Neutrophil Migration through Preexisting Holes in the Basal Laminae of Alveolar Capillaries and Epithelium during Streptococcal Pneumonia

Walker, David C.; Behzad, Ali Reza; Chu, Fanny

doi:10.1006/mvre.1995.1067

Cited by 105 publications

(85 citation statements)

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“…At each time point, for light microscopy and immunohistologic examination, bilateral whole tendons (from 6 runners and 4 controls) were removed with the supraspinatus muscle still attached and fixed in fresh 4% paraformaldehyde for 16-24 hours at 4°C, then subsequently dehydrated, paraffin embedded, and sectioned longitudinally. For transmission electron microscopy (TEM) (4 runner and 2 control tendons per time point), tendons were rapidly dissected, cut into 1-mm 3 pieces, fixed in 2.5% glutaraldehyde in 1M sodium cacodylate buffer for 24 hours, and processed for TEM as previously carried out in the same facility (30).…”

Section: Methodsmentioning

confidence: 99%

Tenocyte responses to mechanical loading in vivo: A role for local insulin‐like growth factor 1 signaling in early tendinosis in rats

Scott

Cook

Hart

et al. 2007

Arthritis & Rheumatism

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143

138

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Objective. To investigate tenocyte regulatory events during the development of overuse supraspinatus tendinosis in rats.Methods. Supraspinatus tendinosis was induced by running rats downhill at 1 km/hour for 1 hour a day. Tendons were harvested at 4, 8, 12, and 16 weeks and processed for brightfield, polarized light, or transmission electron microscopy. The development of tendinosis was assessed semiquantitatively using a modified Bonar histopathologic scale. Apoptosis and proliferation were examined using antibodies against fragmented DNA or proliferating cell nuclear antigen, respectively. Insulin-like growth factor 1 (IGF-1) expression was determined by computer-assisted quantification of immunohistochemical reaction. Local IGF-1 signaling was probed using antibodies to phosphorylated insulin receptor substrate 1 (IRS-1) and ERK-1/2.Results. Tendinosis was present after 12 weeks of downhill running and was characterized by tenocyte rounding and proliferation as well as by glycosaminoglycan accumulation and collagen fragmentation. The proliferation index was elevated in CD90؉ tenocytes in association with tendinosis and correlated with increased local IGF-1 expression by tenocytes and phosphorylation of IRS-1 and ERK-1/2. Both apoptosis and cellular inflammation were absent at all time points. Conclusion. In this animal model, early tendinosis was associated with local stimulation of tenocytes rather than with extrinsic inflammation or apoptosis. Our data suggest a role for IGF-1 in the load-induced tenocyte responses during the pathogenesis of overuse tendon disorders.

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Section: Methodsmentioning

confidence: 99%

Tenocyte responses to mechanical loading in vivo: A role for local insulin‐like growth factor 1 signaling in early tendinosis in rats

Scott

Cook

Hart

et al. 2007

Arthritis & Rheumatism

Self Cite

143

138

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“…Is there a mechanical explanation? Walker and colleagues (21,274) believe that in vivo the basement membrane is perforated with preexisting holes and neutrophils gain access to the interstitial space by migrating through these holes (Fig. 5).…”

Section: B Preexisting Holes In the Basement Membranementioning

confidence: 99%

“…In rabbits and mice, the majority (75-80%) of capillary endothelial tight junctions are located at the intersection of thick and thin walls of the alveolar septum (274). Since the majority of neutrophil migration in the alveolar capillaries appears to occur at tricellular corners (275), it follows that thick walls are the principal site into which neutrophils migrate.…”

Section: B Preexisting Holes In the Basement Membranementioning

confidence: 99%

“…Pericyte profiles are clustered at or near the intersection of the thin and thick wall. Endothelial tight junctions are associated with pericyte profiles in a nonrandom fashion, and ϳ40% of the pericyte profiles around alveolar capillaries are within 0.5 m of endothelial tight junctions (242,274). In other tissues, pericytes surround capillaries and make numerous contacts with the endothelium (209,239,241,261).…”

Section: B Preexisting Holes In the Basement Membranementioning

confidence: 99%

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Unique Structural Features That Influence Neutrophil Emigration Into the Lung

Burns

Smith²,

Walker³

2003

Physiological Reviews

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262

272

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Neutrophil emigration in the lung differs substantially from that in systemic vascular beds where extravasation occurs primarily through postcapillary venules. Migration into the alveolus occurs directly from alveolar capillaries and appears to progress through a sequence of steps uniquely influenced by the cellular anatomy and organization of the alveolar wall. The cascade of adhesive and stimulatory events so critical to the extravasation of neutrophils from postcapillary venules in many tissues is not evident in this setting. Compelling evidence exists for unique cascades of biophysical, adhesive, stimulatory, and guidance factors that arrest neutrophils in the alveolar capillary bed and direct their movement through the endothelium, interstitial space, and alveolar epithelium. A prominent path accessible to the neutrophil appears to be determined by the structural interactions of endothelial cells, interstitial fibroblasts, as well as type I and type II alveolar epithelial cells.

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“…Despite these fi ndings, in the light of the known resistance of the BM to mechanical damage and its impermeable nature, it remains unclear how neutrophils may cross this barrier without disrupting its intricate threedimensional structure. Of relevance, Walker et al previously reported on neutrophil migration through holes in the BM of alveolar capillaries (24), though there is no strong evidence for the existence of such regions in venular BMs.…”

mentioning

confidence: 96%

Venular basement membranes contain specific matrix protein low expression regions that act as exit points for emigrating neutrophils

Wang¹,

Voisin²,

Larbi³

et al. 2006

The Journal of Cell Biology

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Neutrophil Migration through Preexisting Holes in the Basal Laminae of Alveolar Capillaries and Epithelium during Streptococcal Pneumonia

Cited by 105 publications

References 0 publications

Tenocyte responses to mechanical loading in vivo: A role for local insulin‐like growth factor 1 signaling in early tendinosis in rats

Tenocyte responses to mechanical loading in vivo: A role for local insulin‐like growth factor 1 signaling in early tendinosis in rats

Unique Structural Features That Influence Neutrophil Emigration Into the Lung

Venular basement membranes contain specific matrix protein low expression regions that act as exit points for emigrating neutrophils

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