Abstract
Collagen-induced arthritis is a B cell-mediated autoimmune disease. Recently published studies have demonstrated that in some rare cases pathogens can confer protection from autoimmunity. Trypanosoma brucei parasites are tsetse fly transmitted extracellular protozoans causing sleeping sickness disease in humans and Nagana in livestock in sub-Saharan endemic areas. In the past, we demonstrated that trypanosome infections impair B cell homeostasis and abolish vaccine-induced protection against unrelated antigens. Hence, here we hypothesized that trypanosome infection can affect the onset of CIA by specifically dampening specific B-cell responses and type II collagen antibody titers in DBA/1 prone mice. We observed a substantial delay in the onset of collagen-induced arthritis in T. brucei-infected DBA/1 mice that correlates with a drastic decrease of type II collagen titers of the different IgG isotypes in the serum. Treatment of infected mice with Berenil, a trypanocidal drug, restored the development of CIA-associated clinical symptoms. Interestingly, these data were confirmed by the challenge of immunized DBA/1 prone mice with T. brucei-infected tsetse flies. Together, these results demonstrate that T. brucei infection is impairing the maintenance of the antigen specific plasma B cell pool driving the development of CIA in DBA/1 prone mice.
Highlights
Epidemiologists have observed a low occurrence of infectious diseases, coinciding with an increase prevalence of autoimmune diseases in the developed world, whereas theyPLOS ONE | DOI:10.1371/journal.pone.0130431 June 25, 2015Trypanosomosis Delays the Outcome of Collagen-Induced Arthritis found the opposite, namely high incidence of infections associated to low rate of autoimmunity, in the developing countries
As our group already reported that T. brucei infection alters B cell homeostasis, we investigated if trypanosomosis was able to modulate the course of B cell-mediated Collagen-induced arthritis (CIA) in DBA/1 prone mice [14, 17]
The results demonstrated a significant delay in CIA development in the infected group, which is characterized by a significant lower mean of arthritic lesion score at day 42 (Fig 1A)
Summary
Epidemiologists have observed a low occurrence of infectious diseases, coinciding with an increase prevalence of autoimmune diseases in the developed world, whereas theyPLOS ONE | DOI:10.1371/journal.pone.0130431 June 25, 2015Trypanosomosis Delays the Outcome of Collagen-Induced Arthritis found the opposite, namely high incidence of infections associated to low rate of autoimmunity, in the developing countries. The reason is due to the fact that the developed world has managed to eradicate most infectious diseases, but has concomitantly witnessed a rise in autoimmune diseases, while the developing countries have still to battle with a number of infectious diseases with a very small percentage of autoimmune diseases [1]. These observations have led to the hygiene hypothesis, which states that the absence of early childhood exposure to infectious pathogens may give rise to an increased susceptibility to the natural development of autoimmune diseases and allergy [2]. The presence of autoreactive B cells to Type II Collagen (CII), rheumatoid factor and anti-cyclic citrullinated peptide in the sera of RA patients is associated with a higher risk of mortality and morbidity as well as more severe articular cartilage disease [6]
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