Stored Red Blood Cells Selectively Activate Human Neutrophils to Release Il-8 and Secretory Pla2

Zallen, Garret; Moore, Ernest E.; Ciesla, David J.; Brown, Michelle; Biffl, Walter L.; Silliman, Christopher C.

doi:10.1097/00024382-200013010-00006

Cited by 149 publications

(101 citation statements)

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“…For example, RBC can efficiently bind inflammatory mediators such as interleukin-8 (IL-8); regulated on activation, normal T-expressed and secreted (RANTES); and monocyte chemotactic protein 1. These mediators can also be released from the RBC, indicating a role for RBC in the regulation of inflammation (8,9,12,33,53). In line with these data, we have recently demonstrated that RBC can stimulate fibroblast-mediated collagen gel contraction in a time-and concentration-dependent manner and that coculture results in increased release of fibronectin (16).…”

mentioning

confidence: 72%

Red blood cells increase secretion of matrix metalloproteinases from human lung fibroblasts in vitro

Fredriksson

Liu

Lundahl

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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mentioning

confidence: 72%

Red blood cells increase secretion of matrix metalloproteinases from human lung fibroblasts in vitro

Fredriksson

Liu

Lundahl

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…In our previous work, we have postulated that the lipid anomalies associated with MGD and DES might have resulted primarily from diminished lipid turnover, instead of an absolute defi ciency in lipids per se ( 20 ), which is in accordance ductal and acinar epithelia of gland tissues, which could possibly activate mitogen-activated protein kinase activity leading to the downstream release of chemokines and cytokines, therefore eliciting the ocular infl ammatory cascade, as has been previously demonstrated in conjunctival and corneal epithelial tissues ( 31,32 ). The induction of extracellular PLA 2 secretion from various cell types under an infl ammatory milieu has also been extensively documented (33)(34)(35)(36)(37). Therefore, the release of PLA 2 from meibomian gland acinar and ductal epithelia as a result of elevated intraglandular pressure might represent a plausible mechanistic pathway for the enhanced levels of lysophospholipids observed in the tears of MGD patients.…”

Section: Meibum-derived Amphiphilic Lipids In Maintaining Tear Fi Lm mentioning

confidence: 84%

Longitudinal changes in tear fluid lipidome brought about by eyelid-warming treatment in a cohort of meibomian gland dysfunction

Lam

Tong

Duan

et al. 2014

Journal of Lipid Research

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Dry eye syndrome (DES) is a prevalent ophthalmic condition adversely affecting up to 80% of the population over the age of 80, with potential debilitating effects on specifi c segments of the population such as contact lens wearers, people who have undergone refractive surgeries, postmenopausal women, and patients suffering from a variety of autoimmune disorders ( 1 ). DES is a multifactorial disease of the tears and ocular surface caused by a deficiency in tear production or excessive evaporation ( 2 ). Regardless of the initiating causes, chronic dryness and the resultant tear fi lm hyperosmolarity leads to infl ammation that jeopardizes the structural and functional integrity of the lacrimal gland, meibomian gland, and corneal and conjunctival epithelial tissues. The gradual destruction of Abstract Meibomian gland dysfunction (MGD) is a leading cause of evaporative dry eye and ocular discomfort characterized by an unstable tear fi lm principally attributed to affl icted delivery of lipids to the ocular surface. Herein, we elucidated longitudinal tear lipid alterations associated with disease alleviation and symptom improvement in a cohort of MGD patients undergoing eyelid-warming treatment for 12 weeks. Remarkably, eyelid-warming resulted in stark reductions in lysophospholipids ( P < 0.001 for lyso-plasmalogen phosphatidylethanolamine, lysophosphatidylcholine, and lysophosphatidylinositol), as well as numerous PUFAcontaining diacylglyceride species in tears, accompanied by signifi cant increases in several PUFA-containing phospholipids. These changes in tear lipidomes suggest that eyelidwarming leads to diminished activity of tear phospholipases that preferentially target PUFA-containing phospholipids. In addition, treatment led to appreciable increases ( P < 0.001) in O -acyl--hydroxy-FAs (OAHFAs), which are lipid amphiphiles critical to the maintenance of tear fi lm stability. Longitudinal changes in the tear lipids aforementioned also signifi cantly ( P < 0.05) correlated with reduced rate of ocular evaporation and improvement in ocular symptoms. The foregoing data thus indicate that excess ocular surface phospholipase activity detrimental to tear fi lm stability could be alleviated by eyelid warming alone without application of steroids and identify tear OAHFAs as suitable markers to monitor treatment response in MGD. -Man Lam, S

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“…Delayed PMN apoptosis has also been identified in human subjects and animal models by comparison of circulating PMNs with those isolated from bronchoalveolar lavage specimens (20,37), suggesting that our syngeneic bilayer model closely mimics the biology/physiology of the human lungs. However, we acknowledge that factors such as isolation-induced PMN priming (36,41) and cells lines instead of primary cells used in the experiments may interfere with the results, and caution should be taken with direct application of the data to the in vivo situations. Nonetheless, our results with the bilayer model may provide new insight in the molecular basis of PMN apoptosis regulation.…”

Section: Discussionmentioning

confidence: 99%

Regulation of polymorphonuclear leukocyte apoptosis: role of lung endothelium-epithelium bilayer transmigration

Hu¹,

Lin²,

Du³

et al. 2005

American Journal of Physiology-Lung Cellular and Molecular Phys

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Delayed polymorphonuclear leukocyte (PMN) apoptosis exacerbates acute lung injury. To reach the alveolar spaces, PMNs must migrate across both pulmonary endothelial and epithelial cell layers. We hypothesized that transmigration across the endotheliumepithelium bilayer suppresses PMN apoptosis and sought to elucidate the underlying mechanisms. PMNs freshly isolated from normal volunteers were allowed to migrate across polycarbonate membranes alone or membranes coated with a bilayer of human lung endothelial and epithelial cells. After migration toward different chemoattractants (IL-8, formyl-Met-Leu-Phe, or leukotriene B 4), PMN apoptosis and caspase activities were assessed by annexin V, histology, and enzymatic assays, respectively. Messenger RNA and specific protein expression in three receptor ligand-mediated, apoptosis-inducing pathways (Fas, TNF-␣, and TNF-related apoptosis-inducing ligand) were further examined by gene array, RT-PCR, flow cytometry, and Western blot analyses. The data demonstrated that transbilayer migration suppressed PMN apoptosis, and this effect was not chemoattractant type specific. Kinetic analyses further showed that the delay of apoptosis was sustained to at least 18 h. Transbilayer migration caused significant decreases in caspase (-3, -8, and -9) activities. The changes in apoptosis-related gene expression support the survival role of transbilayer migration. Furthermore, the reduced apoptosis was correlated with downregulation of Fas ligand and TNF receptor 1 expression. Our data reveal that migration across a lung endotheliumepithelium bilayer suppresses PMN apoptosis. The decreased activity and/or expression of proapoptotic proteins may provide possible targets for the regulation of inappropriate delay in PMN apoptosis during lung inflammation and injury. neutrophils; chemotaxis; interleukin-8

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Stored Red Blood Cells Selectively Activate Human Neutrophils to Release Il-8 and Secretory Pla2

Cited by 149 publications

References 0 publications

Red blood cells increase secretion of matrix metalloproteinases from human lung fibroblasts in vitro

Red blood cells increase secretion of matrix metalloproteinases from human lung fibroblasts in vitro

Longitudinal changes in tear fluid lipidome brought about by eyelid-warming treatment in a cohort of meibomian gland dysfunction

Regulation of polymorphonuclear leukocyte apoptosis: role of lung endothelium-epithelium bilayer transmigration

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