Background Previous studies have shown the effect of bacterial lipopolysaccharide (LPS) on enhanced cancer cells’ growth and metastasis. However, the effect of LPS on prostate cancer (PCa) cells metastasis has not been investigated in details. This study aimed to investigate the functional role of LPS on PCa cells metastasis and determine the effect of dexamethasone (DEX) on this event. Methods Two different PCa reporter cells lines (DU145‐NF‐κB‐Luc and MAT‐LyLu‐ NF‐κB‐Luc) were used to assess the direct effect of LPS on NF‐κB activation in PCa cells. Plasma collected from LPS‐stimulated human and rodent blood were used to check the indirect effect of LPS on NF‐κB activation in PCa cells. Trans‐well migration assay and two different orthotopic PCa animal models were used to investigate the effect of LPS on DU145 and MAT‐LyLu cells migration or metastasis in vitro and in vivo, respectively. In all the studies DEX was used with or without LPS stimulation. Results LPS and secretory factors present in plasma collected from LPS‐stimulated blood, significantly activated NF‐κB in DU145, and MAT‐LyLu cells and enhanced their migration in vitro. DEX significantly suppressed LPS‐mediated activation of cancer and blood cells and abrogated the direct and indirect pro‐migratory effect of LPS on PCa cells. Systemic administration of LPS activated NF‐κB in DU145 cells in vivo; however, failed to alter the metastatic properties of these cells. On the other hand, systemic administration of LPS to MAT‐LyLu tumor bearing animals significantly enhanced the incidence of metastasis without altering the overall growth of primary tumors. Unexpectedly, though DEX significantly suppressed MAT‐LyLu primary tumor weights, it aggravated metastasis of cancer cells in presence and absence of LPS. Moreover, consecutive DEX pre‐treatment enhanced experimental peritoneal metastasis of MAT‐LyLu cells. At the molecular level, LPS, and/or DEX induced overexpression of immunosuppressive molecules in MAT‐LyLu tumors. Conclusions Overall, our study has shown that LPS and/or LPS induced inflammation can increase PCa metastasis and immunosuppressive dose of DEX might further enhance cancer metastasis.

Background The role of microbiota in the pathophysiology of benign prostate hyperplasia (BPH), especially in creating an inflammatory milieu may not be avoided. The major objectives of this study were to investigate the microbial composition of BPH tissues, its association with inflammation and check the effect of clinically isolated bacteria on prostate epithelial cells. Methods The study includes 36 patients with a pathological diagnosis of BPH. Following strict aseptic measures, tissues were collected after transurethral resection of prostate, multiple pieces of the resected tissues were subjected to histopathological analysis, bacterial culture and genomic DNA extraction. Microbial composition was analyzed by culture and/or next‐generation sequencing methods. Annotation of operational taxonomy unit has been done with an in‐house algorithm. The extent of inflammation was scored through histological evaluation of tissue sections. The effect of clinical isolates on nuclear factor‐κB (NF‐κB) activity and induction of DNA‐damage in the prostate epithelial cells were evaluated. Results Histopathological analysis of the BPH tissues showed the presence of inflammation in almost all the tissues with a varied level at different regions of the same tissue section and the level of overall inflammation was different from patients to patients. Microbial culture of tissue samples showed the presence of live bacteria in 55.5% (20 out of 36) of the patient tissues. Majority of the isolates were coagulase‐positive Staphylococcus, E. coli and Micrococcus spp. Further, V3 16S rRNA sequencing of the DNA isolated from BPH tissues showed the presence of multiple bacteria and the most common phylum in the BPH tissues were found to be Proteobacteria, Actinobacteria, Firmicutes, and Bacteroidetes. The E. coli, isolated from one of the tissue was able to activate NF‐κB and induce DNA damage in prostate epithelial cells. Phospho‐histone γH2A.X staining confirmed the presence of cells with damaged DNA lesion in BPH tissues and also correlated with the severity of inflammation. Conclusion Our study has shown that the BPH tissues do have a divergent microbial composition including the commonly found E. coli (phylum Proteobacteria), and these bacteria might contribute to the BPH‐associated inflammation and/or tissue damage. The BPH‐associated E. coli induced NF‐κB signaling and DNA damage in prostate epithelial cells in vitro.

Results of this study are promising. Larger studies are needed to assess whether RDTs using urine could serve as a practical, reliable method for the detection of P. falciparum in a non-invasive manner where invasive blood taking is less feasible.

Abdominal scar endometriosis is very rare. We report a case of abdominal scar endometriosis in a 32-yearold woman presented with a blue lesion over the abdominal scar for 7 months. She had history of intermittent dull aching pain over the scar for 5 years. Excision of the lump was done with the clinical diagnosis of vascular malformation over the scar. The specimen was sent for histopathological examination. The histopathological report revealed decidual change in the scar tissue suggesting abdominal scar endometriosis. Abdominal scar endometriosis should be kept in mind while dealing a case of the painful lump over the abdominal scar in any woman of childbearing age having a history of obstetric or gynecological procedure.