaling pathway.
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    The significance of M1 macrophage should be highlighted in peripheral nerve regeneration
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2023) Feng, Ruiqin; Zhang, Peixun
    Macrophage influences peripheral nerve regeneration. According to the classical M1/M2 paradigm, the M1 macrophage is an inhibitor of regeneration, while the M2 macrophage is a promoter. However, several studies have shown that M1 macrophages are indispensable for peripheral nerve repair and facilitate many critical processes in axonal regeneration. In this review, we summarized the information on macrophage polarization and focused on the activities of M1 macrophages in regeneration. We also provided some examples where the macrophage phenotypes were regulated to help regeneration. We argued that the coordination of both macrophage phenotypes might be effective in peripheral nerve repair, and a more comprehensive view of macrophages might contribute to macrophage-based immunomodulatory therapies.