Neutrophil Dependence of Vascular Remodeling after Mycoplasma Infection of Mouse Airways

Bałuk, Peter; Phillips, Keeley; Yao, Li‐Chin; Adams, Alicia; Nitschké, Maximilian; McDonald, Donald M.

doi:10.1016/j.ajpath.2014.02.010

Cited by 8 publications

(12 citation statements)

References 65 publications

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Section: Complementary Effects Of Ang2 and Tnf On Neutrophil Influx Amentioning

confidence: 99%

“…45 Neutrophils are known to contribute to vascular remodeling after infection, because vessel changes do not occur if neutrophil influx is blocked. 45 To determine whether inhibition of Ang2 and/or TNF reduced the influx of neutrophils, we quantified cells in the tracheal mucosa stained for the neutrophil marker S100a9 at 7 days after infection. 45 Neutrophils were uncommon in the tracheal mucosa of pathogen-free mice ( Figure 4 ½F4 ½F4 A) 8 but were abundant and widespread, but unevenly distributed, at 7 days after infection ( Figure 4B).…”

Section: Complementary Effects Of Ang2 and Tnf On Neutrophil Influx Amentioning

confidence: 99%

“…45 To determine whether inhibition of Ang2 and/or TNF reduced the influx of neutrophils, we quantified cells in the tracheal mucosa stained for the neutrophil marker S100a9 at 7 days after infection. 45 Neutrophils were uncommon in the tracheal mucosa of pathogen-free mice ( Figure 4 ½F4 ½F4 A) 8 but were abundant and widespread, but unevenly distributed, at 7 days after infection ( Figure 4B). Neutrophil influx was slightly reduced when Ang2 was inhibited during the infection, but was reduced more when TNF was blocked ( Figure 4, C, D, and F).…”

Section: Complementary Effects Of Ang2 and Tnf On Neutrophil Influx Amentioning

confidence: 99%

“…8,20,45 Vascular remodeling is reduced, but not prevented, by TNF blockade or deletion of TNF-a receptors (Tnfr1, Tnfrsf1a). 20 1117 1118 1119 1120 1121 1122 1123 1124 1125 1126 1127 1128 1129 1130 1131 1132 1133 1134 1135 1136 1137 1138 1139 1140 1141 1142 1143 1144 1145 1146 1147 1148 1149 1150 1151 1152 1153 1154 1155 1156 1157 1158 1159 1160 1161 1162 1163 1164 1165 1166 1167 1168 1169 1170 1171 1172 1173 1174...…”

Section: Q27mentioning

confidence: 99%

“…45 Ang2 and TNF contribute to the recruitment of these cells. TNF blockade during M. pulmonis infection reduces leukocyte influx into the lung, 20 and Ang2 blockade reduces CD11b-positive cell recruitment into the airway mucosa.…”

Section: Suppression Of Neutrophil Influx By Inhibition Of Ang2 and Tmentioning

confidence: 99%

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Synergistic Actions of Blocking Angiopoietin-2 and Tumor Necrosis Factor-α in Suppressing Remodeling of Blood Vessels and Lymphatics in Airway Inflammation

Laidlaw

Morehouse³

et al. 2015

The American Journal of Pathology

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Remodeling of blood vessels and lymphatics are prominent features of sustained inflammation. Angiopoietin-2 (Ang2)/Tie2 receptor signaling and tumor necrosis factor-α (TNF)/TNF receptor signaling are known to contribute to these changes in airway inflammation after Mycoplasma pulmonis infection in mice. We determined whether Ang2 and TNF are both essential for the remodeling on blood vessels and lymphatics, and thereby influence the actions of one another. Their respective contributions to the initial stage of vascular remodeling and sprouting lymphangiogenesis were examined by comparing the effects of function-blocking antibodies to Ang2 or TNF, given individually or together during the first week after infection. As indices of efficacy, vascular enlargement, endothelial leakiness, venular marker expression, pericyte changes, and lymphatic vessel sprouting were assessed. Inhibition of Ang2 or TNF alone reduced the remodeling of blood vessels and lymphatics, but inhibition of both together completely prevented these changes. Genome-wide analysis of changes in gene expression revealed synergistic actions of the antibody combination over a broad range of genes and signaling pathways involved in inflammatory responses. These findings demonstrate that Ang2 and TNF are essential and synergistic drivers of remodeling of blood vessels and lymphatics during the initial stage of inflammation after infection. Inhibition of Ang2 and TNF together results in widespread suppression of the inflammatory response.

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Section: Complementary Effects Of Ang2 and Tnf On Neutrophil Influx Amentioning

confidence: 99%

Section: Complementary Effects Of Ang2 and Tnf On Neutrophil Influx Amentioning

confidence: 99%

Section: Complementary Effects Of Ang2 and Tnf On Neutrophil Influx Amentioning

confidence: 99%

Section: Q27mentioning

confidence: 99%

Section: Suppression Of Neutrophil Influx By Inhibition Of Ang2 and Tmentioning

confidence: 99%

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Synergistic Actions of Blocking Angiopoietin-2 and Tumor Necrosis Factor-α in Suppressing Remodeling of Blood Vessels and Lymphatics in Airway Inflammation

Laidlaw

Morehouse³

et al. 2015

The American Journal of Pathology

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Underlying chronic inflammation alters the profile and mechanisms of acute neutrophil recruitment

Whiteford

Nourshargh

et al. 2016

The Journal of Pathology

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Chronically inflamed tissues show altered characteristics that include persistent populations of inflammatory leukocytes and remodelling of the vascular network. As the majority of studies on leukocyte recruitment have been carried out in normal healthy tissues, the impact of underlying chronic inflammation on ongoing leukocyte recruitment is largely unknown. Here, we investigate the profile and mechanisms of acute inflammatory responses in chronically inflamed and angiogenic tissues, and consider the implications for chronic inflammatory disorders. We have developed a novel model of chronic ischaemia of the mouse cremaster muscle that is characterized by a persistent population of monocyte‐derived cells (MDCs), and capillary angiogenesis. These tissues also show elevated acute neutrophil recruitment in response to locally administered inflammatory stimuli. We determined that Gr1low MDCs, which are widely considered to have anti‐inflammatory and reparative functions, amplified acute inflammatory reactions via the generation of additional proinflammatory signals, changing both the profile and magnitude of the tissue response. Similar vascular and inflammatory responses, including activation of MDCs by transient ischaemia–reperfusion, were observed in mouse hindlimbs subjected to chronic ischaemia. This response demonstrates the relevance of the findings to peripheral arterial disease, in which patients experience transient exercise‐induced ischaemia known as claudication.These findings demonstrate that chronically inflamed tissues show an altered profile and altered mechanisms of acute inflammatory responses, and identify tissue‐resident MDCs as potential therapeutic targets. © 2016 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.

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Role of iBALT in Respiratory Immunity

Silva-Sánchez

Randall

2019

Current Topics in Microbiology and Immunology

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Pulmonary respiration inevitably exposes the mucosal surface of the lung to potentially noxious stimuli, including pathogens, allergens, and particulates, each of which can trigger pulmonary damage and inflammation. As inflammation resolves, B and T lymphocytes often aggregate around large bronchi to form inducible Bronchus-Associated Lymphoid Tissue (iBALT). iBALT formation can be initiated by a diverse array of molecular pathways that converge on the activation and differentiation of chemokine-expressing stromal cells that serve as the scaffolding for iBALT and facilitate the recruitment, retention, and organization of leukocytes. Like conventional lymphoid organs, iBALT recruits naïve lymphocytes from the blood, exposes them to local antigens, in this case from the airways, and supports their activation and differentiation into effector cells. The activity of iBALT is demonstrably beneficial for the clearance of respiratory pathogens; however, it is less clear whether it dampens or exacerbates inflammatory responses to non-infectious agents. Here, we review the evidence regarding the role of iBALT in pulmonary immunity and propose that the final outcome depends on the context of the disease.

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Neutrophil Dependence of Vascular Remodeling after Mycoplasma Infection of Mouse Airways

Cited by 8 publications

References 65 publications

Synergistic Actions of Blocking Angiopoietin-2 and Tumor Necrosis Factor-α in Suppressing Remodeling of Blood Vessels and Lymphatics in Airway Inflammation

Synergistic Actions of Blocking Angiopoietin-2 and Tumor Necrosis Factor-α in Suppressing Remodeling of Blood Vessels and Lymphatics in Airway Inflammation

Underlying chronic inflammation alters the profile and mechanisms of acute neutrophil recruitment

Role of iBALT in Respiratory Immunity

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