Effects of Interferon‐α/β and Interferon‐γ Preparations on Phagocytosis by Mouse Peritoneal Macrophages

Rollag, H.; Degré, Miklos; Sonnenfeld, Gerald

doi:10.1111/j.1365-3083.1984.tb00988.x

Cited by 34 publications

(18 citation statements)

References 14 publications

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“…In contrast, efferocytosis suppresses innate immunity and promotes its resolution by suppressing the expression of inflammatory mediators [40]. To that end, IFNα increases phagocytosis by macrophages [41], [42] suggesting that the effect of IFNα in SUH rats may be partially attributable to stimulation of efferocytosis. Additional studies are needed to address the role of apoptosis and efferocytosis in the effect of IFNα on PH and in the pathogenesis of the disease itself.…”

Section: Discussionmentioning

confidence: 99%

Recombinant Human Interferon Alpha 2b Prevents and Reverses Experimental Pulmonary Hypertension

et al. 2014

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Pulmonary hypertension (PH) is a progressive and fatal disease with no cure. Vascular remodeling in PH involves intraluminal growth of endothelial and smooth muscle cells, leading to obliterative vascular lesions. Cell growth in these lesions is quasi-neoplastic, with evidence of monoclonality, apoptosis resistance and cancer-like metabolic derangements. Herein we tested the effect of human interferon alpha 2b (IFNα), a pleiotropic cytokine and anti-cancer therapeutic, on the development and progression of PH in the rat SU5416/hypoxia (SUH) model and mouse hypoxia model of the disease. In both models IFNα attenuated the development of PH and reversed established PH as assessed by measuring right ventricular systolic pressure and right ventricular hypertrophy. The effect of IFNα was dependent on the type I interferon receptor (IFNAR) since mice lacking a subunit of the IFNAR were not protected by IFNα. Morphometric analysis of pulmonary aterioles from hypoxic mice or SUH rats showed that IFNα inhibited pulmonary vascular remodeling in both models and that IFNα reversed remodeling in SUH rats with established disease. Immunohistochemical staining revealed that IFNα decreased the number of PCNA and Tunel positive cells in the wall of pulmonary arterioles. In vitro, IFNα inhibited proliferation of human pulmonary artery smooth muscle cells and as well as human pulmonary artery endothelial cell proliferation and apoptosis. Together these findings demonstrate that IFNα reverses established experimental PH and provide a rationale for further exploration of the use of IFNα and other immunotherpies in PH.

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Section: Discussionmentioning

confidence: 99%

Recombinant Human Interferon Alpha 2b Prevents and Reverses Experimental Pulmonary Hypertension

et al. 2014

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“…Thus, primary human fibroblasts produce IFN-␥ in response to Shigella invasion (38). Among many functions, this cytokine enhances bacterial phagocytosis by macrophages (39). Invasion of intestinal epithelial cells has been shown to trigger the production of IL-8, GM-CSF, monocyte chemoattractant protein-1, and TNF-␣ (40).…”

Section: Discussionmentioning

confidence: 99%

Blockade of CD14 Increases Shigella-Mediated Invasion and Tissue Destruction

Wennerås

Avé

Huerre

et al. 2000

The Journal of Immunology

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Shigella is a diarrheal pathogen that causes disease through invasion of the large intestinal mucosa. The endotoxin of the invading bacterium may play a key role in the disease process by causing inflammation and tissue injury during infection. Earlier studies have shown that various animal species lacking functional CD14 were protected against endotoxin-mediated shock. Rabbits experimentally infected with Shigella were used to test the hypothesis that blockade of endotoxin-induced cell activation with anti-CD14 mAb would diminish inflammation and thus disease severity. Unexpectedly, we observed that the intestinal mucosa of anti-CD14-treated animals exhibited a 50-fold increase in bacterial invasion and more severe tissue injury compared with controls. Despite higher bacterial loads in treated animals, the numbers of polymorphonuclear leukocytes that were recruited to the infection site were similar to those in controls. Furthermore, the phagocytic cells of CD14-blocked animals produced IL-1 and TNF-α. Moreover, in vitro blockade of CD14 did not impede bactericidal activity. Thus, anti-CD14 treatment interfered with host defense mechanisms involved with removal/eradication of Shigella.

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“…Gamma interferon (IFN-␥) is a key monocyte-activating cytokine (3,17,20,27). With IFN-␥ stimulation, the human monocytic cell line THP-1 expresses a number of genes associated with the antigen-presenting function of macrophages, including major histocompatibility complex class II (MHC-II), CD74 (MHC-II-associated invariant chain), and interleukin-1␤ (7,26; our unpublished observation).…”

mentioning

confidence: 99%

Immunocytochemical Analyses and Targeted Gene Disruption of GTPBP1

Senju

Iyama²,

Kaneko

et al. 2000

Molecular and Cellular Biology

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We previously identified a gene encoding a putative GTPase, GTPBP1, which is structurally related to elongation factor 1␣, a key component of protein biosynthesis machinery. The primary structure of GTPBP1 is highly conserved between human and mouse (97% identical at the amino acid level). Expression of this gene is enhanced by gamma interferon in a monocytic cell line, THP-1. Although counterparts of this molecule in Caenorhabditis elegans and Ascaris suum have also been identified, the function of this molecule remains to be clarified. In the present study, our immunohistochemical analyses on mouse tissues revealed that GTPBP1 is expressed in some neurons and smooth muscle cells of various organs as well as macrophages. Immunofluorescence analyses revealed that GTPBP1 is localized exclusively in cytoplasm and shows a diffuse granular network forming a gradient from the nucleus to the periphery of the cells in smooth muscle cell lines and macrophages. To investigate the physiological role of GTPBP1, we used targeted gene disruption in embryonic stem cells to generate GTPBP1-deficient mice. The mutant mice were born at the expected Mendelian frequency, developed normally, and were fertile. No manifest anatomical or behavioral abnormality was observed in the mutant mice. Functions of macrophages, including chemotaxis, phagocytosis, and nitric oxide production, in mutant mice were equivalent to those seen in wild-type mice. No significant difference was observed in the immune response to protein antigen between mutant mice and wild-type mice, suggesting normal function of antigen-presenting cells of the mutant mice. The absence of an eminent phenotype in GTPBP1-deficient mice may be due to functional compensation by GTPBP2, a molecule we recently identified which is similar to GTPBP1 in structure and tissue distribution.

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Effects of Interferon‐α/β and Interferon‐γ Preparations on Phagocytosis by Mouse Peritoneal Macrophages

Cited by 34 publications

References 14 publications

Recombinant Human Interferon Alpha 2b Prevents and Reverses Experimental Pulmonary Hypertension

Recombinant Human Interferon Alpha 2b Prevents and Reverses Experimental Pulmonary Hypertension

Blockade of CD14 Increases Shigella-Mediated Invasion and Tissue Destruction

Immunocytochemical Analyses and Targeted Gene Disruption of GTPBP1

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