Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10145 (IL-8)
 23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An investigation of the porcine response to gastrointestinal infection with Salmonella enterica serovars Choleraesuis (narrow host range) and Typhimurium (broad host range) revealed markedly different transcriptional profiles. Seven genes identified by suppression subtractive hybridization as up-regulated in the mesenteric lymph nodes at 24h (h) post-inoculation (p.i.) in serovar Choleraesuis-infected pigs (ARPC2, CCT7, HSPH1, LCP1, PTMA, SDCBP, VCP) and three genes in serovar Typhimurium-infected pigs (CD47/IAP, CXCL10, SCARB2) were analyzed by real-time PCR at 8h, 24 h, 48 h, 7 days (d) and 21 d p.i. A comparison between the two Salmonella infections revealed significant differences in transcriptional induction early in the infection (8-24h) for the serovar Typhimurium-infected pigs, whereas the serovar Choleraesuis-infected pigs exhibited significantly higher levels of gene expression at the later time points (48h-21 d), except for HSPH1. A similar gene expression trend was observed for immune-related genes involved in innate immunity and the inflammatory T helper 1 (Th1) response. Initial repression of gene expression in the serovar Choleraesuis-infected pigs from 8 to 48h p.i. (IFNG, IL12A, IL4, IL8, CSF2) coincided with extended transcriptional activation throughout the 21 d infection (IFNG, INDO, SOCS1, STAT1, IL1B, IL6, IL8, SLC11A1). The serovar Typhimurium-infected swine presented a more transient induction of immune-related genes (IFNG, INDO, IRF1, SOCS1, STAT1, IL1B, IL8, SLC11A1) early in the infection (24-48 h) followed by a significant repression of IL12A, IL12B, IL4, IL8 and CSF2. Collectively, these data reveal specific porcine genes with differences in gene expression kinetics that may be responsible for the variation in disease progression observed in swine infected with Typhimurium compared to Choleraesuis.
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PMID:Porcine differential gene expression in response to Salmonella enterica serovars Choleraesuis and Typhimurium. 1733 57

Given that gastrointestinal (GI) symptoms are a prominent extrapulmonary manifestation of coronavirus disease 2019 (COVID-19), we investigated the impact of GI infection on disease pathogenesis in three large cohorts of patients in the United States and Europe. Unexpectedly, we observed that GI involvement was associated with a significant reduction in disease severity and mortality, with an accompanying reduction in key inflammatory proteins including IL-6, CXCL8, IL-17A and CCL28 in circulation. In a fourth cohort of COVID-19 patients in which GI biopsies were obtained, we identified severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) within small intestinal enterocytes for the first time in vivo but failed to obtain culturable virus. High dimensional analyses of GI tissues confirmed low levels of cellular inflammation in the GI lamina propria and an active downregulation of key inflammatory genes including IFNG, CXCL8, CXCL2 and IL1B among others. These data draw attention to organ-level heterogeneity in disease pathogenesis and highlight the role of the GI tract in attenuating SARS-CoV-2-associated inflammation with related mortality benefit.
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PMID:Gastrointestinal involvement attenuates COVID-19 severity and mortality. 3305 9