Alternatively activated alveolar macrophages in pulmonary fibrosis—mediator production and intracellular signal transduction

Pechkovsky, Dmitri V.; Prasse, Antje; Kollert, Florian; Engel, Kathrin M.; Dentler, Jan; Luttmann, Werner; Friedrich, Karlheinz; Müller–Quernheim, Joachim; Zissel, Gernot

doi:10.1016/j.clim.2010.06.017

Cited by 287 publications

(207 citation statements)

References 53 publications

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“…Nonetheless, it is known that during fibrogenesis alveolar macrophages acquire a proinflammatory and profibrotic phenotype, which is characterized by elevated expression of both CD11b and CD206 (45,46). There is evidence for increased expression of CD206 + macrophages in alveolar macrophages isolated from patients with IPF versus controls, which is compatible with the fibrogenic role of this subset of alveolar macrophages (47). In the present study, bleomycin treatment induced a selective increase in both the number of CD11b + cells and the cell surface expression of CD11b within 7 days, whereas similar changes in CD206 + cells only appeared 14 days after bleomycin treatment (Figure 8, B and C).…”

Section: Discussionsupporting

confidence: 69%

Cannabinoid CB1 receptor overactivity contributes to the pathogenesis of idiopathic pulmonary fibrosis

Çınar¹,

Gochuico²,

Iyer³

et al. 2017

JCI Insight

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Section: Discussionsupporting

confidence: 69%

Cannabinoid CB1 receptor overactivity contributes to the pathogenesis of idiopathic pulmonary fibrosis

Çınar¹,

Gochuico²,

Iyer³

et al. 2017

JCI Insight

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“…As previously shown, these observations suggest that ER stress in macrophages exposed to chrysotile induces cell survival (38,41,42). Several chronic diseases have demonstrated that macrophage cell survival has an important role in disease progression (43)(44)(45)(46). Our observations suggest that the UPR induce cell survival in macrophages, which mediates fibrosis development in lung.…”

Section: Discussionsupporting

confidence: 66%

Asbestos-induced Disruption of Calcium Homeostasis Induces Endoplasmic Reticulum Stress in Macrophages

Ryan¹,

Larson‐Casey

et al. 2014

Journal of Biological Chemistry

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Background:Macrophages are important cells in fibrotic diseases. Results: Chrysotile increases cytosolic calcium (Ca 2ϩ ) and induces endoplasmic reticulum (ER) stress in macrophages in a Ca 2ϩ -dependent manner. ER stress is found in alveolar macrophages from fibrotic lungs. Conclusion: Chrysotile triggers ER Ca 2ϩ leak and induces ER stress in macrophages. Significance: Macrophages undergo ER stress, which may contribute to pulmonary fibrosis.

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“…By 28 days, macrophages staining positively for these M2 markers were enlarged, vacuolated, and clustered in thickened alveoli surrounding areas of fibrosis, supporting their profibrotic activity (29,30). Epidemiological evidence, as well as experimental models of idiopathic and chemical-induced fibrosis, have shown that CD163 and CD206 M2 macrophages contribute to fibrogenesis in the lung, kidney, and peritoneum (31)(32)(33)(34)(35). Our findings suggest that they may play a similar role in lung fibrosis after NM exposure; however, this remains to be investigated.…”

Section: Discussionmentioning

confidence: 99%

Characterization of Distinct Macrophage Subpopulations during Nitrogen Mustard–Induced Lung Injury and Fibrosis

Venosa¹,

Malaviya²,

Choi³

et al. 2016

Am J Respir Cell Mol Biol

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Nitrogen mustard (NM) is an alkylating agent known to cause extensive pulmonary injury progressing to fibrosis. This is accompanied by a persistent macrophage inflammatory response. In these studies, we characterized the phenotype of macrophages accumulating in the lung over time following NM exposure. Treatment of rats with NM (0.125 mg/kg, intratracheally) resulted in an increase in CD11b 1 macrophages in histologic sections. These cells consisted of inducible nitric oxide synthase 1 (iNOS) proinflammatory M1 macrophages, and CD68 1 M1 macrophages and mature CD43 2 M2 macrophages, which increased sequentially. Time-related increases in M1 (iNOS, IL-12a, COX-2, TNF-a, matrix metalloproteinase-9, matrix metalloproteinase-10) and M2 (IL-10, pentraxin-2, connective tissue growth factor, ApoE) genes, as well as chemokines/ chemokine receptors associated with trafficking of M1 (CCR2, CCR5, CCL2, CCL5) and M2 (CX 3 CR1, fractalkine) macrophages to sites of injury, were also noted in macrophages isolated from the lung after NM. The appearance of M1 and M2 macrophages in the lung correlated with NM-induced acute injury and the development of fibrosis, suggesting a potential role of these macrophage subpopulations in the pathogenic response to NM.

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Alternatively activated alveolar macrophages in pulmonary fibrosis—mediator production and intracellular signal transduction

Cited by 287 publications

References 53 publications

Cannabinoid CB1 receptor overactivity contributes to the pathogenesis of idiopathic pulmonary fibrosis

Cannabinoid CB1 receptor overactivity contributes to the pathogenesis of idiopathic pulmonary fibrosis

Asbestos-induced Disruption of Calcium Homeostasis Induces Endoplasmic Reticulum Stress in Macrophages

Characterization of Distinct Macrophage Subpopulations during Nitrogen Mustard–Induced Lung Injury and Fibrosis

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