Monocytes and Interleukin-1 & Lyme disease
By Linda on Feb 9, 2011 in Infections | comments(0)
Link: http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1001144
Excerpt:
If insufficiently treated, Lyme borreliosis can evolve into an
inflammatory disorder affecting skin, joints, and the CNS. Early
innate immunity may determine host responses targeting infection.
Thus, we sought to characterize the immediate cytokine storm
associated with exposure of PBMC to moderate levels of live
Borrelia burgdorferi. Since
Th17 cytokines are connected to host defense against
extracellular bacteria, we focused on interleukin (IL)-17 and
IL-22. Here, we report that, despite induction of inflammatory
cytokines including IL-23, IL-17 remained barely detectable in
response to B. burgdorferi. In contrast, T cell-dependent
expression of IL-22 became evident within 10 h of exposure to the
spirochetes. This dichotomy was unrelated to interferon-? but to
a large part dependent on caspase-1 and IL-1 bioactivity derived
from monocytes. In fact, IL-1? as a single stimulus induced IL-22
but not IL-17. Neutrophils display antibacterial activity against
B. burgdorferi, particularly when opsonized by antibodies. Since
neutrophilic inflammation, indicative of IL-17 bioactivity, is
scarcely observed in Erythema migrans, a manifestation of skin
inflammation after infection, protective and antibacterial
properties of IL-22 may close this gap and serve essential
functions in the initial phase of spirochete infection.
