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Isolation, Processing and Analysis of Murine Gingival Cells
Published on: July 2, 2013
Porphyromonas gingivalis virulence in a murine lesion model: effects of immune alterations
L Kesavalu1, S C Holt, J L Ebersole
1Department of Periodontics, School of Dentistry, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78284, USA.
Abstract:
This study utilized various mouse strains with documented alterations in immune system components to assess their contribution to modify the virulence of Porphyromonas gingivalis. P. gingivalis W50 was cultivated on blood agar plates, harvested and used to challenge mice by subcutaneous injection on the dorsolateral surface of the back. Soft tissue lesion development was estimated by measuring the area of the spreading lesion formed by this microorganism over a period of 15 days. Challenge of various normal inbred and outbred mouse strains including: BALB/cN, BALB/cJ, BALB/c nu/+, ICR, B10.A(4R), B10.MBR, A/J, C57BL/6J, CBA/CaH, C.B-17/Icv Tacf DF and C3H/HeN with 2 x 10(10) bacteria showed similar lesion size among these strains (approximately 400 mm2). Genetically deficient mouse strains [C.B-17/Icr Tac (SCID); DBA/2 (C5 deficient); BALB/c nu/nu (T cell deficient); CBA/CaHN-XID/J (B cell deficient) and C3H/HeJ (LPS hyporesponsive)] demonstrated a lesion size which was similar to normal animals. C57BL/6J-BgJ (NK cell deficient) mice exhibited a significantly more severe lesion than the other strains tested. Following healing of the lesions, we initiated a secondary infection of the surviving animals to estimate the acquisition of protective immunity following recovery from the primary infection. Normal mice demonstrated a delayed onset and decrease in lesion size of 15 to 30% compared with the primary infection. In contrast, each of the immunodeficient strains appeared unable to develop immune protection to the secondary challenge. The findings suggest that protection against primary infections with P. gingivalis are mediated by innate immune mechanisms (PMN. NK cells). Additionally, it appears that T-cell-dependent humoral responses are critical to developing immunity to subsequent P. gingivalis infection.
Insights
Natural killer (NK) cells are crucial for controlling Porphyromonas gingivalis infections. While innate immunity protects against initial infection, T-cell dependent responses are vital for developing immunity to subsequent challenges.
Area of Science:
- Microbiology
- Immunology
- Oral Health Research
Background:
- Porphyromonas gingivalis is a key pathogen in periodontal disease.
- Understanding host immune responses is critical for developing effective treatments.
Purpose of the Study:
- To investigate the role of different immune system components in modulating Porphyromonas gingivalis virulence.
- To identify immune mechanisms responsible for protection against primary and secondary P. gingivalis infections.
Main Methods:
- Utilized various normal and genetically immunodeficient mouse strains.
- Inoculated mice subcutaneously with P. gingivalis W50.
- Measured soft tissue lesion development over 15 days.
- Assessed secondary infection response to evaluate acquired immunity.
Main Results:
- NK cell deficient mice showed significantly more severe lesions compared to other strains.
- Normal mice developed partial protection after primary infection.
- Immunodeficient mice failed to develop protective immunity to secondary challenge.
- Innate immune mechanisms, including NK cells, mediate primary infection control.
Conclusions:
- NK cells play a significant role in controlling P. gingivalis virulence.
- Innate immunity is essential for initial defense against P. gingivalis.
- T-cell dependent humoral responses are critical for developing long-term immunity to P. gingivalis.
