Genetically distinct Group B Streptococcus strains induce varying macrophage cytokine responses
Autoři:
Rebecca A. Flaherty aff001; Elena C. Borges aff001; Jessica A. Sutton aff002; David M. Aronoff aff003; Jennifer A. Gaddy aff003; Margaret G. Petroff aff001; Shannon D. Manning aff001
Působiště autorů:
Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, MI, United States of America
aff001; Department of Microbiology and Immunology, Meharry Medical College School of Medicine, Nashville, TN, United States of America
aff002; Department of Medicine, Division of Infectious Disease, Vanderbilt University Medical Center, Nashville, TN, United States of America
aff003; Pathobiology and Diagnostic Investigation, Michigan State University, East Lansing, MI, United States of America
aff004
Vyšlo v časopise:
PLoS ONE 14(9)
Kategorie:
Research Article
doi:
https://doi.org/10.1371/journal.pone.0222910
Souhrn
Group B Streptococcus (GBS) is an opportunistic pathogen that causes preterm birth and neonatal disease. Although GBS is known to exhibit vast diversity in virulence across strains, the mechanisms of GBS-associated pathogenesis are incompletely understood. We hypothesized that GBS strains of different genotypes would vary in their ability to elicit host inflammatory responses, and that strains associated with neonatal disease would induce different cytokine profiles than those associated with colonization. Using a multiplexed, antibody-based protein detection array, we found that production of a discrete number of inflammatory mediators by THP-1 macrophage-like cells was universally induced in response to challenge with each of five genetically distinct GBS isolates, while other responses appeared to be strain-specific. Key array responses were validated by ELISA using the initial five strains as well as ten additional strains with distinct genotypic and phenotypic characteristics. Interestingly, IL-6 was significantly elevated following infection with neonatal infection-associated sequence type (ST)-17 strains and among strains possessing capsule (cps) type III. Significant differences in production of IL1-β, IL-10 and MCP-2 were also identified across STs and cps types. These data support our hypothesis and suggest that unique host innate immune responses reflect strain-specific differences in virulence across GBS isolates. Such data might inform the development of improved diagnostic or prognostic strategies against invasive GBS infections.
Klíčová slova:
Biology and life sciences – Physiology – Developmental biology – Molecular development – Neonates – Cell biology – Cellular types – Animal cells – Blood cells – White blood cells – Macrophages – Immune cells – Medicine and health sciences – Immune physiology – Immunology – Immune system – Innate immune system – Cytokines – Immune response – Inflammation – Diagnostic medicine – Signs and symptoms – Sepsis – Neonatal sepsis – Pathology and laboratory medicine – Research and analysis methods – Immunologic techniques – Immunoassays – Enzyme-linked immunoassays
Zdroje
1. Verani JR, McGee L, Schrag SJ. Prevention of perinatal group B streptococcal disease—revised guidelines from CDC, 2010. MMWR Recommendations and reports. 2010;59: 1–36. Available: http://www.ncbi.nlm.nih.gov/pubmed/21088663
2. Horvath B, Lakatos F, Tóth C, Bödecs T, Bódis J. Silent chorioamnionitis and associated pregnancy outcomes: a review of clinical data gathered over a 16-year period. J Perinat Med. 2014;42: 441–7. doi: 10.1515/jpm-2013-0186 24421211
3. Doran KS, Nizet V. Molecular pathogenesis of neonatal group B streptococcal infection: no longer in its infancy. Mol Microbiol. 2004;54: 23–31. doi: 10.1111/j.1365-2958.2004.04266.x 15458402
4. Wennekamp J, Henneke P. Induction and termination of inflammatory signaling in group B streptococcal sepsis. Immunol Rev. 2008;225: 114–127. doi: 10.1111/j.1600-065X.2008.00673.x 18837779
5. Korir ML, Manning SD, Davies HD. Intrinsic maturational neonatal immune deficiencies and susceptibility to group B Streptococcus infection. Clin Microbiol Rev. 2017;30: 973–989. doi: 10.1128/CMR.00019-17 28814408
6. Anders AP, Gaddy JA, Doster RS, Aronoff DM. Current concepts in maternal–fetal immunology: Recognition and response to microbial pathogens by decidual stromal cells. Am J Reprod Immunol. 2017. doi: 10.1111/aji.12623 28044385
7. Jones N, Bohnsack JF, Takahashi S, Oliver KA, Chan MS, Kunst F, et al. Multilocus sequence typing system for group B Streptococcus. J Clin Microbiol. 2003;41: 2530–2536. doi: 10.1128/JCM.41.6.2530-2536.2003 12791877
8. Luan S-L, Granlund M, Sellin M, Lagergård T, Spratt BG, Norgren M. Multilocus sequence typing of Swedish invasive group B Streptococcus isolates indicates a neonatally associated genetic lineage and capsule switching. J Clin Microbiol. 2005;43: 3727–33. doi: 10.1128/JCM.43.8.3727-3733.2005 16081902
9. Lin F-YC, Whiting A, Adderson E, Takahashi S, Dunn DM, Weiss R, et al. Phylogenetic lineages of invasive and colonizing strains of serotype III group B streptococci from neonates: a multicenter prospective study. J Clin Microbiol. 2006;44: 1257–61. doi: 10.1128/JCM.44.4.1257-1261.2006 16597848
10. Manning SD, Springman AC, Lehotzky E, Lewis MA, Whittam TS, Davies HD. Multilocus sequence types associated with neonatal group B streptococcal sepsis and meningitis in Canada. J Clin Microbiol. 2009;47: 1143–1148. doi: 10.1128/JCM.01424-08 19158264
11. Korir ML, Knupp D, LeMerise K, Boldenow E, Loch-Caruso R, Aronoff DM, et al. Association and virulence gene expression vary among serotype III group B Streptococcus isolates following exposure to decidual and lung epithelial cells. Infect Immun. 2014; doi: 10.1128/IAI.02181-14 25135682
12. Springman AC, Lacher DW, Wu G, Milton N, Whittam TS, Davies HD, et al. Selection, recombination, and virulence gene diversity among group B streptococcal genotypes. J Bacteriol. 2009; doi: 10.1128/JB.00369-09 19581371
13. Korir ML, Laut C, Rogers LM, Plemmons JA, Aronoff DM, Manning SD. Differing mechanisms of surviving phagosomal stress among group B Streptococcus strains of varying genotypes. Virulence. 2017;8: 924–937. doi: 10.1080/21505594.2016.1252016 27791478
14. Korir ML, Flaherty RA, Rogers LM, Gaddy JA, Aronoff DM, Manning SD. Investigation of the role that NADH peroxidase plays in oxidative stress survival in group B Streptococcus. Front Microbiol. 2018; doi: 10.3389/fmicb.2018.02786 30515142
15. Manning SD, Lewis MA, Springman AC, Lehotzky E, Whittam TS, Davies HD. genotypic diversity and serotype distribution of group B Streptococcus isolated from Women Before and After Delivery. Clin Infect Dis. 2008;46: 1829–1837. doi: 10.1086/588296 18462173
16. Rogers LM, Gaddy JA, Manning SD, Aronoff DM. Variation in macrophage phagocytosis of Streptococcus agalactiae does not reflect bacterial capsular serotype, multilocus sequence type, or association with invasive infection. Pathog Immun. 2018;
17. Flaherty RA, Donahue DL, Carothers KE, Ross JN, Ploplis VA, Castellino FJ, et al. Neutralization of streptolysin S-dependent and independent inflammatory cytokine IL-1β activity reduces pathology during early group A streptococcal skin infection. Front Cell Infect Microbiol. 2018;8: 211. doi: 10.3389/fcimb.2018.00211 30018884
18. Chaudhry H, Zhou J, Zhong Y, Ali MM, Mcguire F, Nagarkatti PS, et al. Role of cytokines as a double-edged sword in sepsis. In Vivo. 2013;27: 669–684. 24292568
19. Rosati E, Fettucciari K, Scaringi L, Cornacchione P, Sabatini R, Mezzasoma L, et al. Cytokine response to group B Streptococcus infection in mice. Scand J Immunol. 1998;47: 314–323. doi: 10.1046/j.1365-3083.1998.00305.x 9600312
20. Biondo C, Mancuso G, Midiri A, Signorino G, Domina M, Lanza Cariccio V, et al. The interleukin-1β/CXCL1/2/neutrophil axis mediates host protection against group B streptococcal infection. Infect Immun; 2014;82: 4508–17. doi: 10.1128/IAI.02104-14 25114117
21. Berner R, Welter P, Brandis M. Cytokine expression of cord and adult blood mononuclear cells in response to Streptococcus agalactiae. Pediatr Res. Nature Publishing Group; 2002;51: 304–309. doi: 10.1203/00006450-200203000-00007 11861934
22. Vallejo JG, Knuefermann P, Mann DL, Sivasubramanian N. Group B Streptococcus induces TNF-α gene expression and activation of the transcription factors NF-κB and activator protein-1 in human cord blood monocytes. J Immunol. 2000;165: 419–425. doi: 10.4049/jimmunol.165.1.419 10861080
23. Berner R, Csorba J, Brandis M. Different cytokine expression in cord blood mononuclear cells after stimulation with neonatal sepsis or colonizing strains of Streptococcus agalactiae. Pediatr Res. 2001;49: 691–697. doi: 10.1203/00006450-200105000-00014 11328954
24. Phares CR, Lynfield R, Farley MM, Mohle-Boetani J, Harrison LH, Petit S, et al. Epidemiology of invasive group B streptococcal disease in the United States, 1999–2005. JAMA. 2008;299: 2056–2065. doi: 10.1001/jama.299.17.2056 18460666
25. Sugitharini V, Prema A, Berla Thangam E. Inflammatory mediators of systemic inflammation in neonatal sepsis. Inflamm Res. 2013;62: 1025–1034. doi: 10.1007/s00011-013-0661-9 24013483
26. Singh P, Aronoff DM, Davies HD, Manning SD. Draft Genome sequence of an invasive Streptococcus agalactiae isolate lacking pigmentation. Genome Announc. 2016;4: e00015–16. doi: 10.1128/genomeA.00015-16 26950320
27. D'elia R V., Harrison K, Oyston PC, Lukaszewski RA, Clark GC. Targeting the “cytokine storm” for therapeutic benefit. Clin Vaccine Immunol. 2013. doi: 10.1128/CVI.00636-12 23283640
28. Vanderhoeven JP, Bierle CJ, Kapur RP, McAdams RM, Beyer RP, Bammler TK, et al. Group B streptococcal infection of the choriodecidua induces dysfunction of the cytokeratin network in amniotic epithelium: a pathway to membrane weakening. PLoS Pathog. 2014;10. doi: 10.1371/journal.ppat.1003920 24603861
Článek vyšel v časopise
PLOS One
2019 Číslo 9
- Tisícileté topoly, mokří psi, stárnoucí kočky a ospalé octomilky – „jednohubky“ z výzkumu 2024/41
- Jaké jsou aktuální trendy v léčbě karcinomu slinivky?
- Menstruační krev má značný diagnostický potenciál, mimo jiné u diabetu
- Proč jsou nemocnice nepřítelem spánku? A jak to změnit?
- Metamizol jako analgetikum první volby: kdy, pro koho, jak a proč?