Strain differences in susceptibility to murine respiratory mycoplasmosis in C57BL/6 and C3H/HeN mice

Abstract

Not only is murine respiratory mycoplasmosis, due to Mycoplasma pulmonis, a complication of biomedical research, it provides excellent animal models to study the development of a naturally occurring respiratory disease induced by an infectious agent. The understanding of pathogenic mechanisms of disease can be greatly facilitated by studying genetic differences in susceptibility. Five strains of mice with various H-2K haplotypes were examined for their susceptibility to murine respiratory mycoplasmosis; of these, C57BL/6 and C3H/HeN mice were chosen for additional study. There were no significant differences in the incidence of infection in either the upper or lower respiratory tract or in the severity of upper respiratory tract lesions in the two strains as determined at 14 days postinfection. In striking contrast, the C57BL/6 mice were significantly more resistant to the development of gross and microscopic lung lesions and to death due to pneumonia as shown by an almost 100-fold difference in the 50% lethal dose, 50% gross pneumonia dose, and 50% microscopic lesion dose. The most apparent differences in lung lesions between the two strains were in the severity of acute lesions of the bronchial epithelium, the amount of mixed inflammatory response in the alveoli, and the amount of lymphoid infiltrates. All were significantly more severe in C3H/HeN mice. In addition, more C3H/HeN mice developed antibody responses to M. pulmonis. The amount of antibody correlated with lesion severity in both strains.

Mycoplasma pneumoniae Induces Host-Dependent Pulmonary Inflammation and Airway Obstruction in Mice

“…In a similar model using the mouse pathogenic mycoplasma species M. pulmonis, it was demonstrated that certain mouse strains differ markedly in resistance to infection and progression of disease with C3H/HeN mice being more susceptible than C57BL/6 mice (41). The resistance of C57BL/6 mice to M. pulmonis is thought to be related to nonspecific, innate intrapulmonary host immunity which limits the extent of infection (41,42).…”

“…In a similar model using the mouse pathogenic mycoplasma species M. pulmonis, it was demonstrated that certain mouse strains differ markedly in resistance to infection and progression of disease with C3H/HeN mice being more susceptible than C57BL/6 mice (41). The resistance of C57BL/6 mice to M. pulmonis is thought to be related to nonspecific, innate intrapulmonary host immunity which limits the extent of infection (41,42). Cartner and coworkers have also investigated the response of various murine strains to infection with M. pulmonis by evaluating 17 inbred mouse strains, and found that resistance to murine mycoplasmosis is a complex trait controlled by multiple genes (43).…”

Clearance of different strains of Mycoplasma pulmonis from the respiratory tract of C3H/HeN mice

“…Murine respiratory mycoplasmosis is a naturally occurring disease of rats and mice; rats and mice with murine respiratory mycoplasmosis are excellent animal models for the study of infectious respiratory disease (3,4,21). It has been shown previously that C3H/HeN mice are highly susceptible to Mycoplasma pulmonis infection and disease (8). An aerosol model has been described previously (9), and pulmonary clearance of virulent M. pulmonis by C3H/HeN mice has been reported previously (25).…”

Chronic respiratory mycoplasmosis in C3H/HeN and C57BL/6N mice: lesion severity and antibody response

“…Mouse strains differ in susceptibility to M. pulmonis, and studies of these differences give insights into the mechanisms of host defense and pathogenesis of respiratory mycoplasmosis. During the first 2 weeks of infection (acute disease), C3H/ HeN mice are much more susceptible to the infection than C57BL/6N mice, as evidenced by the fact that C3H/HeN mice have a 100-fold-lower 50% gross pneumonia dose, 50% microscopic lesion dose, and 50% lethal dose (10,24). However, it is not known whether the differences in susceptibility persist during the chronic disease (2 weeks to 2 months) or how antibody responses of the two mouse strains relate to progression of the chronic disease.…”