Activation of Alveolar Macrophages via the Alternative Pathway in Herpesvirus-Induced Lung Fibrosis

Mora, Ana L.; Torres-González, Edilson; Rojas, Mauricio; Corredor, Claudia; Ritzenthaler, Jeffrey D.; Xu, Jianguo; Roman, Jesse; Brigham, Kenneth L.; Stecenko, Arlene A.

doi:10.1165/rcmb.2006-0121oc

Cited by 163 publications

(175 citation statements)

References 39 publications

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“…However, the vessel endothelial and other cells also exhibited positive staining of Arg-1. Similar observations of Arg-1 expression have been previously reported (31,32). These results indicate that Arg-1 is the hallmark for alternatively activated macrophages and also for other mediators in other cells, and takes part in the pathogenesis of RILF.…”

Section: Discussionsupporting

confidence: 91%

Th2-like immune response in radiation-induced lung fibrosis

Hân

Zhang²,

Xie

et al. 2011

Oncol Rep

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Section: Discussionsupporting

confidence: 91%

Th2-like immune response in radiation-induced lung fibrosis

Hân

Zhang²,

Xie

et al. 2011

Oncol Rep

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“…On one hand, over-production of inflammatory cytokines can lead to chronic inflammation and a variety of autoimmune diseases, including inflammatory bowel disease, rheumatoid arthritis, asthma and even atherosclerosis. On the other hand, over-production of anti-inflammatory cytokines can lead to persistent infection and tumor tolerance [29,30] . Regulation of macrophage activation by immunomodulatory drugs at specific stage of different diseases can be of important therapeutic benefit.…”

Section: Discussionmentioning

confidence: 99%

Immunomodulatory activity of andrographolide on macrophage activation and specific antibody response

et al. 2010

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Aim: To investigate the immunomodulatory effects of andrographolide on both innate and adaptive immune responses. Methods: Andrographolide (10 µg/mL in vitro or 1 mg/kg in vivo) was used to modulate LPS-induced classical activated (M1) or IL-4-induced alternative activated (M2) macrophages in vitro and humor immune response to HBsAg in vivo. Cytokine gene expression profile (M1 vs M2) was measured by real-time PCR, IL-12/IL-10 level was detected by ELISA, and surface antigen expression was evaluated by flow cytometry, whereas phosphorylation level of ERK 1/2 and AKT was determined by Western blot. The level of anti-HBs antibodies in HBsAg immunized mice was detected by ELISA, and the number of HBsAg specific IL-4-producing splenocyte was enumerated by ELISPOT. Results: Andrographolide treatment in vitro attenuated either LPS or IL-4 induced macrophage activation, inhibited both M1 and M2 cytokines expression and decreased IL-12/IL-10 ratio (the ratio of M1/M2 polarization). Andrographolide down-regulated the expression of mannose receptor (CD206) in IL-4 induced macrophages and major histocompability complex/costimulatory molecules (MHC I, CD40, CD80, CD86) in LPS-induced macrophages. Correspondingly, anti-HBs antibody production and the number of IL-4-producing splenocytes were reduced by in vivo administration of andrographolide. Reduced phosphorylation levels of ERK1/2 and AKT were observed in macrophages treated with andrographolide. Conclusion: Andrographolide can modulate the innate and adaptive immune responses by regulating macrophage phenotypic polarization and Ag-specific antibody production. MAPK and PI3K signaling pathways may participate in the mechanisms of andrographolide regulating macrophage activation and polarization.

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“…These results are not surprising, as several animal models of alternatively activated macrophages have shown significant increases in HIMF production (27,28). Using an HIMF antibody that we developed, Mora and colleagues (39) found that HIMF was expressed by these macrophages in an animal model of herpes virus-induced lung fibrosis. In addition, macrophages collected from the BALF of mice experimentally infected with Pneumocystis pneumonia showed consistent upregulation of HIMF concomitant with the development of fibrosis (40).…”

Section: Discussionmentioning

confidence: 99%

Resistin-Like Molecule-β in Scleroderma-Associated Pulmonary Hypertension

Angelini¹,

Su²,

Yamaji-Kegan³

et al. 2009

Am J Respir Cell Mol Biol

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Scleroderma is a systemic, mixed connective tissue disease that can impact the lungs through pulmonary fibrosis, vascular remodeling, and the development of pulmonary hypertension and right heart failure. Currently, little is known about the molecular mechanisms that drive this condition, but we have recently identified a novel gene product that is up-regulated in a murine model of hypoxia-induced pulmonary hypertension. This molecule, known as hypoxia-induced mitogenic factor (HIMF), is a member of the newly described resistin gene family. We have demonstrated that HIMF has mitogenic, angiogenic, vasoconstrictive, inflammatory, and chemokine-like properties, all of which are associated with vascular remodeling in the lung. Here, we demonstrate that the human homolog of HIMF, resistin-like molecule (RELM)-b, is expressed in the lung tissue of patients with scleroderma-associated pulmonary hypertension and is up-regulated compared with normal control subjects. Immunofluorescence colocalization revealed that RELM-b is expressed in the endothelium and vascular smooth muscle of remodeled vessels, as well as in plexiform lesions, macrophages, T cells, and myofibroblastlike cells. We also show that addition of recombinant RELM-b induces proliferation and activation of ERK1/2 in primary cultured human pulmonary endothelial and smooth muscle cells. These results suggest that RELM-b may be involved in the development of scleroderma-associated pulmonary hypertension.

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Activation of Alveolar Macrophages via the Alternative Pathway in Herpesvirus-Induced Lung Fibrosis

Cited by 163 publications

References 39 publications

Th2-like immune response in radiation-induced lung fibrosis

Th2-like immune response in radiation-induced lung fibrosis

Immunomodulatory activity of andrographolide on macrophage activation and specific antibody response

Resistin-Like Molecule-β in Scleroderma-Associated Pulmonary Hypertension

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