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Demonstrates induction of Kawasaki-like coronary arteritis by bacterial cell walls in mice, suggesting an essential role for macrophages.
We describe the induction of an asymmetric, focal, inflammatory coronary arteritis by a single intraperitoneal injection of group B Lactobacillus casei cell wall fragments in various inbred mouse strains. This coronary arteritis resembles the arteritis which is responsible for the 1-2% fatality rate among children with mucocutaneous lymph node syndrome. Coronary arteritis developed in 18 of 26 C57BL/6, 14 of 26 A/J, 7 of 15 Balb/c, and 8 of 15 C3Heb/FeJ mice injected. It also developed in 2 of 4 "nude" A/J background mice and 3 of 4 "nude" C57BL/6 mice, but in 0 of 15 C3H/HeJ mice. Lesions were evident as early as 3 days following injection. The development of arteritis was accompanied by disruption of the arterial intima and media with true aneurysm formation. Measurement of serial IgG and IgM titers indicated no relationship between the development of coronary arteritis and immunoglobulin response to L casei cell walls or the development of antibodies cross-reactive with normal myocardium. The absence of disease in only the C3H/HeJ mice, which are known to have defective macrophages, suggests that macrophages may play an essential role in the pathogenesis of coronary arteritis.
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Lehman et al. (1985) studied this question.
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