Objective To investigate the clinical and histopathologic features of patients with primary gastrointestinal malignant lymphoma ( PGIML). Methods The clinical and histopathologic data of 22 patients with PGIML were reviewed and analyzed retrospectively. All cases were confirmed with histological specimen obtained from endoscopic biopsies or surgery. Results Abdominal pain was the most common presenting symptom, seen in 15 of 22 patients (68.2% ). The incidence of PGIML was highest in stomach, seen in 12 of 22 patients (54. 5% ). Modularity of the mucosal surface was the most common endoscopic finding, seen in 15 of 21 patients (71. 4% ). The positive rate of endoscopic biopsy for the diagnosis of PGIML was 52. 6% (10/19 biopsy cases). All cases were non-Hodgkins lymphomas ( NHL). Twenty cases were muco-sa associated lymphoid tissue (MALT) lymphoma, and 13 of 20 cases were extra-nodal marginal zone B-cell lymphoma of MALT. Conclusions Abdominal pain is the most common symptom and the stomach was the most common location in PGIML. Extra nodal marginal zone B-cell lymphoma of MALT is the main histopathologic feature. The prognosis of PGIML is related to the surgical procedure and the post operative chemotherapy.

ObjectiveDepression is a common mental illness with a profound impact on physical health. Depression has been associated with a higher risk of bacterial infection； however， whether this relationship is causal and how depression affects infection remains unclear. Therefore， we aimed to investigate the effects of depressive phenotype in infected mice by constructing a chronic unpredictable mild stress （CUMS） model. MethodsMice were induced with CUMS for 4 weeks. The depressive phenotype was evaluated using behavioral tests. Subsequently， the mice were intraperitoneally injected with Klebsiella pneumoniae to establish bacterial infection. Serum and abdominal tissues were collected 48 h after infection. Hematoxylin-eosin （HE） staining was used to observe the pathological changes in the tissues， and enzyme-linked immunosorbent assay （ELISA） was used to measure the levels of inflammatory factors. In addition， the fecal samples collected before infection were analyzed for 16S rDNA gene of gut microbiota， and the expression levels of NF-κB/NLRP3 signaling pathway in colon tissues of uninfected mice were detected. ResultsBehavioral tests showed that compared with the control mice， CUMS mice had significantly lower body weight （P<0.000 1， t=5.426）， lower sucrose preference rate （P<0.001， t=4.937）， increased swimming stationary time （P<0.001， t=16.37）， and decreased time spent in the central area of the open field （P<0.01， t=3.575）. Survival analysis showed that compared with the control mice， the survival rate of CUMS mice significantly decreased after infection （P<0.05）. Additionally， histochemical staining showed that tissue damage in the liver （P<0.05， t=4.025）， kidney （P<0.05， t=2.828）， and mesentery （P<0.01， t=5.367） significantly increased. Furthermore， ELISA results showed that the levels of the inflammatory cytokines IL-6 （P<0.01， t=3.365）， IL-1β （P<0.01， t=4.061）， TNF-α （P<0.01， t=4.460） and LPS （P<0.000 1， t=27.24） were elevated. The difference was statistically significant. According to 16S rDNA sequencing， CUMS-induced changes in the intestinal bacterial community structure of mice， making them significantly different from the control mice. Compared with the control mice， the expression levels of NF-κB （P<0.01， t=6.825） and NLRP3 （P<0.001， t=9.561） were upregulated in CUMS mice. ConclusionThe CUMS model was successfully constructed and CUMS mice developed more severe bacterial infection. Gut microbiota was dysregulated and the expression of NF-κB/NLRP3 signaling pathway was up-regulated in CUMS mice， which was related to the susceptibility to bacterial infection.