Direct Leukocyte Migration across Pulmonary Arterioles and Venules into the Perivascular Interstitium of Murine Lungs during Bleomycin Injury and Repair

Wang, Ping M.; Kachel, Diane L.; Cesta, Mark F.; Martin, William J.

doi:10.1016/j.ajpath.2011.02.047

Cited by 10 publications

(12 citation statements)

References 66 publications

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“…It is a connective tissue composed of extracellular matrix (ECM) which has a clear structural function in the maintenance of lung architecture but also in the migration of leukocytes [43]. Indeed ECM collagen fibers present in PVS may provide an attachment point for leukocyte motility around these pulmonary arteries or veins [44]. Accumulation of leukocytes has been observed in the PVS in models of lung infections, fibrosis, and allergic reactions [45–47].…”

Section: Discussionmentioning

confidence: 99%

IL-4 receptor dependent expansion of lung CD169+ macrophages in microfilaria-driven inflammation

Fercoq¹,

Remion²,

Frohberger³

et al. 2019

PLoS Negl Trop Dis

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Lung disease is regularly reported in human filarial infections but the molecular pathogenesis of pulmonary filariasis is poorly understood. We used Litomosoides sigmodontis, a rodent filaria residing in the pleural cavity responsible for pleural inflammation, to model responses to human filarial infections and probe the mechanisms. Wild-type and Th2-deficient mice (ΔdblGata1 and Il-4receptor(r)a -/-/IL-5 -/-) were infected with L. sigmodontis. Survival and growth of adult filariae and prevalence and density of microfilariae were evaluated. Cells and cytokines in the pleural cavity and bronchoalveolar space were characterized by imaging, flow cytometry and ELISA. Inflammatory pathways were evaluated by transcriptomic microarrays and lungs were isolated and analyzed for histopathological signatures. 40% of WT mice were amicrofilaremic whereas almost all mutant mice display blood microfilaremia. Microfilariae induced pleural, bronchoalveolar and lung-tissue inflammation associated with an increase in bronchoalveolar eosinophils and perivascular macrophages, production of mucus, visceral pleura alterations and fibrosis. Inflammation and pathology were decreased in Th2-deficient mice. An IL-4R-dependent increase of CD169 was observed on pleural and bronchoalveolar macrophages in microfilaremic mice. CD169 + tissue-resident macrophages were identified in the lungs with specific localizations. Strikingly, CD169 + macrophages increased significantly in the perivascular area in microfilaremic mice. These data describe lung inflammation and pathology in chronic filariasis and emphasize the role of Th2 responses according to the presence of microfilariae. It is also the first report implicating CD169 + lung macrophages in response to a Nematode infection.

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Section: Discussionmentioning

confidence: 99%

IL-4 receptor dependent expansion of lung CD169+ macrophages in microfilaria-driven inflammation

Fercoq¹,

Remion²,

Frohberger³

et al. 2019

PLoS Negl Trop Dis

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“…Our experiments have revealed the major accumulation of neutrophils in the perivascular compartment, which is recognized as an important part of lung architecture, with inflammatory cells having been repeatedly observed in this compartment in inflamed lungs (Pabst and Tschernig 2002;Tschernig et al 2008;Wang et al 2011). Recently, direct evidence of leukocyte recruitment into the perivascular compartment of the lung has been provided (Wang et al 2011).…”

Section: Discussionmentioning

confidence: 84%

“…Recently, direct evidence of leukocyte recruitment into the perivascular compartment of the lung has been provided (Wang et al 2011). The role of integrin β3 -/-in the perivascular recruitment of leukocytes in the inflamed lung might be of interest and requires further investigation.…”

Section: Discussionmentioning

confidence: 99%

Integrin β3 is not critical for neutrophil recruitment in a mouse model of pneumococcal pneumonia

et al. 2012

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Streptococcus pneumoniae is one of the most common causes of bacterial pneumonias in humans. Neutrophil migration into lungs infected with S. pneumoniae is central to the host defense but the mechanisms of neutrophil recruitment, as mediated by S. pneumoniae, into lungs are incompletely understood. Therefore, we have assessed the role of integrin αvβ3 by evaluating its subunit β3 in a mouse model of lung inflammation induced by S. pneumonia. Integrin subunit β3 knockout (β3(-/-)) and wild-type (WT) mice were intratracheally instilled with either S. pneumoniae or saline. Other groups of WT mice were treated intraperitoneally with 25 μg or 50 μg of antibody against integrin β3 or with isotype-matched antibody at 1 h before instillation of S. pneumoniae. Mice were killed 24 h after infection. Flow cytometry confirmed the absence or presence of integrin subunit β3 on peripheral blood neutrophils in β3(-/-) or WT mice, respectively. Neutrophil numbers in bronchoalveolar lavage (BAL) from infected β3(-/-) and WT mice showed no differences. Neutrophil numbers in BAL of infected WT mice treated with β3 antibody were lower compared with those without antibody but similar to those of mice administered isotype-matched antibody. Many neutrophils were present in the perivascular spaces of the lungs in β3(-/-) mice. Lungs from infected β3(-/-) mice had negligible mitogen-activated protein kinase expression compared with those of infected WT mice. Thus, integrin β3 or its heterodimer αvβ3 is not critical for neutrophil migration into lungs infected with S. pneumoniae.

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“…Our study provides rst immunohistochemical data showing increased pulmonary expression of ICAM-1, VCAM-1 and vWF proteins in glyphosate treated mice. It is well known that ICAM-1 and VCAM-1 engage selectins to slow-down rolling neutrophils and vWF secreted from Weibel-Palade bodies in endothelial cells facilitates recruitment of platelets (23,24) and is a marker of in ammation (25)(26)(27). The higher levels of cytokines such as IL-13 and IL-5 likely caused the observed increase in the expression of adhesion molecules in lungs of animals treated with glyphosate.…”

Section: Discussionmentioning

confidence: 97%

Lung Inflammation from Single and Repetitive Exposure to Glyphosate

Pandher

Kirychuk

Schneberger

et al. 2021

Preprint

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Background: Glyphosate is an active ingredient in herbicides used in agriculture worldwide. Exposure to glyphosate has been associated with respiratory dysfunctions in agricultural workers. However, the ability of glyphosate to induce inflammation in the lung is not well studied. Therefore, we evaluated lung inflammatory response to glyphosate at agricultural relevant dose for single and repetitive exposures. Methods: Male C57BL/6 mice were intranasally exposed to glyphosate (1 μg/40 μl) for 1-day or once daily for 5-days, and 10-days. After the exposure periods, mice were euthanized to collect the bronchoalveolar lavage (BAL) fluid and lung tissue. Results: Repetitive exposure to glyphosate for 5-days and 10-days showed an increase of neutrophils in BAL fluid and eosinophil peroxidase levels in lungs, a marker for eosinophils. Leukocyte infiltration in lungs was further confirmed through lung histology. Th2 cytokines including IL-5 and IL-13 were increased in BAL fluid after 10-days of glyphosate exposure whereas IL-4 was not increased. Lung sections from all glyphosate groups showed higher expression for ICAM-1, VCAM-1, and vWF adhesion molecules. TLR-4 and TLR-2 expression was increased in lungs after repetitive exposure to glyphosate. Conclusions: We conclude that repetitive exposure to glyphosate induces migration of neutrophils and eosinophils and release of Th2 cytokines. This study, for the first time, provides evidence for the role of ICAM-1, VCAM-1 and vWF in lungs of glyphosate-treated animals.

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Direct Leukocyte Migration across Pulmonary Arterioles and Venules into the Perivascular Interstitium of Murine Lungs during Bleomycin Injury and Repair

Cited by 10 publications

References 66 publications

IL-4 receptor dependent expansion of lung CD169+ macrophages in microfilaria-driven inflammation

IL-4 receptor dependent expansion of lung CD169+ macrophages in microfilaria-driven inflammation

Integrin β3 is not critical for neutrophil recruitment in a mouse model of pneumococcal pneumonia

Lung Inflammation from Single and Repetitive Exposure to Glyphosate

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