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Infect Immun
Institute for Biological Sciences, National Research Council Canada, Ottawa, Ontario, Canada.
Published: March 2009
Acinetobacter baumannii is an emerging bacterial pathogen that rapidly develops multiple-drug resistance and is responsible for many nosocomial pulmonary infections. This study investigated the role of the NADPH phagocyte oxidase (phox) and inducible nitric oxide synthase (NOS2) in the host defense against respiratory infection with A. baumannii in mouse models of intranasal A. baumannii infection. gp91(phox-/-) mice showed higher susceptibility to A. baumannii infection than wild-type (WT) C57BL/6 mice, with significantly greater bacterial counts in their lungs (1,000-fold) (P < 0.005) and spleens (10-fold) (P < 0.05). Moreover, all of the gp91(phox-/-) mice succumbed to infection within 48 h. In contrast, only a moderate increase in bacterial burdens was detected in the lungs of NOS2(-/-) mice, and all NOS2(-/-) mice survived infection. Compared to WT mice, the pulmonary influx of inflammatory cells and serum and local inflammatory cytokine/chemokine responses were not obviously impaired at 4 h and were significantly higher at 24 h (P < 0.05) in gp91(phox-/-) mice, but NADPH-deficient neutrophils were unable to control bacterial replication and extrapulmonary dissemination. Thus, NADPH phagocyte oxidase appears to play a crucial role in the neutrophil-mediated host defense against A. baumannii.
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http://dx.doi.org/10.1128/IAI.01029-08 | DOI Listing |
J Immunol Methods
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Department of Natural Sciences, Kawasaki Medical School, 577 Matsushima Kurashiki, Okayama 701-0192, Japan.
Reactive oxygen species (ROS)-producing NADPH oxidase (Nox) family proteins are involved in host defense. The overproduction of ROS leads to oxidative stress, which is associated with a myriad of diseases. The Nox subunit p22 is essential for Nox1-4 activity, and p22 and Nox2 proteins are mutually stabilized in phagocytic cells.
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March 2025
Department of Hepatobiliary Pancreatic Surgery, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
NAD(P)H dehydrogenase quinone 1 (NQO1) is overexpressed in various cancers and is strongly associated with an immunosuppressive microenvironment and poor prognosis. In this study, we explored the role of NQO1 in the microenvironment, prognosis and immunotherapy of Hepatocellular carcinoma (HCC) using multi-omics analysis and machine learning. The results revealed that NQO1 was significantly overexpressed in HCC cells.
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March 2025
Faculté de Pharmacie, Université de Montréal, Montréal, QC H3C 3J7, Canada.
Macrophage mitochondrial dysfunction, caused by oxidative stress, has been proposed as an essential event in the progression of chronic inflammation diseases, such as atherosclerosis. The cluster of differentiation-36 (CD36) and lectin-like oxLDL receptor-1 (LOX-1) scavenger receptors mediate macrophage uptake of oxidized low-density lipoprotein (oxLDL), which contributes to mitochondrial dysfunction by sustained production of mitochondrial reactive oxygen species (mtROS), as well as membrane depolarization. In the present study, the antioxidant mechanisms of action of the selective synthetic azapeptide CD36 ligand MPE-298 have been revealed.
View Article and Find Full Text PDFBMC Med
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Department of Rheumatology and Immunology, the First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230001, China.
Background: Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by disrupted bone homeostasis. This study investigated the effect and underlying mechanisms of one-carbon metabolism enzyme methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) on osteoclast differentiation and bone loss in RA.
Methods: The expression of MTHFD2 was examined in CD14 + monocytes and murine bone marrow-derived macrophages (BMMs).
Sci Rep
February 2025
Department of Comparative Biochemistry and Bioanalytics, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Kraków, Poland.
Candida albicans, a prevalent fungal pathogen, employs aspartyl proteases such as Sap6 to evade immune defenses, challenging our understanding of host‒pathogen interactions. This research examined the impact of Sap6 on neutrophil responses, which are crucial for innate immunity. Employing flow cytometry and fluorescence microscopy, we explored how Sap6 affects neutrophil functions, particularly by focusing on reactive oxygen species (ROS) production, neutrophil extracellular traps release (NETosis), and apoptosis.
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