Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.37 (neutrophil elastase)
 4,078 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have examined the expression of three endothelial adhesion molecules (intercellular adhesion molecule-1 [ICAM-1], endothelial leukocyte adhesion molecule-1 [ELAM-1], and vascular cell adhesion molecule-1 [VCAM-1]) in normal human skin following intradermal injection of stratum corneum-derived interleukin-1 alpha (SCIL-1 alpha). In control skin, constitutive expression of ICAM-1 was found on endothelial cells and at low levels on dermal dendritic cells but not on keratinocytes. ELAM-1 and VCAM-1 were present in low levels on endothelium and perivascular dendritic cells, respectively. SCIL-1 alpha injection produced marked endothelial ELAM-1 upregulation. Double staining with neutrophil elastase demonstrated that many ELAM-1-positive vessels contained marginating neutrophils and that interstitial neutrophils were clustered around ELAM-1-positive vessels. An increase in dermal dendritic cell ICAM-1 expression occurred and in two of three biopsies there was keratinocyte expression of ICAM-1 in the SCIL-1 alpha-injected tissue. Also, there was upregulation of VCAM-1 on vascular endothelium and an increase in the dermal dendritic cell expression of this molecule. These results give in vivo confirmation that SCIL-1 alpha modulated endothelial and dermal dendritic cell adhesion molecule expression, and show that endothelial VCAM-1 is regulated in vivo by SCIL-1 alpha, thus providing a regulatable ICAM-1-independent means of mononuclear cell recruitment.
 ...
PMID:Effect of in vivo interleukin-1 on adhesion molecule expression in normal human skin. 137 29

Baboons were subjected to septic or traumatic/hypovolemic shock and their tissues were examined for the de novo expression of endothelial leukocyte adhesion molecule 1 (ELAM-1), using immunohistochemical techniques. In animals with septic shock induced with live Escherichia coli, there was widespread expression of ELAM-1, recognized by monoclonal antibodies H4/18 or ENA-1 in most tissues examined with strong staining in the lung, liver, and kidneys. Endothelial leukocyte adhesion molecule 1 expression was evident in capillaries, venules, small veins, arterioles, and arteries. In contrast, baboons with traumatic/hypovolemic shock had minimal levels of focal ELAM expression in all organs studied. Similarly evidence of neutrophil activation, measured by granulocyte elastase levels in the plasma was much more pronounced in animals with septic shock. The study documents that lipopolysaccharide (LPS)- and cytokine-induced endothelial activation occurs in vivo in septic shock. Much higher levels of ELAM-1 expression and plasma granulocyte-elastase titer in septic shock, as contrasted with traumatic/hypovolemic shock, are consistent with the higher levels of circulating tumor necrosis factor, other cytokines, and LPS in sepsis.
 ...
PMID:Expression of endothelial leukocyte adhesion molecule-1 in septic but not traumatic/hypovolemic shock in the baboon. 171 43

Twenty-nine psoriatics were examined using a model with clinical, physiological and pathological assessment parameters. The three parts in this assessment model include: (1) clinical assessment: psoriasis area and severity index (PASI); (2) assessment of skin physiology and microcirculation: water content of stratum corneum, water-holding capacity of stratum corneum, transepidermal water loss, intravital dynamic videocapillaroscopy-measuring the capillary diameters and blood cell velocity in proximal nailfold of ring finger, and fluorescence angiography-measuring transcapillary Na-fluorescein(NAF) diffusion; and (3) immunohistochemistry examination: markers of proliferation (Ki67Ag), differentiation (involucrin), and inflammation (neutrophil elastase, intercellular adhesion molecule-1(ICAM-1), endothelial leukocyte adhesion molecule-1(ELAM-1)). Our results showed both the transcapillary diffusion of NAF and the expression of cell markers-dermal neutrophil elastase, epidermal ELAM-1 and Ki67Ag--correlated significantly to PASI scores (P < 0.05, linear regression). According to our results, the increased capillary permeability and inflammation markers, and enhanced expression of Ki67Ag correlated very well with PASI score. These markers could serve as alternative methods for assessment of the clinical severity of psoriatic patients.
 ...
PMID:Quantitative assessments of physiological and biological parameters in psoriatic lesions and its correlations to the clinical severity of psoriasis. 1171 40

Mucosal Leishmaniasis (ML) may occur in both nasal and oral mucosa. However, despite the impressive tissue destruction, little is known about the oral involvement. To compare some changes underlying inflammation in oral and nasal ML, we performed immunohistochemistry on mucosal tissue of 20 patients with ML (nasal [n = 12]; oral [n = 8] lesions) and 20 healthy donors using antibodies that recognize inflammatory markers (CD3, CD4, CD8, CD22, CD68, neutrophil elastase, CD1a, CLA, Ki67, Bcl-2, NOS2, CD62E, Fas and FasL). A significantly larger number of cells, mainly T cells and macrophages, were observed in lesions than in healthy tissue. In addition, high nitric oxide synthase 2 (NOS2) expression was associated with a reduced detection of parasites, highlighting the importance of NOS2 for parasite elimination. Oral lesions had higher numbers of neutrophils, parasites, proliferating cells and NOS2 than nasal lesions. These findings, together with the shorter duration of oral lesions and more intense symptoms, suggest a more recent inflammatory process. It could be explained by lesion-induced oral cavity changes that lead to eating difficulties and social stigma. In addition, the frequent poor tooth conservation and gingival inflammation tend to amplify tissue destruction and symptoms and may impair and confuse the correct diagnosis, thus delaying the onset of specific treatment.
 ...
PMID:Comparative study of the in situ immune response in oral and nasal mucosal leishmaniasis. 2209 33