Inflammatory Immune Response

Prior exposure to a stressor can potentiate CNS pro-inflammatory immune responses to a peripheral immune challenge. However, the neuroimmune substrate(s) mediating this effect has not been determined. The present investigation examined whether microglia serve as this neuroimmune substrate given that microglia are the primary immune effector cell in the CNS. The effect of inescapable shock (IS) on glial activation (MHC

The mild inflammatory response against stented bioprosthetic heart valves in the sheep model is often opposed by a more distinct response in failing human implants. With the emergence of stentless root prostheses with their significantly larger proportion of tissue interacting with the immune system of the host, a more relevant animal model than the sheep may be needed. Valved, porcine aortic roots of 5 cm length were fixed in 0.2% glutaraldehyde and implanted in the upper descending aorta of Merino sheep (n = 5; 43+/-3 kg) and Chacma baboons (n = 5; 17+/-3 kg). After 6 weeks of tissue calcification, pannus outgrowth and inflammation were assessed by atomic absorption spectrophotometry, histologic damage scoring (0 to 3), image analysis, and transmission electron microscopy. The main difference between the two animal models was in aortic wall calcification (64.8+/-39.8 microg/mg in the sheep model versus 4.1+/-5.9 microg/mg in the primate model; p > 0.005). In both models, leaflet calcification was negligible (2.6+/-2.4 microg/mg in the sheep versus 2.5+/-1.9 microg/mg in the primate), and the overall extent of inflammation was comparable (1.2+/-0.8 versus 0.98+/-0.7; p = 0.18 in the sheep and the primate, respectively). Qualitatively, the sheep demonstrated a macrophage-dominated reaction whereas the inflammatory demarcation often resembled a granulocyte-dominated xenograft response in the primate. Pannus outgrowth was comparable in length (8.4+/-2.3 mm versus 9.1+/-4.3 mm proximally and 7.1+/-3.4 mm versus 7.4+/-5.1 mm distally, in the sheep and baboon, respectively; p > 0.05). Our results confirm the sheep as a significantly stronger calcification model for stentless aortic heart valves than the primate. Remaining antigenicity of porcine tissue as a result of incomplete cross-linking, however, elicits a distinctly stronger xenograft-type reaction in the primate model.

Although innate immunity is crucial to pulmonary host defense and can initiate immune and inflammatory responses independent of adaptive immunity, it remains unstudied in the context of transplant rejection. To investigate the role of innate immunity in the development of allograft ...

This chapter looks at these interconnected
biological changes in people presenting with
depression, both MDD and BD, and the implications
that this may have for the etiology, course,
and treatment of mood disorders. Firstly, we
review Oxidative and nitrosative stress (O&NS) before looking at their role in MDD and BD.

Migraine treatment has evolved from the realms of the supernatural into the scientific arena, but it seems still controversial whether migraine is primarily a vascular or a neurological dysfunction. Irrespective of this controversy, the levels of serotonin (5-hydroxytryptamine; 5-HT), a vasoconstrictor and a central neurotransmitter, seem to decrease during migraine (with associated carotid vasodilatation) whereas an i.v. infusion of 5-HT can abort migraine. In fact, 5-HT as well as ergotamine, dihydroergotamine and other antimigraine agents invariably produce vasoconstriction in the external carotid circulation. The last decade has witnessed the advent of sumatriptan and second generation triptans (e.g. zolmitriptan, rizatriptan, naratriptan), which belong to a new class of drugs, now known as 5-HT1B/1D/1F receptor agonists. Compared to sumatriptan, the second-generation triptans have a higher oral bioavailability and longer plasma half-life. In line with the vascular and neurogeni...

Objective:  This paper intends to evaluate inflammatory proteins and
hematological factors  concurrently blood obtained during the
cupping and with the venous blood.
Methods:  About 30 samples of 10 men participated in this clinical
evaluative study aged between 23 and 58 years. The hematological
factors were evaluated by by KX-. Cytokines (IL-10) &  hs-CRP were
measured by a sensitive sandwich ELISA kit.
Results:  Analysis of the results showed  a significant difference  in
many of the inflammatory proteins, hematological factors between
the venous blood and the cupping blood.
Conclusion: Based on the results of the comparison between venous
blood and cupping blood, the cupping blood is different, both in
components and immunologic response.

Background: There is evidence that immune-inflammatory and oxidative and nitrosative stress
(O&NS) pathways play a role in the pathophysiology of Myalgic Encephalomyelitis (ME) / chronic
fatigue syndrome (CFS). There is also evidence that these neuro-immune diseases are accompanied
by hypothalamic-pituitary-adrenal (HPA) axis hypoactivity as indicated by lowered baseline
glucocorticoid levels.
Aims: This paper aims to review the bidirectional communications between immune-inflammatory
and O&NS pathways and HPA axis hypoactivity in ME/CFS, considering two possibilities: a)
activation of immune-inflammatory pathways is secondary to HPA-axis hypofunction via
attenuated negative feedback mechanisms; or b) chronic activated immune-inflammatory and
O&NS pathways play a causative role in HPA-axis hypoactivity.
Methods: Electronic databases, i.e. PUBMED, Scopus and Google Scholar were used as sources for
this narrative review using keywords: CFS, ME, cortisol, ACTH, CRH, HPA-axis, glucocorticoid
receptor, cytokines, immune, immunity, inflammation, O&NS.
Results: Findings show that activation of immune-inflammatory and O&NS pathways in ME/CFS
are probably not secondary to HPA-axis hypoactivity and that activation of these pathways may
underpin HPA-axis hypofunction in ME/CFS. Mechanistic explanations comprise: increased levels
of tumor necrosis factor-; T regulatory responses with elevated levels of interleukin-10 and
transforming growth factor-; elevated levels of nitric oxide; and viral/bacterial mediated
mechanisms.
Conclusions: HPA-axis hypoactivity in ME/CFS is most likely a consequence and not a cause of a
wide variety of activated immune-inflammatory and O&NS pathways in that illness.

Inflammation clearly occurs in pathologically vulnerable regions of the Alzheimer's disease (AD) brain, and it does so with the full complexity of local peripheral inflammatory responses. In the periphery, degenerating tissue and the deposition of highly insoluble abnormal materials are classical stimulants of inflammation. Likewise, in the AD brain damaged neurons and neurites and highly insoluble amyloid beta peptide deposits and neurofibrillary tangles provide obvious stimuli for inflammation. Because these stimuli are discrete, microlocalized, and present from early preclinical to terminal stages of AD, local upregulation of complement, cytokines, acute phase reactants, and other inflammatory mediators is also discrete, microlocalized, and chronic. Cumulated over many years, direct and bystander damage from AD inflammatory mechanisms is likely to significantly exacerbate the very pathogenic processes that gave rise to it. Thus, animal models and clinical studies, although still in their infancy, strongly suggest that AD inflammation significantly contributes to AD pathogenesis. By better understanding AD inflammatory and immunoregulatory processes, it should be possible to develop anti-inflammatory approaches that may not cure AD but will likely help slow the progression or delay the onset of this devastating disorder.