Eosinophilic gastroenteritis presenting as small bowel obstruction: A case report and review of the literature

Eosinophilic gastroenteritis is a rare disease of unknown etiology. It is characterized by eosinophilic infiltration of the bowel wall to a variable depth and symptoms associated with gastrointestinal tract. Recently, the authors experienced a case of eosinophilic gastroenteritis presenting as small bowel obstruction. A 51-year old woman was admitted to our hospital complaining of abdominal pain and vomiting. Physical examination revealed a distended abdomen with diffuse tenderness. Complete blood count showed mild leukocytosis without eosinophilia. Computed tomography confirmed a dilatation of the small intestine with ascites. An emergency laparotomy was performed for a diagnosis of peritonitis due to intestinal obstruction. Segmental resection of the ileum and end to end anastomosis were performed. Histologically, there was a dense infiltration of eosinophils throughout the entire thickness of ileal wall and eosinophilic enteritis was diagnosed. The patient recovered well, and was free from gastrointestinal symptoms at the time when we reported her disease.

Eosinophilic Gastroenteritis in Tropical Area: about 6 Cases from Senegal

The aetiologies of hypereosinophilia are dominated by digestive parasitosis and drug intake. In the tropics, because of the frequency of parasitosis, eosinophilic digestive pathologies of primary origin, which are rare, may be overlooked. We report 6 cases of eosinophilic gastroenteritis with polymorphic digestive manifestations testifying to the different locations of eosinophilic infiltration in the digestive parietal layer. Three patients had ascites rich in eosinophils, indicative of serous involvement, while the other two had a muscular form, and the last a mucosal involvement. The evolution was favourable in all cases with corticosteroid therapy, but a recurrence was noted in 4 cases when treatment was stopped.

Characterization of SHARPIN knockout Syrian hamsters developed using CRISPR/Cas9 system

Background : SHARPIN (SHANK- associated RH domain interactor) is a component ofthe linear ubiquitination complex that regulates the NF- κB signaling pathway. To betterunderstand the function of SHARPIN, we sought to establish a novel geneticallyengineered Syrian hamster with SHARPIN disruption using the CRISPR/Cas9 system.Methods : A single- guide ribonucleic acid targeting exon 1 of SHARPIN gene was designedand constructed. The zygotes generated by cytoplasmic injection of the Cas9/gRNA ribonucleoprotein were transferred into pseudopregnant hamsters. Neonatalmutants were identified by genotyping. SHARPIN protein expression was detectedusing Western blotting assay. Splenic, mesenteric lymph nodes (MLNs), and thymicweights were measured, and organ coefficients were calculated. Histopathologicalexamination of the spleen, liver, lung, small intestine, and esophagus was performedindependently by a pathologist. The expression of lymphocytic markers and cytokineswas evaluated using reverse transcriptase- quantitative polymerase chain reaction.Results : All the offspring harbored germline- transmitted SHARPIN mutations.Compared with wild- type hamsters, SHARPIN protein was undetectable in SHARPIN −/−hamsters. Spleen enlargement and splenic coefficient elevation were spotted inSHARPIN −/− hamsters, with the descent of MLNs and thymuses. Further, eosinophilinfiltration and structural alteration in spleens, livers, lungs, small intestines, and esophagiwere obvious after the deletion of SHARPIN. Notably, the expression of CD94 and CD22 was downregulated in the spleens of knockout (KO) animals. Nonetheless,the expression of CCR3, CCL11, Il4 , and Il13 was upregulated in the esophagi. Theexpression of NF- κB and phosphorylation of NF- κB and IκB protein significantly diminishedin SHARPIN −/− animals.Conclusions : A novel SHARPIN KO hamster was successfully established using theCRISPR/Cas9 system. Abnormal development of secondary lymphoid organs andeosinophil infiltration in multiple organs reveal its potential in delineating SHARPINfunction and chronic inflammation.

Semaphorin 3A controls allergic and inflammatory responses in experimental allergic conjunctivitis

AIM: To assess the efficacy of topical Semaphorin 3A(SEMA3A) in the treatment of allergic conjunctivitis.METHODS: Experimental allergic conjunctivitis(EAC)mice model induced by short ragweed pollen(SRW) in 4-week-old of BALB/c mice, mice were evaluated using haematoxylin and eosin(H&E) staining, immunofluor-escence and light microscope photographs. Early phase took the samples in 24 h after instillation and late phase took the samples between 4 to 14 d after the start of treatment. The study use of topical SEMA3A(10 U, 100 U,1000 U) eye drops and subconjunctival injection of SEMA3 A with same concentration. For comparison, five types of allergy eyedrops were quantified using clinical characteristics.· RESULTS: Clinical score of composite ocular symptoms of the mice treated with SEMA3 A were significantly decreased both in the immediate phase and the late phase compared to those treated with commercial ophthalmic formulations and non-treatment mice. SEMA3 A treatment attenuates infiltration of eosinophils entering into conjunctiva in EAC mice. The score of eosinophil infiltration in the conjunctiva of SEMA3 A 1000 U-treated group were significantly lower than low-concentration of SEMA3 A treated groups and non-treated group. SEMA3 A treatment also suppressed T-cell proliferation in vitro and decreased serum total Ig E levels in EAC mice. Moreover, treatment of SEMA3 A suppressed Th2-related cytokines(IL-5, IL-13 and IL-4)and pro-inflammatory cytokines(IFN-γ, IL-17 and TNF-α)release, but increased regulatory cytokine IL-10 concentration in the conjunctiva of EAC mice.CONCLUSION: SEMA3 A as a biological agent, showed the beneficial activity in ocular allergic processes with the less damage to the intraocular tissue. It is expected that SEMA3 A may be contributed in patients with a more severe spectrum of refractory ocular allergic diseases including allergic conjunctivitis in the near future.