Folia Microbiologica

, 56:373 | Cite as

Changes in Caenorhabditis elegans life span and selective innate immune genes during Staphylococcus aureus infection

  • Gnanasekaran JebaMercy
  • Shunmugiah Karutha Pandian
  • Krishnaswamy Balamurugan
Article

Abstract

Caenorhabditis elegans has been increasingly used to study the innate immunity and for the screening of microbe/host-specific pathogenic factors. Staphylococcus aureus-mediated infections with live C. elegans were performed on solid (full-lawn) and liquid assays. S. aureus required 90 ± 10 h for the complete killing of C. elegans, but the infection was started only after 32 h of exposure with 20% inoculum of S. aureus. The short time exposure studies revealed that, in 20% of inoculum, continuous exposure to the pathogen was required for the killing of nematode. In 100% of inoculum, only 8 h of exposure was sufficient to kill the C. elegans. To evaluate kinetically at the innate immune level, the regulation of representative candidate antimicrobial genes was investigated. Both semi-quantitative reverse transcriptase polymerase chain reaction (PCR) and real-time PCR analyses indicated the regulation of candidate immune regulatory genes of lysozyme (lys-7), cysteine protease (cpr-2), and C-type lectin (clec-60 and clec-87) family members during the course of S. aureus infections, indicating the possible contribution of the above players during the host immune response against S. aureus exposures.

Keywords

Reverse Transcriptase Polymerase Chain Reaction Alpha Toxin Lysozyme Gene Bacterial Accumulation Complete Killing 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Abbreviations

TSS

Toxic shock syndrome

PAMPs

Pathogen-associated molecular patterns

PRRs

Pattern-recognition receptors

HSMPs

Host-specific molecular patterns

ATCC

American Type Culture Collection

CGC

Caenorhabditis Genetic Centre

NGM

Nematode growth medium

CFU

Colony-forming unit(s)

PCR

Polymerase chain reaction

LT50

Median lethal time

Notes

Acknowledgment

We thank Caenorhabditis Genetics Center for providing C. elegans N2 WT strain and E. coli OP50. KB thankfully acknowledges the financial support received through DBT-RGYI (BT/PR10270/GBD/27/83/2007 dated 18 Dec 2007) and UGC [F. No. 33-237/2007 (SR)], GOI, India. Authors gratefully acknowledge the Alagappa University BIF (BT/BI/25/001/2006).

Supplementary material

12223_2011_60_Fig5_ESM.jpg (4 kb)
ESM 1

The level of mRNA expression of an immune effector gene lys-7 during the continuous infection of S. aureus. A semi-quantitative RT-PCR was performed using gene specific primers as described in Materials and methods. The pattern of expression was analyzed during the linear range of amplifications (22–28 cycle). A representative 12% PAGE showing the PCR products. (Lane: 1–0 h sample, 2–12 h OP50-exposed C. elegans, 3–12 h M9-buffer-exposed C. elegans, 4–12 h S. aureus-exposed C. elegans, 5–100 bp ladder; 6–24 h OP50-exposed C. elegans, 7–24 h M9-buffer-exposed C. elegans, 8–24 h S. aureus-exposed C. elegans, 9–36 h S. aureus-exposed C. elegans, 10–100 bp ladder; 11–48 h S. aureus-exposed C. elegans, 12–60 h S. aureus-exposed C. elegans, 13–72 h S. aureus-exposed C. elegans, 14–72 h OP50-exposed C. elegans) (JPEG 4 kb)

12223_2011_60_MOESM1_ESM.tif (1.3 mb)
High-resolution image (TIFF 1,290 kb)
12223_2011_60_Fig6_ESM.jpg (15 kb)
ESM 2

The level of mRNA expression of an immune effector gene, cpr-2. A semi-quantitative RT-PCR was performed using gene-specific primers as described in Materials and methods. The pattern of expression was analyzed during the linear range of amplifications (22–28 cycle). A representative 12% PAGE showing the PCR products. (Lane: 1–0 h sample, 2–12 h S. aureus-exposed C. elegans, 3–24 h S. aureus-exposed C. elegans, 4–36 h S. aureus-exposed C. elegans, 5-100 bp ladder; 6–48 h S. aureus-exposed C. elegans, 7–60 h S. aureus-exposed C. elegans, 8–72 h S. aureus-exposed C. elegans) (JPEG 14 kb)

12223_2011_60_MOESM2_ESM.tif (2.3 mb)
High-resolution image (TIFF 2,323 kb)
12223_2011_60_Fig7_ESM.jpg (5 kb)
ESM 3

The level of expression of a pathogen recognizing receptor gene, clec-60 of C. elegans during the continuous infection of S. aureus. A semi-quantitative RT-PCR was performed using gene-specific primers as described in Materials and methods. The pattern of expression was analyzed during the linear range of amplifications (22–28 cycle). A representative 12% PAGE showing the PCR products. (Lane: 1–100 bp ladder, 2–0 h sample, 3–12 h OP50-exposed C. elegans, 4–12 h M9-buffer-exposed C. elegans, 5–12 h S. aureus-exposed C. elegans, 6–24 h OP50-exposed C. elegans, 7–24 h M9-buffer-exposed C. elegans, 8–24 h S. aureus-exposed C. elegans, 9–36 h S. aureus-exposed C. elegans; 10-100 bp ladder, 11–48 h S. aureus-exposed C. elegans, 12–60 h S. aureus-exposed C. elegans, 13–72 h S. aureus-exposed C. elegans, 14–72 h OP50-exposed C. elegans) (JPEG 5 kb)

12223_2011_60_MOESM3_ESM.tif (1.7 mb)
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12223_2011_60_Fig8_ESM.jpg (6 kb)
ESM 4

The level of expression of a pathogen recognizing receptor gene, clec-87 of C. elegans during the continuous infection of S. aureus.(Lane 1–0 h sample, 2–12 h OP50-exposed C. elegans, 3–12 h S. aureus-exposed C. elegans, 4–24 h S. aureus-exposed C. elegans, 5–36 h S. aureus-exposed C. elegans, 6-100 bp ladder; 7–48 h S. aureus-exposed C. elegans, 8–60 h S. aureus-exposed C. elegans, 9–72 h S. aureus-exposed C. elegans, 10–72 h OP50-exposed C. elegans) (JPEG 6 kb)

12223_2011_60_MOESM4_ESM.tif (2.8 mb)
High-resolution image (TIFF 2,890 kb)

References

  1. Alper S, Mcbride SJ, Lackford B, Freedman JH, Schwartz DA (2007) Specificity and complexity of the Caenorhabditis elegans innate immune response. Mol Cell Biol 27:5544–5553PubMedCrossRefGoogle Scholar
  2. Bachali S, Jager M, Hassanin A, Schoentgen F, Jolles P, Fiala-Medioni (2002) A phylogenetic analysis of invertebrate lysozymes and the evolution of lysozyme function. J Mol Evol 54:652–664PubMedCrossRefGoogle Scholar
  3. Drickamer K (1993) Evolution of Ca (2+)-dependent animal lectins. Prog Nucleic Acid Res Mol Biol 45:207–232PubMedCrossRefGoogle Scholar
  4. Garsin DA, Sifri CD, Mylonakis E, Qin X, Singh KV, Murray BE, Calderwood SB, Ausubel FM (2001) A simple model host for identifying Gram-positive virulence factors. Proc Natl Acad Sci USA 98:10892–10897PubMedCrossRefGoogle Scholar
  5. Garvis S, Mei JM, Ruiz-Albert J, Holden DH (2002) Staphylococcus aureus svrA: a gene required for virulence and expression of the agr locus. Microbiology 148:3235–3243PubMedGoogle Scholar
  6. Hodgkin J, Kuwabara PE, Corneliussen B (2000) A novel bacterial pathogen, Microbacterium nematophilum, induces morphological change in the nematode C. elegans. Curr Biol 10:1615–1618PubMedCrossRefGoogle Scholar
  7. Irazoqui JE, Troemel ER, Feinbaum RL, Luhachack LG, Cezairliyan BO (2010) Distinct pathogenesis and host responses during infection of C. elegans by P. aeruginosa and S. aureus. PLoS Pathog 6:e1000982PubMedCrossRefGoogle Scholar
  8. Kesika P, Pandian SK, Balamurugan K (2011) Analysis of Shigella flexneri-mediated infections in model organism Caenorhabditis elegans. Scand J Infect Dis 43:286–295PubMedCrossRefGoogle Scholar
  9. Mallo GV, Kurz CL, Couillault C, Pujol N, Granjeaud S, Kohara Y (2002) Inducible antibacterial defense system in C. elegans. Curr Biol 12:1209–1214PubMedCrossRefGoogle Scholar
  10. Morse DP, Bass BL (1999) Long RNA hairpins that contain inosine are present in Caenorhabditis elegans poly(A)+ RNA. Proc Natl Acad Sci USA 96:6048–6053PubMedCrossRefGoogle Scholar
  11. O’Rourke D, Baban D, Demidova M, Mott R, Hodgkin J (2006) Genomic clusters, putative pathogen recognition molecules, and antimicrobial genes are induced by infection of C. elegans with M. nematophilum. Genome Res 16:1005–1016PubMedCrossRefGoogle Scholar
  12. Shapira M, Hamlin BJ, Rong J, Chen K, Ronen M, Tan MW (2006) A conserved role for a GATA transcription factor in regulating epithelial innate immune responses. Proc Natl Acad Sci USA 103:14086–14091PubMedCrossRefGoogle Scholar
  13. Sherris JC, Plorde JJ (1990) Staphylococci. In: Sherris JC (ed) Medical microbiology: an introduction to infectious diseases. Elsevier, New York, pp 275–289Google Scholar
  14. Sifri CD, Begun J, Ausubel FM, Calderwood SB (2003) Caenorhabditis elegans as a model host for Staphylococcus aureus pathogenesis. Infect Immun 71:2208–2217PubMedCrossRefGoogle Scholar
  15. Todome Y, Ohkuni H, Mizuse M, Okibayashi F, Ohtani N, Suzuki H, Song C, Igarashi H, Harada K, Sakurai S, Kotani S (1999) Superantigenic exotoxin production by isolates of Staphylococcus aureus from the Kawasaki syndrome patients and age-matched control children. J Med Microbiol 42:91–95CrossRefGoogle Scholar
  16. Troemel ER, Chu SW, Reinke V, Lee SS, Ausubel FM, Kim DH (2006) p38 MAPK regulates expression of immune response genes and contributes to longevity in C. elegans. PLoS Genet 2:1725–1739CrossRefGoogle Scholar
  17. Turk D, Guncar G (2003) Lysosomal cysteine proteases (cathepsins): promising drug targets. Acta Crystallogr D Biol Crystallogr 59:203–213PubMedCrossRefGoogle Scholar
  18. Waldvogel FA (2000) Staphylococcus aureus (including staphylococcal toxic shock). In: Mandell GL, Bennett IE, Dolin R (eds) Principles and practice of infectious diseases, 5th edn. Churchill Livingstone Inc., New York, pp 2069–2092Google Scholar
  19. Wong D, Bazopoulou D, Pujol N, Tavernarakis N, Ewbank JJ (2007) Genome-wide investigation reveals pathogen-specific and shared signatures in the response of Caenorhabditis elegans to infection. Genome Biol 8:R194PubMedCrossRefGoogle Scholar

Copyright information

© Institute of Microbiology, Academy of Sciences of the Czech Republic, v.v.i. 2011

Authors and Affiliations

  • Gnanasekaran JebaMercy
    • 1
  • Shunmugiah Karutha Pandian
    • 1
  • Krishnaswamy Balamurugan
    • 1
  1. 1.Department of BiotechnologyAlagappa UniversityKaraikudiIndia

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