[10] Animal chamber models for study of host-parasite interactions

Genco, Caroline A.; Arko, R J

doi:10.1016/0076-6879(94)35136-8

Cited by 37 publications

(32 citation statements)

References 48 publications

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“…This model of infection allows both the growth of bacteria and the immune response to be monitored over a period of weeks. As the bacteria cannot escape from the chamber, but host cells and fluids can enter, this model is a compromise between the open-ended chamber models, from which bacteria may translocate, and the enclosed chambers, which do not allow interaction of the bacteria with host cells (Genco & Arko, 1994). The model is useful, not only because it yields data about fundamental aspects of the immune response to bacterial infection, but it also provides a model for prolonged infection.…”

Section: Discussionmentioning

confidence: 99%

Immune reactions to Bacteroides fragilis populations with three different types of capsule in a model of infection

1995

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The survival and growth of populations of the obligately anaerobic pathogenic bacterium Bacteroides fragi/is enriched for large capsules (LCs), small capsules (SCs) or an electron-dense layer (EDL; non-capsulate by light microscopy) were examined in a mouse model of infection over a minimum period of 20 d. Chambers which allowed the influx of leukocytes, but not the efflux of bacteria, were implanted in the mouse peritoneal cavity. The LC and EDL populations consistently attained viable cell densities of the order of 108-109 c.f.u. ml-l within 24 h, whereas the SC population did not. However, after 3 d, all three bacterial populations maintained total viable numbers of 108-1 O9 c.f.u. ml-l within the chambers. LC expression was selected against within 24 h in the model, the populations becoming non-capsulate by light microscopy, whereas in the SC population expression of the SC was retained by approximately 90% of the population. The EDL population remained noncapsulate by light microscopy throughout. Lymphocytes infiltrated the chambers to an equal extent for all three B. tiegilis populations and at approximately 1000 times higher concentration than chambers which contained only quarter-strength Ringer's solution. The presence of neutrophils within the chambers did not cause a decrease in the total viable bacterial count. Each population elicited antibodies specific for outer-membrane proteins and polysaccharide, as detected by immunoblotting, which crossreacted with the other populations. Differences were observed in the immunogenicity of the outer-membrane proteins within the three populations. Neutrophils were initially the predominant cell type in the chambers, but as the total leukocyte count increased with incubation time, neutrophils were outnumbered by other leukocytes. Flow cytometric investigations indicated that by day 7 the majority of these leukocytes were B-cells. Bearing in mind the constraints of this model system, it appears that all three populations of B. fragiris have the potential for in wivo growth and that each elicits an immune reaction.

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Section: Discussionmentioning

confidence: 99%

Immune reactions to Bacteroides fragilis populations with three different types of capsule in a model of infection

1995

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“…After the healing period, the chambers were used as a biological compartment for inducing in¯ammation. 13 Experimental design (Fig. 1) Fifty-four mice were divided into three groups of 18 mice each: a repeat-challenge group (REP), a single-challenge group (SIN) and a control group (CON).…”

Section: The Experimental Modelmentioning

confidence: 99%

“…To test this hypothesis, we used a P. gingivalis induced in¯ammatory response in the subcutaneous chamber model in mice. 13,14 This model provides a localized in¯amma-tory exudate that is easily accessible for sampling and quanti®cation of its contents. We followed the development of the in¯ammatory response by measuring leucocyte recruitment and the local accumulation of TNF-a, IFN-c, and IL-10, after a single challenge compared to two repeated challenges with P. gingivalis.…”

Section: Introductionmentioning

confidence: 99%

Repeat bacterial challenge in a subcutaneous chamber model results in augmented tumour necrosis factor‐α and interferon‐γ response, and suppression of interleukin‐10

et al. 2000

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SUMMARYThe present study compared the effect of a single or a repeat challenge with the Gram-negative pathogen Porphyromonas gingivalis on the local in¯ammatory response within subcutaneous chamber model in mice. Subcutaneous chambers were implanted 2 weeks prior to the ®nal challenge. The repeat-challenge (REP) group received two intrachamber bacterial injections 14 days apart, while the single-injection group (SIN) received only a single bacterial challenge. Injection of saline was used as the control. The cellular contents of the chamber exudates were used for differential cell counts, and the supernatants were analysed for tumour necrosis factor-a (TNF-a), interferon-c (IFN-c), and interleukin (IL)-10 levels. Immunoglobulin G1 (IgG1) and IgG2a levels to P. gingivalis in the exudates were also determined. The results showed that the leucocyte counts increased signi®cantly post-challenge, and the REP group showed the highest number of lymphocytes and neutrophils. Both P. gingivalis-challenged groups exhibited signi®cant increase in TNF-a and IL-10 levels at day 1 post-challenge. TNF-a levels in the chamber exudate were threefold higher in the REP group compared with the SIN group on day 1 post-challenge (P<0 . 05). In contrast, IL-10 levels were signi®cantly lower in the REP group 1 day post-challenge compared with the SIN group. The REP group had signi®cantly higher levels of IFN-c at baseline, and this difference remained signi®cant 1 day post-challenge. Analysis of antibody levels to P. gingivalis showed that while the control and the SIN groups had no anti-P. gingivalis IgG in the chamber exudate during the 7-day study period, the REP group showed high anti-P. gingivalis IgG levels. In addition, the titres of IgG2a were ®vefold higher than the IgG1 titres. The results showed that a repeat local challenge with P. gingivalis augmented the proin¯ammatory cytokines TNF-a and IFN-c, while inhibiting the accumulation of the anti-in¯ammatory cytokine IL-10. This shift towards a T helper 1 (Th1)-dominant response was re¯ected in the relatively high anti-P. gingivalis IgG2a titres in the local in¯ammatory environment 7 days post-challenge.

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“…17) Male C57BL/6J mice (7 weeks old) were used in these studies. Coil-shaped chambers were prepared from 0.5-mm stainless-steel wire and surgically implanted into the dorsolumbar region subcutaneously.…”

Section: Methodsmentioning

confidence: 99%

The Periodontal Pathogen Aggregatibacter Actinomycetemcomitans Deteriorates Ventricular Remodeling After Myocardial Infarction in Mice

et al. 2012

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SummaryChronic inflammation plays a fundamental role in coronary heart disease (CHD). Periodontal disease is a common infectious disease and is a potential source of systemic inflammation. However, the effect of periodontal infection on CHD has not yet been proven. The purpose of this study was to determine the effect of periodontopathic bacteria on experimental myocardial infarction (MI). We implanted a chamber into the subcutaneous tissue of each male mouse. Aggregatibacter actinomycetemcomitans (A.a. n = 8), which is a major periodontal pathogen, or PBS (n = 6) was injected into the chamber. Then, MI was induced by permanent ligation of the left anterior descending coronary artery. To exclude the nonspecific effect of the pathogen, we injected A.a. into the mice without MI (n = 4). The plasma level of anti-A.a. antibody was statistically higher in A.a.-infected mice than in vehicle control mice. Seven days after the myocardial ischemia, the A.a.-positive MI hearts showed a larger infarct size and length than the A.a.-negative MI mice. The A.a.-positive MI hearts showed more MOMA-2 positive myocardial infiltrating cells compared to the A.a.-negative MI mice. The injection of A.a. into the mice without MI did not affect their hearts. We concluded that a periodontal pathogen infection might deteriorate ventricular remodeling after MI through inflammatory cell infiltration. (Int Heart J 2012; 53: 253-256)

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[10] Animal chamber models for study of host-parasite interactions

Cited by 37 publications

References 48 publications

Immune reactions to Bacteroides fragilis populations with three different types of capsule in a model of infection

Immune reactions to Bacteroides fragilis populations with three different types of capsule in a model of infection

Repeat bacterial challenge in a subcutaneous chamber model results in augmented tumour necrosis factor‐α and interferon‐γ response, and suppression of interleukin‐10

The Periodontal Pathogen Aggregatibacter Actinomycetemcomitans Deteriorates Ventricular Remodeling After Myocardial Infarction in Mice

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