How to reconstruct an upper full-thickness abdomen wall defect in austere environment? Interests of the pedicled myofascial latissimis dorsi flap

Upper abdominal wall defects secondary to trauma are not amenable to immediate closure in most cases. After a primary coverage, the definitive reconstruction can be done at a later date, using prosthetic mesh or flap. The majority of these complex procedures is, however, not available in the austere environment. The authors report a clinical case of upper full-thickness defects of the abdominal wall secondary to an explosion in Afghanistan. The patient was managed by a French Forward Surgical Team. The defect was immediately reconstructed in a one-stage surgery using a pedicled myofascial latissimus dorsi flap with good functional results. The pedicled latissimus dorsi flap is commonly used for coverage of both extrathoracic and intrathoracic defects. It is, therefore, possible to extend the harvesting of the muscle to the thoracolumbar fascia and the posterior third of the iliac crest. It provides a very large flap to cover an upper full-thickness abdomen wall defect. The harvest technique is simple, short, and largely accessible to a general surgeon. It provides immediate and definitive closure with a short hospital stay, what is clearly adapted in austere environment

CX₃CL1 (fractalkine) and its receptor CX₃CR1 regulate atopic dermatitis by controlling effector T cell retention in inflamed skin.

International audienceAtopic dermatitis (AD) is a chronic allergic dermatosis characterized by epidermal thickening and dermal inflammatory infiltrates with a dominant Th2 profile during the acute phase, whereas a Th1 profile is characteristic of the chronic stage. Among chemokines and chemokine receptors associated with inflammation, increased levels of CX3CL1 (fractalkine) and its unique receptor, CX3CR1, have been observed in human AD. We have thus investigated their role and mechanism of action in experimental models of AD and psoriasis. AD pathology and immune responses, but not psoriasis, were profoundly decreased in CX3CR1-deficient mice and upon blocking CX3CL1-CX3CR1 interactions in wild-type mice. CX3CR1 deficiency affected neither antigen presentation nor T cell proliferation in vivo upon skin sensitization, but CX3CR1 expression by both Th2 and Th1 cells was required to induce AD. Surprisingly, unlike in allergic asthma, where CX3CL1 and CX3CR1 regulate the pathology by controlling effector CD4(+) T cell survival within inflamed tissues, adoptive transfer experiments established CX3CR1 as a key regulator of CD4(+) T cell retention in inflamed skin, indicating a new function for this chemokine receptor. Therefore, although CX3CR1 and CX3CL1 act through distinct mechanisms in different pathologies, our results further indicate their interest as promising therapeutic targets in allergic diseases