Penicillium purpurogenum produces a novel endo-1,5-arabinanase, active on debranched arabinan, short arabinooligosaccharides and on the artificial substrate p-nitrophenyl arabinofuranoside.

Penicillium purpurogenum secretes numerous lignocellulose-degrading enzymes, including four arabinofuranosidases and an exo-arabinanase. In this work, the biochemical properties of an endo-arabinanase (ABN1) are presented. A gene, coding for a potential ABN was mined from the genome. It includes three introns. The cDNA is 975 bp long and codes for a mature protein of 324 residues. The cDNA was expressed in Pichia pastoris. The enzyme is active on debranched arabinan and arabinooligosaccharides. In contrast to other characterized ABNs, inactive on p-nitrophenyl-α-L-arabinofuranoside (pNPAra), ABN1 is active on this substrate. The enzyme has an optimal pH of 4.5 and an optimal temperature of 30-35 °C. Calcium does not activate ABN1. ABN1 belongs to GH family 43 sub-family 6, and a Clustal alignment with sequences of characterized fungal ABNs shows highest identity (54.6%) with an ABN from Aspergillus aculeatus. A three-dimensional model of ABN1 was constructed and the docking with pNPAra was compared with similar models of an enzyme very active on this substrate and another lacking activity, both from GH family 43. Differences in the number of hydrogen bonds between enzyme and substrate, and distance between the substrate and the catalytic residues may explain the differences in activity shown by these enzymes.

Pioderma gangrenoso: terapias clásicas y emergentes / Pyoderma gangrenosum: Classic and emerging therapies

El pioderma gangrenoso es una dermatosis ulceronecrótica que representa un desafío importante para el clínico no solo porque puede simular otras dermatosis, sino porque en general no responde a los tratamientos habituales. Durante el último año han surgido nuevos estudios acerca de la eficacia real de los tratamientos convencionales, tales como la ciclosporina y los glucocorticoides sistémicos. Estos estudios han demostrado que los tratamientos clásicos son comparables pero insuficientes como monoterapia. Han surgido nuevos tratamientos, como los agentes ahorradores de glucocorticoides, los inhibidores del factor de necrosis tumoral y la cirugía. Esta revisión es una puesta al día de la evidencia actual para el tratamiento del pioderma gangrenoso (AU)

Pyoderma gangrenosum is an ulceronecrotising dermatosis that represents a challenge for any clinician, not only for its ability to mimic other dermatoses but also for its lack of response to treatment. During the past year, there have been new studies about the efficacy of standard therapies, such as cyclosporine and systemic corticosteroids. These studies showed that classic treatment was comparable, but they are insufficient as monotherapy. That being said, new emerging therapies are becoming important, as the use of corticosteroid-sparing agents, tumour necrosis factor inhibitors or even surgery. This review updates the current evidence for the treatment of pyoderma gangrenosum (AU)

Pyoderma gangrenosum: Classic and emerging therapies. / Pioderma gangrenoso: terapias clásicas y emergentes.

Pyoderma gangrenosum is an ulceronecrotising dermatosis that represents a challenge for any clinician, not only for its ability to mimic other dermatoses but also for its lack of response to treatment. During the past year, there have been new studies about the efficacy of standard therapies, such as cyclosporine and systemic corticosteroids. These studies showed that classic treatment was comparable, but they are insufficient as monotherapy. That being said, new emerging therapies are becoming important, as the use of corticosteroid-sparing agents, tumour necrosis factor inhibitors or even surgery. This review updates the current evidence for the treatment of pyoderma gangrenosum.

Enfermedad de Mucha-Habermann febril ulceronecrótica con respuesta favorable a minociclina, a propósito de un caso / Febrile ulceronecrotic Mucha-Habermann disease: report of one case

Pityriasis lichenoides et varioliformis acuta (PLEVA), pityriasis lichenoides chronica (PLC) and febrile ulceronecrotic Mucha-Habermann disease (FUMHD) are considered different manifestations of the same disease. Febrile ulceronecrotic Mucha-Habermann disease is a rare, and potentially lethal illness which is characterized by fast progression of numerous papules that converge, ulcerate and form a plaque with a necrotic center, together with hemorrhagic vesicles and pustules that are associated with high fever and variable systemic symptoms. We report a 16 years old male presenting with erythematous papules with crusts and fever. The diagnosis of febrile ulceronecrotic Mucha-Habermann disease was confirmed with the pathological study of the lesions. He was successfully treated with minocycline after a failed attempt of treatment with prednisone.

[Febrile ulceronecrotic Mucha-Habermann disease]. / Enfermedad de Mucha-Habermann febril ulceronecrótica con respuesta favorable a minociclina, a propósito de un caso: Report of one case.

Pityriasis lichenoides et varioliformis acuta (PLEVA), pityriasis lichenoides chronica (PLC) and febrile ulceronecrotic Mucha-Habermann disease (FUMHD) are considered different manifestations of the same disease. Febrile ulceronecrotic Mucha-Habermann disease is a rare, and potentially lethal illness which is characterized by fast progression of numerous papules that converge, ulcerate and form a plaque with a necrotic center, together with hemorrhagic vesicles and pustules that are associated with high fever and variable systemic symptoms. We report a 16 years old male presenting with erythematous papules with crusts and fever. The diagnosis of febrile ulceronecrotic Mucha-Habermann disease was confirmed with the pathological study of the lesions. He was successfully treated with minocycline after a failed attempt of treatment with prednisone.

Imprinting of CCR9 on CD4 T cells requires IL-4 signaling on mesenteric lymph node dendritic cells.

It has recently been shown that IL-4 can educate dendritic cells (DC) to differentially affect T cell effector activity. In this study, we show that IL-4 can also act upon DC to instruct naive T cells to express the gut-associated homing receptor CCR9. Thus, effector T cells generated after coculture with mesenteric lymph node (MLN)-DC show a higher expression of CCR9 when activated in the presence of IL-4. In contrast, IL-4 had no effect on CCR9 expression when naive T cells were polyclonally activated in the absence of MLN-DC, suggesting that the effect of IL-4 on CCR9 expression passed through DC. Indeed, T cells activated by MLN-DC from IL-4Ralpha(-/-) mice showed a much lower CCR9 expression and a greatly reduced migration to the small intestine than T cells activated by wild-type MLN-DC even in the presence of IL-4. Consistent with the finding that the vitamin A metabolite retinoic acid (RA) induces gut-homing molecules on T cells, we further demonstrate that IL-4 up-regulated retinaldehyde dehydrogenase 2 mRNA on MLN-DC, a critical enzyme involved in the synthesis of RA. Moreover, LE135, a RA receptor antagonist, blocked the increased expression of CCR9 driven by IL-4-treated MLN-DC. Thus, besides the direct effect of RA on T cell gut tropism, our results show that the induction of a gut-homing phenotype on CD4(+) T cells is also influenced by the effect of IL-4 on gut-associated DC.