Evidence for autoantibody production associated with polyclonal B-cell activation by Pseudomonas aeruginosa

Abstract

Experimental infection of mice with Pseudomonas aeruginosa resulted in the polyclonal activation of B lymphocytes, as assessed by the spontaneous plaque-forming cell (PFC) response to trinitrophenyl and sheep erythrocytes. Additionally, a PFC response to bromelain-treated syngeneic erythrocytes (Br-MRBC) could be detected in infected mice, suggesting that P. aeruginosa infection might also induce activation of self-reactive B-cell clones and consequently lead to autoantibody production. Furthermore, in cultures of mouse peritoneal cells, heat-killed P. aeruginosa enhanced the development of anti-Br-MRBC PFC, even under conditions where cell division was blocked, suggesting that the in vitro P. aeruginosa-induced enhancement of anti-Br-MRBC PFC was essentially related to cell differentiation, cell division playing only a minor role. The mechanism of the in vivo and in vitro P. aeruginosa-induced activation of anti-Br-MRBC PFC are discussed.

T suppressor cells as well as anti-hapten and anti-idiotype B lymphocytes regulate contact sensitivity to oxazolone in mice injected with purified protein derivative from Mycobacterium tuberculosis

“…Many microorganisms or bacterial constituents are polyclonal B-cell activators (PBAs) (6,10,21,26), in that they induce B lymphocytes to proliferate and mature into immunoglobulin-secreting cells. Under appropriate conditions, PBAs cause several alterations in immune reactivity, which include the replacement of the need for T cells in antibody formation to antigens which normally require cellular cooperation (13), the inhibition or enhancement of antibody production when given before or after the antigen, respectively (8,20,23), and the depression of cell-mediated immunity (12,15,19).…”