Inflammatory cytokine profile and T cell responses in African tick bite fever patients

Abstract

African tick bite fever, an acute febrile illness, is caused by the obligate intracellular bacterium Rickettsia africae. Immune responses to rickettsial infections have so far mainly been investigated in vitro with infected endothelial cells as the main target cells, and in mouse models. Patient studies are rare and little is known about the immunology of human infections. In this study, inflammatory mediators and T cell responses were examined in samples from 13 patients with polymerase chain reaction-confirmed R. africae infections at different time points of illness. The Th1-associated cytokines IFNγ and IL-12 were increased in the acute phase of illness, as were levels of the T cell chemoattractant cytokine CXCL-10. In addition, the anti-inflammatory cytokine IL-10 and also IL-22 were elevated. IL-22 but not IFNγ was increasingly produced by CD4+ and CD8+ T cells during illness. Besides IFNγ, IL-22 appears to play a protective role in rickettsial infections.

When a travel bug gets you down[SS1]: severe, hypotensive African tick bite fever and response to therapy

“…Rickettsia africae infection induces Th1-type immune responses including the cytokines interferon gamma and interleukin 12 during the acute febrile phase [5], which may lead to some of the common constitutional symptoms. Common features of R. africae infection include inoculation eschars, fever,…”