Nerve damage is a common feature of leprosy although the mechanism responsible for the damage is not clearly understood. In the tuberculoid end of the leprosy spectrum where both intraneural Mycobacterium leprae or their antigens and cell-mediated hypersensitivity to M. leprae co-exist, acute neuritis affecting major nerve trunks can occur during reversal reactions. These reactions are known to be associated with increased hypersensitivity to M. leprae antigens. The nerve involvement is therefore thought to be a direct consequence of the patient's hypersensitivity to M. leprae. So far the only indirect evidence based on in vitro studies have been produced to support such a contention. We sensitized rabbits with M. leprae and then injected M. leprae sonicate into the sciatic nerves at the peak of hypersensitivity. Seventy-two hours later, the nerves were dissected out and studied histologically. Our results show that cellular infiltration and axonal degeneration can occur as a direct consequence of hypersensitivity to intraneural M. leprae antigens. This study, therefore, offers direct evidence for the involvement of specific cell-mediated hypersensitivity to M. leprae antigens in the pathogenesis of major nerve trunk damage in the tuberculoid end of the leprosy spectrum especially during acute reversal reactions.
BT - Clinical and experimental immunology C1 - http://www.ncbi.nlm.nih.gov/pubmed/6345041?dopt=Abstract DA - 1983 May IS - 2 J2 - Clin. Exp. Immunol. LA - eng N2 -Nerve damage is a common feature of leprosy although the mechanism responsible for the damage is not clearly understood. In the tuberculoid end of the leprosy spectrum where both intraneural Mycobacterium leprae or their antigens and cell-mediated hypersensitivity to M. leprae co-exist, acute neuritis affecting major nerve trunks can occur during reversal reactions. These reactions are known to be associated with increased hypersensitivity to M. leprae antigens. The nerve involvement is therefore thought to be a direct consequence of the patient's hypersensitivity to M. leprae. So far the only indirect evidence based on in vitro studies have been produced to support such a contention. We sensitized rabbits with M. leprae and then injected M. leprae sonicate into the sciatic nerves at the peak of hypersensitivity. Seventy-two hours later, the nerves were dissected out and studied histologically. Our results show that cellular infiltration and axonal degeneration can occur as a direct consequence of hypersensitivity to intraneural M. leprae antigens. This study, therefore, offers direct evidence for the involvement of specific cell-mediated hypersensitivity to M. leprae antigens in the pathogenesis of major nerve trunk damage in the tuberculoid end of the leprosy spectrum especially during acute reversal reactions.
PY - 1983 SP - 441 EP - 8 T2 - Clinical and experimental immunology TI - Nerve damage following intraneural injection of Mycobacterium leprae into rabbits pre-sensitized to mycobacteria. VL - 52 SN - 0009-9104 ER -