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Infect Immun, August 1998, p. 3485-3491, Vol. 66, No. 8
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Roles of Innate and Adaptive Immunity in Respiratory Mycoplasmosis

Samuel C. Cartner,1 * J. Russell Lindsey,1 Julie Gibbs-Erwin,1 Gail H. Cassell,2 and Jerry W. Simecka3

Departments of Comparative Medicine1 and Microbiology,2 Schools of Medicine and Dentistry, University of Alabama at Birmingham, Birmingham, Alabama 35294, and Department of Molecular Biology and Immunology, University of North Texas Health Science Center, Fort Worth, Texas 761073

Received 12 January 1998/Returned for modification 4 May 1998/Accepted 13 May 1998

Current evidence suggests that host defense in respiratory mycoplasmosis is dependent on both innate and humoral immunity. To further delineate the roles of innate and adaptive immunity in antimycoplasmal defenses, we intranasally infected C3H/HeSnJ-scid/scid (C3H-SCID), C3H/HeSnJ (C3H), C57BL/6J-scid/scid (C57-SCID), and C57BL/6N (C57BL) mice with Mycoplasma pulmonis and at 14 and 21 days postinfection performed quantitative cultures of lungs and spleens, quantification of lung lesions, and histopathologic assessments of all other major organs. We found that numbers of mycoplasmas in lungs were associated with genetic background (C3H susceptible, C57BL resistant) rather than functional state of adaptive immunity, indicating that innate immunity is the main contributor to antimycoplasmal defense of the lungs. Extrapulmonary dissemination of mycoplasmas with colonization of spleens and histologic lesions in multiple organs was a common occurrence in all mice. The absence of adaptive immune responses in severe combined immunodeficient (SCID) mice resulted in increased mycoplasmal colonization of spleens and lesions in extrapulmonary sites, particularly spleens, hearts, and joints, and also reduced lung lesion severity. The transfer of anti-M. pulmonis serum to infected C3H-SCID mice prevented extrapulmonary infection and disease, while the severity of lung lesions was restored by transfer of naive spleen cells to infected C3H-SCID mice. Collectively, our results strongly support the conclusions that innate immunity provides antimycoplasmal defense of the lungs and humoral immunity has the major role in defense against systemic dissemination of mycoplasmal infection, but cellular immune responses may be important in exacerbation of mycoplasmal lung disease.

* Corresponding author. Mailing address: Department of Comparative Medicine, Schools of Medicine and Dentistry, University of Alabama at Birmingham, Birmingham, AL 35294-0019. Phone: (205) 934-8213. Fax: (205) 975-4418. E-mail: scartner{at}uab.edu.

Infect Immun, August 1998, p. 3485-3491, Vol. 66, No. 8
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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