Differences in mouse strain influence leukocyte and immunoglobulin phenotype response to Porphyromonas gingivalis

Abstract

This study examined the nature of the infiltrating cells in Porphyromonas gingivalis-induced lesions and immunoglobulins in the serum samples of BALB/c (H-2d), C57BL6 (H-2b), DBA/2J (H-2d) and CBA/CaH (H-2k) mice. Mice were immunized intraperitoneally with P. gingivalis outer membrane antigens or sham-immunized with phosphate-buffered saline followed by subcutaneous challenge with live organisms 1 week after the final immunization. The resulting skin abscesses were excised 7 days later, cryostat sections cut and an immunoperoxidase method used to detect the presence of CD4+ and CD8+ T-cell subsets, CD14+ macrophages and CD19+ B cells. Peroxidase positive neutrophils and IgG1- and IgG2a-producing plasma cells were also identified. Anti P. gingivalis IgG1 and IgG2a subclass antibodies were determined in serum obtained by cardiac puncture. Very few CD8+ T cells and CD19+ B cells were found in any of the lesions. The percentages of CD4+ cells, CD14+ cells and neutrophils were similar in lesions of immunized BALB/c and C57BL6 mice, with a trend towards a higher percentage of CD14+ cells in sham-immunized mice. The percentage of CD14+ cells was higher than that of CD4+ cells in immunized compared with sham-immunized DBA/2J mice. The percentages of CD4+ and CD14+ cells predominated in immunized CBA/CaH mice and CD4+ cells in sham-immunized CBA/CaH mice. The percentage of neutrophils in immunized CBA/CaH mice was significantly lower than that of CD14+ cells and CD4+ cells in sham-immunized mice. IgG1+ plasma cells were more dominant than IgG2a+ cells in immunized BALB/c, C57BL6 and DBA/2J mice, whereas IgG2a+ plasma cells were more obvious in sham-immunized mice. IgG2a+ plasma cells were predominant in immunized and sham-immunized CBA/CaH mice. In the serum, specific anti-P. gingivalis IgG2a antibody levels (Th1 response) were higher than IgG1 levels (Th2 response) in sham-immunized CBA/CaH and DBA/2J mice. In immunized BALB/c mice, IgG2a levels were lower than IgG1 levels, while IgG2a levels were higher in immunized C57BL6 mice. In conclusion, this study has shown differences in the proportion of infiltrating leukocytes and in the subclasses of immunoglobulin produced locally and systemically in response to P. gingivalis in different strains of mice, suggesting a degree of genetic control over the response to P. gingivalis.

Clinical evaluation of highly pathogenic tick‐borne flavivirus infection in the mouse model

“…The fact that this spike occurs only in balb/c mice and that balb/c mice have a shorter average survival time than do C57BL/6 mice suggests that underlying characteristics of host immunity may play a role in disease progression. This is in agreement with several reports of a preferential bias for C57BL/6 mouse strains to develop Th1-type response with the Balb/c strain biased towards a Th2-type cytokine polarization to some infectious agents [Heinzel et al, 1989;Locksley et al, 1991;von Stebut et al, 2000;Gemmell et al, 2003;Pinto et al, 2003;Ritchie et al, 2003;Misslitz et al, 2004].…”

Leukocyte infiltration in experimental stroke

“…Immunological differences as well as similarities between these animals have been shown [60,61]. Examination of the literature reveals immunological differences between specific rat [62-65] as well as mouse strains [66,67]. This issue could have an impact on the analysis and should be taken into account when considering the results of this review.…”

Animal Models to Study Host-Bacteria Interactions Involved in Periodontitis

“…BALB/c, AKR/J, DBA/2J and C3H/HeN mice are more susceptible than C57/Bl6, A/J, 129/J, SJL/J and C3H/HeJ [36, 47]. These differences are related to genetic variances among the strains affecting components of the immune response, such as the point mutation on Toll-like receptor 4 (TLR4) in C3H/HeJ mice or differences in adaptive immunity [48]. Normal genetic variation (as well as genetically engineered alterations) in mice provides a potentially rich avenue to establish a cause-and-effect relationship between periodontal disease and aspects of the host response.…”