Serum amyloid P attenuates M2 macrophage activation and protects against fungal spore–induced allergic airway disease

Moreira, Ana Paula; Cavassani, Karen A.; Hullinger, Rikki; Rosada, Rogério Silva; Fong, Daniel J.; Murray, Lynne A.; Hesson, Dave; Hogaboam, Cory M.

doi:10.1016/j.jaci.2010.06.010

Cited by 115 publications

(104 citation statements)

References 45 publications

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“…Elevated numbers of IL-4R + macrophages have been reported in asthmatic patients with defective lung function (76). Moreover, the presence of IL-4R + macrophages exacerbates allergen-induced airway inflammation, whereas reduction of IL-4R + macrophages alleviates this disease (77,78).…”

Section: Hypoxia and Hypoxia-inducible Factorsmentioning

confidence: 99%

Hypoxia-inducible factors: key regulators of myeloid cells during inflammation

Lin¹,

Simon²

2016

Journal of Clinical Investigation

119

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Section: Hypoxia and Hypoxia-inducible Factorsmentioning

confidence: 99%

Hypoxia-inducible factors: key regulators of myeloid cells during inflammation

Lin¹,

Simon²

2016

Journal of Clinical Investigation

119

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“…7,21,39). Experimental studies have not adequately clarified the role of IL-17A in experimental asthmatic responses, since this cytokine can negatively regulate (40)(41)(42) or exacerbate (26,43) features of this disease. In addition, IL-17A drives neutrophil-mediated pulmonary fibrosis in a model of bleomycin-induced fibrosis (44).…”

Section: Figurementioning

confidence: 99%

The protective role of TLR6 in a mouse model of asthma is mediated by IL-23 and IL-17A

Moreira¹,

Cavassani²,

Ismailoglu³

et al. 2011

J. Clin. Invest.

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TLRs are a family of receptors that mediate immune system pathogen recognition. In the respiratory system, TLR activation has both beneficial and deleterious effects in asthma. For example, clinical data indicate that TLR6 activation exerts protective effects in asthma. Here, we explored the mechanism or mechanisms through which TLR6 mediates this effect using mouse models of Aspergillus fumigatus-induced and house dust mite antigen-induced (HDM antigen-induced) chronic asthma. Tlr6 -/-mice with fungal-or HDM antigen-induced asthma exhibited substantially increased airway hyperresponsiveness, inflammation, and remodeling compared with WT asthmatic groups. Surprisingly, whole-lung levels of IL-23 and IL-17 were markedly lower in Tlr6 -/-versus WT asthmatic mice. Tlr6 -/-DCs generated less IL-23 upon activation with lipopolysaccharide, zymosan, or curdlan. Impaired IL-23 generation in Tlr6 -/-mice also corresponded with lower levels of expression of the pathogen-recognition receptor dectin-1 and expansion of Th17 cells both in vivo and in vitro.

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“…In vitro, macrophage polarization to an M2 phenotype has only been shown robustly with mouse cells. Here the differentiation of a monocyte to an M2 phenotype requires a cocktail of cytokines including IL13 and CCL17/TARC 75 . Therefore the Th2 cytokine profile observed in remodeled lungs contributes to the appearance of M2 macrophages.…”

Section: Fibroblast Cell: Cell Interactionsmentioning

confidence: 99%

“…SAP promotes the differentiation of M1 classically activated macrophages in a tuberculosis model of lung infection 145 . We have recently demonstrated that SAP has prominent immunomodulatory effects on mouse macrophages, thereby providing a mechanism for its ability to prevent the development and reverse established experimental fungal airway disease 75 . Moreover, human SAP has been shown to potently inhibit the differentiation of monocytes into fibrocytes 146 and it has consequently been used therapeutically in animal models to inhibit lung fibrosis and fibrosis in a number of organ sites.…”

Section: Pentraxinsmentioning

confidence: 99%

“…Moreover, human SAP has been shown to potently inhibit the differentiation of monocytes into fibrocytes 146 and it has consequently been used therapeutically in animal models to inhibit lung fibrosis and fibrosis in a number of organ sites. In addition, SAP causes an inhibition of the differentiation of peripheral blood mononuclear cells into CD45 + /collagen I + cells called fibrocytes 76,146,147 , as well as reducing M2 macrophage number 75,77 .…”

Section: Pentraxinsmentioning

confidence: 99%

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