An autochthonous chikungunya outbreak is ongoing near Anzio, a coastal town in the province of Rome. The virus isolated from one patient and mosquitoes lacks the A226V mutation and belongs to an East Central South African strain. As of 20 September, 86 cases are laboratory-confirmed. The outbreak proximity to the capital, its late summer occurrence, and diagnostic delays, are favouring transmission. Vector control, enhanced surveillance and restricted blood donations are being implemented in affected areas.

On the basis of previous studies demonstrating that a breach of the colonic epithelial barrier is associated with a microbiota-dependent increase in lamina propria (LP) regulatory cells, we investigated if the lack of spontaneous intestinal inflammation observed in nucleotide-binding oligomerization domain 2 (Nod2)−/− mice was due to enhanced intestinal regulatory function. We found that the LP CD4+ T-cell population of Nod2−/− mice contains an increased percentage of CD4+ regulatory T cells bearing transforming growth factor -β/latency peptide (LP CD4+LAP (latency-associated peptide) + T cells) both under baseline conditions and following an intentional breach of the colonic barrier induced by ethanol administration. In addition, we found that Nod2−/− mice manifest decreased severity of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-colitis and that TNBS-colitis in Nod2−/− or Nod2+/+ mice is ameliorated by adoptive transfer of LP cells from ethanol-treated mice before, but not after, depletion of LAP+ T cells. This increased regulatory T-cell response in Nod2−/− mice could explain why NOD2 polymorphisms in humans are not in themselves sufficient to establish inflammatory lesions.

Background: A CD4+CD25- regulatory T cell population expressing the surface TGF-β in its latent form LAP+ (Latency Associated Peptide) cells was proved to be protective in experimental colitis and be suppressive of human peripheral blood (PB) T proliferation. We investigated the frequency and function of lamina propria (LP) CD4+LAP+ T cells in inflammatory bowel disease (IBD) patients. Methods: Specimens from patients undergoing colonoscopy or bowel resection for IBD and colonic cancer were used as source of lamina propria mononuclear cells (LPMC). Ulcerative Colitis (UC) group was divided according to endoscopic activity evaluated with modified Baron Score. IL-17, IFN-γ, IL-10, LAP and Foxp3 expression in in CD3+CD8- (CD4) or CD3+/CD4+ gated cell population was assessed by immunofluorescence. The ability of FACS-sorted LP CD3+CD8-(CD4) LAP+CD25- to inhibit stimulated autologous PB CD3+CD8-(CD4) LAP- CD25- cells proliferation was assessed. Results: LP CD4LAP+ cells were significantly increased, when compared to controls, in active UC patients and not in Crohn’s Disease patients. The majority of LP CD4+LAP+ cells were Foxp3-. The % of IL-17+ cells in LP CD3+CD8-(CD4) LAP+ cells was significantly higher in active UC patients when compared to controls. LP CD3+CD8-(CD4)LAP+CD25- isolated from UC patients showed reduced or no ability to inhibit autologous PB CD3+CD8-(CD4)LAP-CD25- cell proliferation when compared to controls. Removal of IL-17+ cells from LP CD3+CD8-(CD4) LAP+ cells increases their suppressive ability. Conclusions: % of LP CD4 LAP+ cells is increased in active UC, showing reduced suppressor activity due to their increased proportion of intracellular IL-17 expression.

Background: Pandemic coronavirus disease 2019 (COVID-19) disease represents a challenge for healthcare structures. The molecular confirmation of samples from infected individuals is crucial and therefore guides public health decision making. Clusters and possibly increased diffuse transmission could occur in the context of the next influenza season. For this reason, a diagnostic test able to discriminate severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) from influenza viruses is urgently needed. Methods: A multiplex real-time reverse-transcription polymerase chain reaction (PCR) assay was assessed using 1 laboratory protocol with different real-time PCR instruments. Overall, 1000 clinical samples (600 from samples SARS-CoV-2–infected patients, 200 samples from influenza-infected patients, and 200 negative samples) were analyzed. Results: The assay developed was able to detect and discriminate each virus target and to intercept coinfections. The limit of quantification of each assay ranged between 5 and 10 genomic copy numbers, with a cutoff value of 37.7 and 37.8 for influenza and SARS-CoV-2 viruses, respectively. Only 2 influenza coinfections were detected in COVID-19 samples. Conclusions: This study suggests that multiplex assay is a rapid, valid, and accurate method for the detection of SARS-CoV-2 and influenza viruses in clinical samples. The test may be an important diagnostic tool for both diagnostic and surveillance purposes during the seasonal influenza activity period.