This study centred on the host cell-mediated immune response to
experimentally-induced infection with Dermatophilus congolensis. A review
of the literature explored the characteristics of both chronic and
acute infections and, in particular, the host response. Defence
mechanisms of the skin were also considered.
Spleen mononuclear cells were isolated from experimentally-infected
Wistar rats and cultured with a
range of doses of inactivated
D. congolensis cocci. The outcome was assessed with a lymphocyte
transformation test. Mononuclear cells from infected rats responded well
and in a dose-dependent fashion to in vitro stimulation, with
proliferation rates which were significantly greater than those of
controls (P < 0.01). The supernatants of the stimulated mononuclear cells
were assayed for lymphokine activity and were found to cause significant
inhibition of macrophage migration <P < 0.05).
The immunophenotype of the responding population was determined with an
indirect fluorescent-antibody test using a range of anti-rat mononuclear
cell monoclonals. A significant increase occurred in the T-helper
population of cells from infected rats to form 56 per cent of the total
in the presence of an optimal concentration of D. congolensis cocci
<P < 0.05).
The in situ host response to D. congolensis was studied by identifying
the immunophenotypes within the cellular infiltrate which collects at an
infection site. Sections of skin were screened with a range of anti-rat
monoclonal antibodies. Initially, polymorphonuclear leucocytes
predominated but were soon superseded by a T-cell infiltrate. Both
T-helper and T-cytotoxic/suppressor cells were present and were in an
activated state, demonstrated by the expression of interleukin-2 receptor
and class II. The T-helper cells were observed in the dermis and the
epidermis, whereas the T-cytotoxic/suppressor cells were only rarely seen
in the epidermis. In common with some other skin diseases, the epidermis
expressed class II antigens.
Epidermal hyperproliferation may be an important defence mechanism
against pathogens such as D.congolensis. Several different types of
epidermal culture system were first investigated to assess their
suitability as indicators of epidermal proliferation. Low calcium
concentrations induced stable, monolayer cultures whereas cultures under
normal calcium conditions were inherently unstable, although the cells
grew well short-term. Both types of culture system were then used to
determine whether stimulated mononuclear cells might play a role in
epidermal defence by causing hyperproliferation. Thus, culture
supernatants from D. congo1 ensis-stimulated mononuclear cells were added,
at various dilutions, to the epidermal cultures and the cell
proliferation rates assessed with a 3H-thymidine incorporation assay. The
supernatants caused either significant inhibition or stimulation of
proliferation (P < 0.01), the net effect being concentration-dependent.
In contrast, culture supernatants derived from naive rats had no
stimulatory effect on the proliferation of rat epidermal cells; but at
the highest concentration caused significant proliferation inhibition
CP < 0.01).
The results were discussed in relation to the likely immune effector
mechanisms responsible for the rapid resolution of experimentally-induced
infections and the possible defects in this response which allow
progression to the generalised, chronic form of the disease.