Monocyte Recruitment into the Lungs in Pneumococcal Pneumonia

Goto, Yukinobu; Hogg, James C.; Whalen, Beth A.; Shih, Chih-Horng; Ishii, Hiroshi; Eeden, Stephan F. van

doi:10.1165/rcmb.2003-0312oc

Cited by 37 publications

(40 citation statements)

References 25 publications

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“…The whole blood transfusion method (18,20) that has been developed in our laboratory does not require purification procedures and therefore avoids activation of the cells during a purification process. The protocol that we used to label the dividing monocytes in the bone marrow with the thymidine analog BrdU has been reported previously, and it labels Ͼ80% of circulating monocytes when blood is harvested from donors at 24 h from the first BrdU injection (20).…”

Section: Discussionmentioning

confidence: 99%

“…EHC-93 contained mainly fine particles, which composed 20% of the mass. Details about elemental composition and solubility of EHC-93 are described elsewhere (1,20,52). The endotoxin level in EHC-93 (0.096 endotoxin unit/ml) was too small to induce a systemic inflammatory response when instilled into the rabbit lungs (51).…”

Section: Pm10 Particlesmentioning

confidence: 99%

“…The monocytes of the donor rabbits were labeled in the marrow 3 days after the last (8th) instillation of either particles or saline by following the protocol previously described (18,20). Briefly, the thymidine analog BrdU (Sigma, St. Louis, MO) was injected intravenously at a dose of 100 mg/kg every 2 h for a total of five injections.…”

Section: Experimental Protocolmentioning

confidence: 99%

“…This results in BrdU labeling of ϳ80% of the monocytes present in whole blood harvested 24 h after the first BrdU injection, and Ͻ3% of BrdU-labeled cells in the blood sample are other than monocytes (PMN and lymphocytes) (18). These labeled cells were transfused into serum-compatible WHHL recipient rabbits in whole blood as previously described (20). Three days after the transfusion the recipient rabbits were killed with an overdose of pentobarbital, and thoracic and abdominal aorta were harvested.…”

Section: Experimental Protocolmentioning

confidence: 99%

“…The present study was designed to determine whether PM 10 exposure accelerates the recruitment of these monocytes into atherosclerotic plaques by transfusing whole blood (18,20) harvested from donor animals in which dividing monocytes in the marrow have been labeled with the thymidine analog 5-bromo-2Ј-deoxyuridine (BrdU) into recipient animals.…”

mentioning

confidence: 99%

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Particulate matter air pollution exposure promotes recruitment of monocytes into atherosclerotic plaques

Yatera

Hsieh²,

Hogg³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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demiologic studies have shown an association between exposure to ambient particulate air pollution Ͻ10 m in diameter (PM10) and increased cardiovascular morbidity and mortality. We previously showed that PM10 exposure causes progression of atherosclerosis in coronary arteries. We postulate that the recruitment of monocytes from the circulation into atherosclerotic lesions is a key step in this PM10-induced acceleration of atherosclerosis. The study objective was to quantify the recruitment of circulating monocytes into vessel walls and the progression of atherosclerotic plaques induced by exposure to PM10. Female Watanabe heritable hyperlipidemic rabbits, which naturally develop systemic atherosclerosis, were exposed to PM10 (EHC-93) or vehicle by intratracheal instillation twice a week for 4 wk. Monocytes, labeled with 5-bromo-2Ј-deoxyuridine (BrdU) in donors, were transfused to recipient rabbits as whole blood, and the recruitment of BrdU-labeled cells into vessel walls and plaques in recipients was measured by quantitative histological methodology. Exposure to PM10 caused progression of atherosclerotic lesions in thoracic and abdominal aorta. It also decreased circulating monocyte counts, decreased circulating monocytes expressing high levels of CD31 (platelet endothelial cell adhesion molecule-1) and CD49d (very late antigen-4 ␣-chain), and increased expression of CD54 (ICAM-1) and CD106 (VCAM-1) in plaques. Exposure to PM10 increased the number of BrdU-labeled monocytes adherent to endothelium over plaques and increased the migration of BrdU-labeled monocytes into plaques and smooth muscle underneath plaques. We conclude that exposure to ambient air pollution particles promotes the recruitment of circulating monocytes into atherosclerotic plaques and speculate that this is a critically important step in the PM10-induced progression of atherosclerosis. atherosclerosis; adhesion molecules EPIDEMIOLOGIC STUDIES have associated exposure to ambient particulate air pollution Ͻ10 m in diameter (PM 10

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Section: Discussionmentioning

confidence: 99%

Section: Pm10 Particlesmentioning

confidence: 99%

Section: Experimental Protocolmentioning

confidence: 99%

Section: Experimental Protocolmentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Particulate matter air pollution exposure promotes recruitment of monocytes into atherosclerotic plaques

Yatera

Hsieh²,

Hogg³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

Self Cite

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Ischemic stroke alters immune cell niche and chemokine profile in mice independent of spontaneous bacterial infection

Farris

Monaghan

Zheng

et al. 2019

Immunity Inflam & Disease

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Introduction Stroke‐associated pneumonia (SAP) is a major cause of mortality in patients who have suffered from severe ischemic stroke. Although multifactorial in nature, stroke‐induced immunosuppression plays a key role in the development of SAP. Previous studies using a murine model of transient middle cerebral artery occlusion (tMCAO) have shown that focal ischemic stroke induction results in functional defects of lymphocytes in the spleen, thymus, and peripheral blood, leading to spontaneous bacterial infection in the lungs without inoculation. However, how ischemic stroke alters immune cell niche and the expression of cytokines and chemokines in the lungs has not been fully characterized. Methods Ischemic stroke was induced in mice by tMCAO. Immune cell profiles in the brain and the lungs at 24‐ and 72‐hour time points were compared by flow cytometric analysis. Cytokine and chemokine expression in the lungs were determined by multiplex bead arrays. Tissue damage and bacterial burden in the lungs following tMCAO were evaluated. Results Ischemic stroke increases the percentage of alveolar macrophages, neutrophils, and CD11b+ dendritic cells, but reduces the percentage of CD4+ T cells, CD8+ T cells, B cells, natural killer cells, and eosinophils in the lungs. The alteration of immune cell niche in the lungs coincides with a significant reduction in the levels of multiple chemokines in the lungs, including CCL3, CCL4, CCL5, CCL17, CCL20, CCL22, CXCL5, CXCL9, and CXCL10. Spontaneous bacterial infection and tissue damage following tMCAO, however, were not observed. Conclusion This is the first report to demonstrate a significant reduction of lymphocytes and multiple proinflammatory chemokines in the lungs following ischemic stroke in mice. These findings suggest that ischemic stroke directly impacts pulmonary immunity.

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Alcohol abuse and Streptococcus pneumoniae infections: consideration of virulence factors and impaired immune responses

Bhatty

Pruett

Swiatlo

et al. 2011

Alcohol

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Alcohol is the most frequently abused substance in the world. Both acute and chronic alcohol consumption have diverse and well documented effects on the human immune system, leading to increased susceptibility to infections like bacterial pneumonia. S. pneumoniae is the most common bacterial etiology of community acquired pneumonia world-wide. The frequency and severity of pneumococcal infections in individuals with a history of alcohol abuse is much higher than the general population. Despite this obvious epidemiological relevance, very few experimental studies have focused on the interaction of pneumococci with the immune system of a host acutely or chronically exposed to alcohol. Understanding these host-pathogen interactions is imperative for designing effective prophylactic and therapeutic interventions for such populations. Recent advances in pneumococcal research have greatly improved our understanding of pneumococcal pathogenesis and virulence mechanisms. Additionally, a large body of data is available on the effect of alcohol on the physiology of the lungs and the innate and adaptive immune system of the host. The purpose of this review is to integrate the available knowledge in these diverse areas of for a better understanding of the how the compromised immune system derived from alcohol exposure responds to pneumococcal infections.

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Monocyte Recruitment into the Lungs in Pneumococcal Pneumonia

Cited by 37 publications

References 25 publications

Particulate matter air pollution exposure promotes recruitment of monocytes into atherosclerotic plaques

Particulate matter air pollution exposure promotes recruitment of monocytes into atherosclerotic plaques

Ischemic stroke alters immune cell niche and chemokine profile in mice independent of spontaneous bacterial infection

Alcohol abuse and Streptococcus pneumoniae infections: consideration of virulence factors and impaired immune responses

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