concanavalin-a and Deafness

A study was made of the behavior of peripheral blood lymphocytes in healthy controls and patients with various types of hearing loss. Hearing loss of auto-immune origin was studied in the presence and absence of melatonin, activated or not by concanavalin A. In patients with auto-immune hearing loss, lymphocytes showed hyporeactivity to type II collagen in terms of proliferative activity in the presence of concavalin A. Hyporeactivity was especially relevant in melatonin-incubated cells. In different nosologic entities, lymphocyte hyporeactivity to type II collagen was similar in bilateral sensorineural hearing loss, Ménière's disease and otosclerosis. We conclude that the lymphocytes of patients with autoimmune hearing loss showed hyporeactivity to type II collagen when compared to lymphocytes from control subjects. This hyporeactivity was revealed when lymphocytes were activated in the presence of melatonin.

Topics: Adolescent; Adult; Aged; Autoimmune Diseases; Cell Movement; Collagen; Concanavalin A; Deafness; Female; Humans; Lymphocytes; Male; Melatonin; Meniere Disease; Middle Aged; Pineal Gland

Degeneration of hair cells (HC) and/or spiral ganglion neurons (SGN) is a major cause of hearing loss. Postnatal rat cochlear explant cultures are used to study the toxic actions of different classes of ototoxins and to identify molecules that can protect SGN and HC from ototoxic damage. Various ototoxins induce differential damage to HC and/or SGN. While gentamicin preferentially causes HC death, sodium salicylate selectively induces degeneration of SGN. In contrast, cisplatin results in destruction of both SGN and HC. Specific neurotrophins, including NT-4/5, BDNF, and NT-3, greatly protect SGN from all three types of ototoxins. In contrast, NGF and other growth factors have no effect. Of the 51 compounds examined, only concanavalin A (Con A), a lectin molecule, significantly protects HC from gentamicin. A dose-dependent study of Con A shows that maximal protection occurred at 100 nM. Further experiments indicates that preincubation of Con A with gentamicin does not form a complex, and coaddition of Con A and gentamicin to bacterial cultures, such as E. Coli cultures, does not interfere with the antibiotic activity of gentamicin. When the other 21 lectins are examined, Erythrina cristagalli lectin and Detura stramonium lectin also show activity similar to Con A. These findings may help elucidate the mechanisms of ototoxins and suggest that specific neurotrophins and lectins may be of therapeutic value in the prevention of ototoxin-induced hearing loss.

Topics: Animals; Anti-Bacterial Agents; Cell Survival; Cells, Cultured; Concanavalin A; Deafness; Gentamicins; Hair Cells, Auditory; Lectins; Nerve Growth Factors; Nerve Regeneration; Rats; Spiral Ganglion

We have studied the behavior of peripheral blood lymphocytes in healthy controls and in patients with various hearing losses. These hearing losses were of an autoimmune origin in which type II collagen and melatonin were either present or absent, activated or not with concanavalin A (Con A). In patients with autoimmune hearing losses, the results showed lymphocytes that displayed hyporeactivity to type II collagen in terms of their proliferative activity in the presence of Con A. The hyporeactivity is specially relevant in those cells which are melatonin incubated. When different nosologic entities were studied, we observed similar lymphocyte hyporeactivity to type II collagen in bilateral sensorineural hearing loss, Ménière's disease and otosclerosis. We conclude that in the lymphocytes of patients with autoimmune hearing losses, there is hyporeactivity to type II collagen when compared to the hyporeactivity of lymphocytes in control groups. This hyporeactivity is revealed when the lymphocytes are activated in the presence of melatonin.

Topics: Adolescent; Adult; Aged; Autoimmune Diseases; Case-Control Studies; Cell Division; Child; Collagen; Concanavalin A; Deafness; Female; Humans; Lymphocytes; Male; Melatonin; Meniere Disease; Middle Aged; Otosclerosis