Medical tranfer is a core activity of the Laboratoire Adhesion et Inflammation. This transfer relies on several peculiarities of this laboratory, which are the gathering of medical doctors and physicists, the location of a facility of the laboratory inside the university hospitals of Marseilles, and the dedication of the team members to the set-up of original methodology.
Medical transfer in LAI is done both by technological transfer and scientific or conceptual transfer to medical questions. It works mostly by applying the quantitative methods developed for the fundamental study of the immune response to relevant medical questions. The LAI facility is indeed in the immunology laboratory of Marseilles university hospital, and LAI has tackled several questions relative to the activity of this medical laboratory, as follows :
-In 2011, the ability do detect immune defects relative to adhesion molecules was added to the medical laboratory, using functional tests (laminar flo chamber and RICM) that allow diagnosis regardless of genetics. A first pediatric diagnosis of a LAD-III variant was then made (JI 2011). (Fig. 1)
-A patent was given in 2014 for an automated system for detection of positive in the immunofluorescence antinuclear antibodies test. This system is routinely used in the hospital laboratory both for diagnosis and medical residents formation (Patent).
-A collaboration with the critical care unit of Pr Papazian allowed us to test both leukocyte deformability (using a microfluidic device) and leukocyte adhesion (using a laminar flow chamber) while cells were incubated with ARDS or sepsis patients. ARDS serum itself triggers rigidification (Fig.2) but not adhesion of leukocytes to endothelial cells, Il-1 an TNF-alpha blockade reverses this phenotype (CritCare 2016).
Figure 1 : Neutrophil adhesion under flow. Neutrophils from control (white bars), LAD-III (black bars), or from another patient with LAD-I (gray bars) were driven along ICAM-1–coated surfaces in a laminar flow chamber. The motion of individual cells was monitored (1205 control cells, 414 cells from LAD-III patient, and 692 cells from a patient with LAD-I) for quantitative determination of the number of (A) total detectable arrests (duration >200 ms) and (B) durable arrests (>1 min duration). Experiments were done in control medium with unstimulated cells, cells that had been incubated in EDTA or stimulated with fMLF (fMLP), PMA, or in medium supplemented with Mn2+. Results are expressed in mean (SD). Decrease significant at *p < 0.05 and **p < 0.01.
Figure 2 : Stiffness vs. lung injury. Distributions of the median entry times in a microfluidic constriction (ETs) measured after 1-h incubation of THP-1 cells with the sera of healthy donors (control; n = 5), patients with acute cardiogenic pulmonary edema (ACPE; n = 6), patients with mild acute respiratory distress syndrome (ARDS; n = 9, among whom 5 had septic shock [SS]), and patients with moderate to severe ARDS (n = 13, among whom 10 had septic shock). b Stiffness vs. SS. Distributions of the median ETs measured after 1-h incubation of THP-1 cells with the sera of healthy subjects (n = 5), patients with ACPE (n = 6), patients with ARDS but without septic shock (n = 7), and patients with both ARDS and septic shock (n = 15). The number of tested cells per patient was 50. Box plots represent the median (black bar inside box), interquartile range (box), and minimum and maximum values (whiskers). *p < 0.05; **p < 0.0025; ***p < 0.0001 (Mann-Whitney U test).