PORPHYROMONAS-GINGIVALIS VIRULENCE IN A MURINE LESION MODEL - EFFECTSOF IMMUNE ALTERATIONS

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 cultivat ed on blood agar plates, harvested and used to challenge mice by subcu taneous injection on the dorsolateral surface of the back. Soft tissue lesion development was estimated by measuring the area of the spreadi ng lesion formed by this microorganism over a period of 15 days. Chall enge of various normal inbred and outbred mouse strains including: BAL B/cN, BALB/cJ, BALB/c nu/+, ICR, B10.A(4R), B10.MBR, A/J, C57BL/6J, CB A/CaH, C.B-17/lcv Tacf DF and C3H/HeN with 2 x 10(10) bacteria showed similar lesion size among these strains (similar to 400 mm(2)). Geneti cally deficient mouse strains [C.B-17/lcr Tac (SCID); DBA/2 (C5 defici ent); BALB/c nu/nu (T cell deficient); CBA/CaHN-XID/J (B cell deficien t) and C3H/HeJ (LPS hyporesponsive)] demonstrated a lesion size which was similar to normal animals. C57BL/6J-BgJ (NK cell deficient) mice e xhibited a significantly more severe lesion than the other strains tes ted. Following healing of the lesions, we initiated a secondary infect ion of the surviving animals to estimate the acquisition of protective immunity following recovery from the primary infection. Normal mice d emonstrated a delayed onset and decrease in lesion size of 15 to 30% c ompared with the primary infection. In contrast, each of the immunodef icient strains appeared unable to develop immune protection to the sec ondary challenge. The findings suggest that protection against primary infections with P. gingivalis are mediated by innate immune mechanism s (PMN. NK cells). Additionally, it appears that T-cell-dependent humo ral responses are critical to developing immunity to subsequent P. gin givalis infection. (C) 1997 Academic Press Limited.