Mediators of inflammation
-
Mediators of inflammation · Jan 2008
Case ReportsExpression of endothelial nitric oxide synthase and endothelin-1 in skin tissue from amputated limbs of patients with complex regional pain syndrome.
Impaired microcirculation during the chronic stage of complex regional pain syndrome (CRPS) is related to increased vasoconstriction, tissue hypoxia, and metabolic tissue acidosis in the affected limb. Endothelial dysfunction is suggested to be the main cause of diminished blood flow. The aim of this study was to examine the distribution of endothelial nitric oxide synthase (eNOS) and endothelin-1(ET-1) relative to vascular density represented by the endothelial marker CD31-immunoreactivity in the skin tissue of patients with chronic CRPS. ⋯ We found indications that endothelial dysfunction plays a role in chronic CRPS.
-
Mediators of inflammation · Jan 2008
Inhibitory effect on cerebral inflammatory response following traumatic brain injury in rats: a potential neuroprotective mechanism of N-acetylcysteine.
Although N-acetylcysteine (NAC) has been shown to be neuroprotective for traumatic brain injury (TBI), the mechanisms for this beneficial effect are still poorly understood. Cerebral inflammation plays an important role in the pathogenesis of secondary brain injury after TBI. However, it has not been investigated whether NAC modulates TBI-induced cerebral inflammatory response. ⋯ Measures of IL-6 showed no change after NAC treatment. NAC administration reduced brain edema, BBB permeability, and apoptotic index in the injured brain. The results suggest that post-TBI NAC administration may attenuate inflammatory response in the injured rat brain, and this may be one mechanism by which NAC ameliorates secondary brain damage following TBI.
-
Mediators of inflammation · Jan 2008
ReviewExercise as a mean to control low-grade systemic inflammation.
Chronic noncommunicable diseases (CNCDs), which include cardiovascular disease, some cancers, for example, colon cancer, breast cancer, and type 2 diabetes, are reaching epidemic proportions worldwide. It has now become clear that low-grade chronic inflammation is a key player in the pathogenesis of most CNCDs. ⋯ Recently, IL-6 was introduced as the first myokine, defined as a cytokine, which is produced and released by contracting skeletal muscle fibres, exerting its effects in other organs of the body. We suggest that skeletal muscle is an endocrine organ and that myokines may be involved in mediating the beneficial effects against CNCDs associated with low-grade inflammation.
-
Mediators of inflammation · Jan 2008
Serum amyloid A, procalcitonin, tumor necrosis factor-alpha, and interleukin-1beta levels in neonatal late-onset sepsis.
Sepsis is an important cause of mortality in newborns. However, a single reliable marker is not available for the diagnosis of neonatal late-onset sepsis (NLS). The aim of this study is to evaluate the value of serum amyloid A (SAA) and procalcitonin (PCT) in the diagnosis and follow-up of NLS. ⋯ Present study suggests that CRP seems to be the most helpful indicator and PCT and TNF-alpha may be useful markers for the early diagnosis of NLS. However, SAA, IL-1beta, and TSS are not reliable markers for the diagnosis and follow-up of NLS.
-
The pathogenesis of pruritus in psoriasis remains unclear. Many possible mediators were implicated to transmit or modulate this sensation in psoriasis, but none has been clearly proven to be a causative agent of itching. The most often discussed theory mentioned the importance of impaired innervations and neuropeptides imbalance in psoriatic skin. ⋯ Whether these mechanisms are also involved in pruritus accompanying psoriasis requires further investigation. Limited knowledge of pruritus origin in psoriasis is responsible for the lack of the effective antipruritic treatments for psoriatics. Here, we summarize the current knowledge about the pathogenesis of pruritus in psoriasis and point out possible directions of future studies aiming the pathogenesis of this symptom in psoriasis.