Expression of natural antimicrobial peptide β-defensin-2 and Langerhans cell accumulation in epidermis from human non-healing leg ulcers

Chronic wounds like venous calf and diabetic foot ulcers are frequently contaminated and colonized by bacteria and it remains unclear whether there is sufficient expression of defensins and recruitment of epidermal Langerhans cells in the margin of ulcer compared to normal skin. The aim of this study was to examine immunohistochemically the expression of β-defensin-2 (hBD2), GM-CSF, VEGF growth factors and accumulation of CD1a+ Langerhans cells (LC) in epidermis from chronic skin ulcers and to compare it to normal skin from the corresponding areas. Studies were carried out in 10 patients with diabetic foot, 10 patients with varicous ulcers of the calf and 10 patients undergoing orthopedic surgery (normal skin for control). Biopsy specimens were immunostained using specific primary antibodies, LSAB+ kit based on biotin-avidinperoxidase complex technique and DAB chromogen. Results were expressed as a mean staining intensity. Statistical analysis of staining showed significantly higher staining of hBD2 in both normal and ulcerated epidermis from foot sole skin compared to calf skin (normal and ulcerated,

Lymphedema is more than excess of fluid; a lympho-fibro-adipo-edema

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Staphylococcal and enterococcal virulence -a review

The microbial adherence to cells and extracellular matrix is considered as an essential first step in the process of colonization and infection. A well-characterized family of staphylococcal surface adhesins, called MSCRAMMs ("microbial surface components recognizing adhesive matrix molecules") are known to mediate adherence to host extracellular matrix components, such as fibrinogen, fibronectin and collagen The virulence mechanisms that characterize Escherichia coli are genetically coded by chromosomal, plasmid, and bacteriophage DNAs and include heat-labile (LTI, LTIIa, and LTIIb) and heat-stable (STI and STII) toxins, verotoxin types 1, 2, and 2e (VT1, VT2, and VT2e, respectively), cytotoxic necrotizing factors (CNF1 and CNF2), attaching and effacing mechanisms (eaeA), enteroaggregative mechanisms (Eagg), and enteroinvasive mechanisms (Einv) Adhesins Human staphylococcal infections are frequent. There are numerous portals of entry to the human's body: hair follicle, break in the skin, surgical wound, foreign bodies, respiratory tract

Optimal intermittent pneumatic compression in lymphedema

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Expression of natural antimicrobial peptide β-defensin-2 and Langerhans cell accumulation in epidermis from human non-healing leg ulcers

Chronic wounds like venous calf and diabetic foot ulcers are frequently contaminated and colonized by bacteria and it remains unclear whether there is sufficient expression of defensins and recruitment of epidermal Langerhans cells in the margin of ulcer compared to normal skin. The aim of this study was to examine immunohistochemically the expression of β-defensin-2 (hBD2), GM-CSF, VEGF growth factors and accumulation of CD1a+ Langerhans cells (LC) in epidermis from chronic skin ulcers and to compare it to normal skin from the corresponding areas. Studies were carried out in 10 patients with diabetic foot, 10 patients with varicous ulcers of the calf and 10 patients undergoing orthopedic surgery (normal skin for control). Biopsy specimens were immunostained using specific primary antibodies, LSAB+ kit based on biotin-avidinperoxidase complex technique and DAB chromogen. Results were expressed as a mean staining intensity. Statistical analysis of staining showed significantly higher staining of hBD2 in both normal and ulcerated epidermis from foot sole skin compared to calf skin (normal and ulcerated, p<0.05). Chronic ulcers showed the same expression of hBD2 as normal skin. There was significantly lower accumulation of CD1a+ LC in normal epidermis from foot sole skin compared to normal calf skin (p<0.05). Accumulation of CD1a+ LC and GM-CSF upregulation at the border area of diabetic foot ulcer and reduction of LC concentration at the margin of venous calf ulcer compared to normal skin were observed. It seems that normal calf and sole epidermis is, unlike in the mechanisms of innate immunity, influenced by the different keratinocyte turnover and bacterial flora colonizing these regions. Insufficient upregulation of hBD2 in both diabetic foot and venous calf ulcers may suggest the pathological role of this protein in the chronicity of ulcers

The long-term arterial assist intermittent pneumatic compression generating venous flow obstruction is responsible for improvement of arterial flow in ischemic legs.

BACKGROUND:There is a large group of patients with ischemia of lower limbs not suitable for surgical reconstruction of arteries treated with the help of external assist by intermittent pneumatic compression devices (IPC). Until recently the generally accepted notion was that by compressing tissues below the knee, veins become emptied, venous pressure drops to zero and the increased arterial-venous pressure gradient enables greater arterial flow. We used a pump that, in contradiction to the "empty veins" devices, limited the limb venous outflow by venous obstructions and in a long period therapy expanded the perfusion vessels and brought about persistent reactive hyperemia. AIM:To check the toe and calf arterial inflow measured by venous stasis plethysmography and capillary flow velocity during arterial assist IPC in a long-term therapy of ischemic legs. MATERIAL AND METHODS:Eighteen patients (12M, 6F) age 62 to 75 with leg peripheral arterial disease (PAD, Fontaine stage II) were studied. Pneumatic device with two 10cm wide cuffs (foot, calf) (Bio Compression Systems, Moonachie, NJ, USA) inflated to 120 mmHg for 5-6 sec to obstruct the venous flow, deflation time 16 sec, applied for 45-60 min daily for a period of 2 years. RESULTS:At pump inflation increase in toe arterial pressure, volume, capillary blood flow velocity and one-minute arterial inflow test was observed. Increased toe volume appeared concomitantly with the inflated chamber venous obstruction. Resting pressure in the great saphenous vein increased. The two years therapy showed persistence of the resting limb increased toe capillary flow. Intermittent claudication distance increased by 20-120%. After two years arterial assist TBI increased from 0.2 to 0.6 (range 0.3 to 0.8) (p<0.05 vs pre-therapy). The toe arterial inflow dominated over that in calf skin and muscles, nevertheless, there was prolongation of the claudication distance presumably due to dilatation of exchange vessels also in muscles. CONCLUSIONS:Our arterial assist IPC brought about increase in the toe capillary flow, long lasting dilatation of toe capillaries and extension of painless walking distance. The crucial factor of rhythmic repeated venous outflow obstructions should be taken into account in designing effective assist devices