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Biographical Sketch  Lindsey received his master’s of science degree from Auburn University and his degree in veterinary medicine from the University of Georgia in Athens. Since retiring from UAB in 2001, Lindsey continues to teach and consult for universities and research institutions worldwide, including UAB’s department of anesthesiology.

Research/Clinical Interest Title Mechanisms of antimycoplasmal defenses; rodent diseases Description My research group is interested in the mechanisms of antimycoplasmal defenses in the lungs. Mycoplasmal infections account for up to 30% of all pneumonias and exacerbate other respiratory diseases such as asthma in humans. Mycoplasma pulmonis infections in resistant C57BL/6 (B6) and susceptible C3H/He (C3H) mice mimic the human disease and are used in our laboratory to study the mechanisms of antimycoplasmal lung defense. We have found that (i) innate immunity is the major contributor to antimycoplasmal defense, (ii) alveolar macrophages (AMs) are the main effector cells in resistance of B6 mice, (iii) AMs in C3H mice have impaired killing activity, and (iv) killing by B6 AMs is mediated by surfactant protein A (SPA) through production of peroxynitrite. Current studies are designed to elucidate the molecular mechanisms of killing by B6 AMs and the defect in killing by C3H AMs. Some studies use B6 congenic mice lacking SPA and inducible nitric oxide synthase (iNOS). We also have shown that resistance in mice is a complex genetic trait not explained by H-2 or Bcg genotypes. To determine the genetic basis of resistance, we will use mice of the parental strains (B6, C3H) and their F1 and F2 progeny in chromosomal linkage analysis of intrapulmonary M. pulmonis killing. Resistance alleles will be mapped to specific chromosomal regions by use of polymorphic DNA microsatellites. Candidate gene(s) will be characterized through sequence and expression analysis. Our ultimate goal is to identify and elucidate the molecular mechanisms of pulmonary host defense in mycoplasmosis and subsequently, other bacterial pneumonias.

Selected Publications  Publication PUBMEDID Hickman-Davis, JM, Lindsey, JR, Zhu, S and Matalon, S: Surfactant protein A mediates mycoplasmacidal activity of alveolar macrophages. Amer. J. Physiol.: Lung Cell Mol. Physiol. 274 (Lung Cell Mol Physiol 18):L270-L277, 1998.    Hickman-Davis, JM, Michalek, SM, Gibbs-Erwin, J and Lindsey, JR: Depletion of alveolar macrophages exacerbates respiratory mycoplasmosis in mycoplasma-resistant C57BL mice but not mycoplasma-susceptible C3H mice. Infect. Immun. 65: 2278-2282, 1997.    Cartner, SC, Simecka, JW, Briles, DE, Cassell, GH and Lindsey, JR: Resistance to mycoplasmal lung disease in mice is a complex genetic trait. Infect. Immun. 64:5326-5331, 1996.    Bowden, JJ, Baluk, P, Lefevre, PM, Schoeb, TR, Lindsey, JR and McDonald, DM: Sensory denervation by neonatal capsaicin treatment exacerbates Mycoplasma pulmonis infection in rat airways. Amer. J. Physiol. 270:L393-L403, 1996.    Cartner, SC, Simecka, JW, Lindsey, JR, Cassell, GH and Davis, JK: Chronic respiratory mycoplasmosis in C3H/HeN and C57BL/6N mice: lesion severity and antibody response. Infect .Immun. 63:4138-4142, 1995.

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