Adhesion assay formats

P-selectin Static Cell Adhesion Assay Formats... 

In vitro platelet-tumor cell adhesion assay If the ability of tumor cells to induce platelet aggregation has a prominent role in metastasis formation, it could be expected that its inhibition by specific drugs would reduce the amount of metastases produced by tumor cells with a pronounced TCIPA activity. 

The antiinflammatory effects of statins likely result from their ability to inhibit the formation of mevalonic acid. Downstream products of this molecule include not only the end product, cholesterol, but also several isoprenoid intermediates that covalently modify ( pre-nylate ) certain key intracellular signaling molecules. Statin treatment reduces leukocyte adhesion, accumulation of macrophages, MMPs, tissue factor, and other proinflammatory mediators. By acting on the MHC class II transactivator (CIITA), statins also interfere with antigen presentation and subsequent T-cell activation. Statin treatment can also limit platelet activation in some assays as well. All these results support the concept that in addition to their favorable effect on the lipid profile, statins can also exert an array of antiinflammatory and immunomodulatory actions. 

Stark, J. M., E. A. van, J. J. Zimmerman, S. K. Carabell, and M. F. Tosi. 1992. Detection of enhanced neutrophil adhesion to parainfluenza-infected airway epithelial cells using a modified myeloperoxidase assay in a microtiter format. J Virol Methods 40 225 -2. 

Other Cell Culture-Based Assays for Cell/Tissue Compatibility In addition biocompatibility behavior can be evaluated by seeding cells directly on the test material (similar to the wash-and-plate assay described in Section 4.4.8) and subsequent analysis of cell adhesion, cell proliferation, cell morphology, and cytoskeletal organization and the presence of cell-secreted extracellular matrix (ECM). A proper cell adhesion and the formation of ECM proteins, like fibronectin, are, for instance, essential steps for successful tissue integration of biomaterials. 

It is important to note that antimicrobial and biofilm resistance are two different characteristics though some materials show both properties at the same time. Antimicrobial materials do not automatically prevent biofilm formation and vice versa. Antimicrobial surfaces could kill bacteria on contact but if dead bacteria cell debris blocks the active biocidal surface, biofilm formation could eventually occur. For example, quaternary anunonium polymers can effectively kill bacteria but when the surface is fouled with dead bacteria debris, biofilm formation is inevitable [188]. Materials with antibiofilm properties will repel the bacterial adhesion very effectively but may not kill the bacteria when they do colonize the surface. PEG surfaces are well known to repel bacteria adhesion. However, PEG surfaces show little antimicrobial activity. Quantitative antibiofilm efficacy tests can be divided into two categories static (minimum biofilm eradication concentration assay, MBEC) and dynamic (flow cell assay). In addition, SEM is a semiquantitative assay, which is discussed in Section 2.5. 

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