Gut microbiota-mediated therapeutic effect of Shengmai formula (SMF) on sepsis in mice / 中国药科大学学报

@#To investigate the effects of Shengmai formula (SMF) on tissue damages, serum inflammatory factors and the proportion of innate immunocytes in peripheral blood, sepsis models using either intraperitoneal injection of 20 mg/kg lipopolysaccharide (LPS) or cecal ligation and puncture (CLP) were established.The role of gut microbiota in septic mice during SMF treatment was further investigated.LPS-induced sepsis model was carried out 4 days after daily gavage administration with 0.3 g/kg, 0.6 g/kg, 1.2 g/kg SMF or intraperitoneal injection with 0.6 g/kg SMF.Survival rates of septic mice were determined.Histological evaluations of liver, lung and kidney were analyzed by H&E staining. Serum IL-6, TNF-α, Alanine transaminase (ALT), Aspartate aminotransferase (AST), Blood urea nitrogen (BUN) and Creatinine (Cr) levels were determined.LPS and CLP-induced sepsis models were established, and the proportion of monocytes, macrophages and neutrophils in peripheral blood were analyzed by flow cytometry after gavage administration or intraperitoneal injection of SMF.The therapeutic effects of SMF after antibiotics treatment were further determined, and the therapeutic effects of fecal microbiota from SMF-treated mice were investigated.The results show that LPS-induced sepsis caused death of mice, damages in liver, lung and kidney with increased infiltration of leukocytes and elevated levels of serum IL-6, ALT, AST, BUN and Cr, which were all reversed by gavage administration of SMF.Gavage administration of SMF could significantly reduce the proportion of peripheral macrophages in LPS model and monocytes, macrophages, neutrophils in CLP model.Intraperitoneal injection of SMF showed no therapeutic benefits in septic mice.Depletion of gut microbiota using antibiotics cocktail reversed the therapeutic effects of SMF on sepsis, indicating the involvement of gut microbiota.Fecal microbiota from SMF-treated donors was transplanted into pseudo-sterile recipients, and we found FMT could significantly ameliorate sepsis of recipients.These results showed that gavage administration of SMF reduced serum inflammatory factors and alleviated tissue damages in septic mice by regulating gut microbiota. This study provides a theoretical basis for the treatment of clinical sepsis with SMF.

Purification and characterization of an extracellular alkaline protease produced from an isolated bacillus subtilis.

This paper describes the studies on the purification and partial characterization of serine alkaline protease produced through submerged fermentation process from a locally isolated Bacillus subtilis. This strain, grown in a highly alkaline medium (pH 10), produces an extracellular proteolytic enzyme. The alkaline protease was purified in a simple two-step procedure involving ammonium sulphate precipitation and gel filtration. Sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE) analysis of the purified alkaline protease indicated an estimated molecular mass of 30KDa. It was more active in the range of 20-60ºC and had an optimum activity at 55ºC with optimum pH of 10.5. Characterization of the protease showed that it required certain cations such as Mg++, Mn++ and Ca++ for maximal activity. The serine nature of the alkaline protease was confirmed by PMSF inhibition. The temperature and pH stability of this Alkaline Protease from Bacillus Subtilismakes it potentially useful forindustrial applications.

Síndrome de Miller Fisher. A propósito de un caso / Miller Fisher syndrome. A case report

El síndrome de Miller Fisher es una variedad clínica del síndrome de Guillain-Barré, que se caracteriza por oftalmoplejía, arreflexia y ataxia. Se presenta el caso de una paciente de 6 años de edad, atendida en el Hospital Pediátrico Docente Pepe Portilla de Pinar del Río, en noviembre de 2010; con antecedentes de salud anterior, que 5 días previos al inicio del cuadro tuvo una infección respiratoria alta aguda, seguida de un cuadro de debilidad bucofaríngea y facial, ataxia y debilidad muscular intensa de las extremidades. Se interconsulta con el servicio de Neurología, donde se constata diplejía facial periférica, parálisis del IV par izquierdo, ataxia e hiporreflexia; se le realizan varias investigaciones e ingresa en la Unidad de Cuidados Intensivos con el diagnóstico de síndrome de Miller Fisher. Se comienza el tratamiento con terapéuticocon, intacglobin y vitaminoterapia, logrando una evolución satisfactoria de la paciente a los 10 días de su ingreso en el servicio de UCI con regresión del cuadro.

Miller Fisher syndrome is a clinical variant of Guillain-Barré syndrome it is characterized by ophthalmoplegia, areflexia and ataxia. A six-year old female patient attended to "Pepe Portilla" Children Hospital, Pinar del Rio in November 2010; with past health records, who 5 days before the onset of the disorder suffered from an acute upper respiratory infection that was followed by a picture of buccopharyngeal and facial weakness, ataxia and acute muscular debility of the limbs. A referral to Neurology service verified peripheral facial diplegia, paralysis of the IV left pair, ataxia and hyporeflexia; several examinations were performed before admitting her to the Intensive Care Unit (ICU) with the diagnosis of Miller Fisher syndrome. The therapeutic treatment included intacglobin and vitamins, achieving a satisfactory progress; the patient was discharged from the ICU 10 days after her admission with a total regression of the clinical picture.

Síndrome de Guillain Barré en pediatría / Guillain-Barré syndrome in pediatrics

Este trabajo revisa el conocimiento actual sobre el síndrome de Guillain-Barré (SGB) en niños. El SGB se define como una parálisis flácida arrefléxica aguda y se clasifica en 4 subgrupos: polirradiculopatía aguda inflamatoria desmielinizante (AIDP), neuropatía axonal sensitivo-motora aguda (AMSAN), neuropatía axonal motora aguda (AMAN) y síndrome de Miller-Fisher (SMF). La AIDP se asocia en un 30-50% a compromiso de pares craneales, lo cual no se observa en la AMAN. El SMF se caracteriza por ataxia, oftalmoplejía y arreflexia, pero puede presentar también compromiso de pares craneales. Datos recientes de la anatomía patológica y la fisiopatología del SGB destacan la importancia de la infección por Campylobacter jejuni en la generación de anticuerpos anti-gangliósidos (GM1 en AIDP, GQ1b en SMF y GD1a en AMAN) que lesionan la mielina en AIDP y SMF y el axón en AMAN. El diagnóstico diferencial debe descartar enfermedades del sistema nervioso central (SNC) (encefalitis, encefalomielitis, mielitis), síndromes miasténicos, neuropatías tóxicas por metales pesados, fármacos, substancias químicas o toxinas animales y cuadros miopáticos, especialmente la miositis aguda infecciosa benigna y la neuromiopatía del paciente en la unidad de cuidados intensivos. Es importante el tratamiento con inmunoglobulina en dosis total de 2 gramos por kilogramo a administrar en 48 horas. La plasmaféresis puede ser igualmente eficaz. El SGB tiene buen pronóstico en niños, con una recuperación total en el 85% de los casos. La rehabilitación es fundamental para lograr una recuperación más rápida e integral.

This paper reviews the current knowledge about Guillain- Barré syndrome (GBS). GBS is defined as an acute, areflexic, flaccid paralysis, which is classified into 4 subgroups: acute inflammatory demyelinating polyneuropathy (AIDP), acute motor-sensory axonal neuropathy (AMSAN), acute motor axonal neuropathy (AMAN) and Miller-Fisher syndrome (MFS). AIDP is associated in 30-50% of cases with cranial nerve involvement, which is not observed in AMAN. MFS is characterized by ataxia, ophthalmoplegia and areflexia, but it may also present cranial nerve dysfunction. Recent data on the pathology and pathophysiology of GBS emphasize the important role of Campylobacter jejuni infection in generating anti-ganglioside antibodies (GM1 in AIDP, GQ1b in MFS and GD1a in AMAN), which damage myelin in AIDP and MFS and axons in AMAN. The differential diagnosis must rule out other disorders of the central nervous system (encephalitis, encephalomyelitis, myelitis), myasthenic syndromes, toxic neuropathies induced by heavy meals, drugs, chemical substances or animal toxins, and myopathic conditions, especially acute benign infectious myositis and neuromyopathy of the intensive care unit patient. It is important the treatment with immune globulin, at a total dose of 2 grams per kilogram administered over 48 hours. Plasmapheresis can be equally effective. GBS has a good prognosis in children with a total recovery in 85% of cases. Rehabilitation is crucial to attain a more rapid and global improvement.