CXCL10, MCP-1, and Other Immunologic Markers Involved in Neural Leprosy
2015
Nerve damage in leprosy can be directly induced by
Mycobacterium leprae in the early stages of infection, however,
immunomediated mechanisms add gravity to the impairment of
neural function in symptomatic periods of the disease. This study
investigated the immunohistochemical expression of immunomarkers
involved in the pathogenic mechanisms of leprosy nerve damage.
These markers selected were CXCL10, CCL2 chemokines and
immunomarkers as CD3, CD4, CD8, CD45RA, CD45RO, CD68,
HLA-DR, and metalloproteinases 2 and 9 (MMP2 and MMP9)
occurring in nerve biopsy specimens collected from leprosy (23) and
nonleprosy patients (5) suffering peripheral neuropathy. CXCL10,
CCL2, MMP2, and MMP9 immunoreactivities were found in the
leprosy nerves but not in nonleprosy samples. Immunolabeling was
predominantly found in recruited macrophages and Schwann cells
composing the inflammatory cellular population in the leprosy-affected
nerves. The immunohistochemical expression of all the markers,
but CXCL10, was associated with fibrosis, however, only CCL2
was, independently from the others, associated with this excessive
deposit of extracellular matrix. No difference in the frequency of the
immunolabeling was detected between the AFB+ and AFB leprosy
subgroups of nerve, exception made to some statistical trend to
difference in regard to CD68 and HLA-DR+ cells in the AFB
nerves exhibiting epithelioid granuloma. MMP9 expression associated
with fibrosis is consistent with previous results of research group. The
findings conveys the idea that CCL2 and CXCL10 chemokines at
least in advanced stages of leprosy nerve lesions are not determinant
for the establishment of AFB+ or AFB leprosy lesions, however,
CCL2 is associated with macrophage recruitment and fibrosis.
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