All Posts Tagged With: "monocytes"

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.

Full article: http://www.biomedcentral.com/content/pdf/1471-2334-10-205.pdf

Excerpt:

Results

An informative pattern was obtained by combining two of the analysed parameters: (i), the fractions of HLA-DR-expressing CD4+ T cells and CD8+ T cells, respectively, and (ii), the level of CD40 on CD14+ CD16- monocytes. Patients infected with gram-negative bacteria or EBV showed a marked increase in monocyte CD40, while this effect was less pronounced for tuberculosis, borrelia and influenza. The bacterial agents could be distinguished from the viral agents by the T cell result; CD4+ T cells reacting in bacterial infection, and the CD8+ T cells dominating for the viruses. Patients with systemic autoimmunity also showed a increased activation, but with similar engagement of CD4+ and CD8+ T cells. Analysis of soluble TNF alpha receptors was less informative due to a large inter-individual variation.

Conclusion

Immunophenotyping including the combination of the fractions of HLA-DR expressing T cell subpopulations with the level of CD40 on monocytes produces an informative pattern, differentiating between bacterial origin, viral origin and systemic autoimmunity. Furthermore, it provides some indication of a subacute bacterial infection, such as borreliosis or tuberculosis. This flow cytometric method is suitable for clinical diagnostic laboratories, and may help in the assessment of patients with uncharacteristic inflammatory symptoms.

Full article: http://ukpmc.ac.uk/articles/PMC1490240;jsessionid=7D7D2D45FB70B5A24793992EDD921DFB.jvm4

Excerpt:

Abstract

A case of 65-year-old male is reported who presented with myalgias, headache, and fever. He subsequently developed myocarditis and was diagnosed to have anaplasmosis on peripheral blood smear. He was treated with doxycycline for 30 days. A coronary angiogram done after recovery showed normal epicardial arteries. The case illustrates the importance of a careful examination of the peripheral smear, with a high index of clinical suspicion, which led to prompt treatment and complete recovery of the patient

Ehrlichiosis, first discovered before 1910, has been recognized to cause human infection since 1986.1 It belongs to Rickettsiaceae family. Ehrlichiae are small, obligate intracellular bacteria that grow in cytoplasmic vacuoles to form clusters called morulae. Three distinct species cause human ehrlichiosis. E. chaffeensis predominantly affects the monocytes and is hence termed human monocytic ehrlichiosis (HME) while E. phagocytophilium, and E. ewingii cause human granulocytic ehrlichiosis.2E. phagocytophiliumE. equi are now recognized as the same organism and has been renamed Anaplasma phagocytophilum; the disease is now known as Human Granulocytic Anaplasmosis (HGA). Both HME and HGA share similar clinical and laboratory features and are treated with the same antimicrobials.