Identification and topography of neuronal cell populations expressing; TNFα and IL‐1α in response to hippocampal lesion

Abstract

In previous studies, we have shown that a traumatic lesion to the hippocampus of adult mice induces the transitory expression of TNF alpha and IL-1 alpha by neurons of different brain areas and also by glial cells at the site of injury. The aim of the present study was to establish whether the expression of TNF alpha and IL-1 alpha is restricted to defined subpopulations, or else is common to most of the central neuronal populations. Using polyclonal anti-GAD 67, anti-TH and monoclonal anti-ChAT, and anti-5-HT antibodies in a double-labeling immunohistochemical procedure in combination with murine anti-TNF alpha and anti-IL-1 alpha polyclonal antibodies, we show that most GABAergic, catecholaminergic, and serotoninergic neurons, and a subgroup of the cholinergic neurons, express these cytokines. Although not immunohistochemically characterized, neurons in some glutamatergic structures such as the hippocampus and the prefrontal cortex also express these cytokines. Thus, we conclude that the capacity of central neurons to express cytokines like TNF alpha and IL-1 alpha in reaction to a brain injury is not restricted to peculiar neuronal subtypes, but could include most of the neuronal populations of the brain.

Inflammation and Alzheimer’s disease

“…Neurons also produce several chemokines and cytokines such as IL-1 (Tchelingerian et al, 1996;Friedman, 2001), IL-6 (Li et al, 2000) and TNF-α (Tchelingerian et al, 1996). In particular, neuronal chemokines act as messengers between neurons and glial cells (de Haas et al, 2007;Biber et al, 2008).…”

Cytokine Interactions with Adrenal Medullary Chromaffin Cells

“…TNF-a is secreted by a range of cell types in addition to activated macrophages, including keratinocytes, fibroblasts and neuronal cells in response to inflammation, injury, infection or other stressors (Kern et al 1995;Tchelingerian et al 1996). In situ hybridization revealed that in the human adrenal gland, TNF-a is expressed in not only resident macrophages but also in steroid-producing cells within the zona reticularis and medulla.…”

Insulin Resistance and Alzheimer’s Disease

“…In brains of AD model mice and AD patients, A plaque and NFTs activate astrocytes and microglia, resulting in the release of inflammatory molecules (cytokines and chemokines) and the production of complement, and ultimately causing neuroinflammation Hoozemans et al, 2002;McGeer and McGeer, 2003;Tansey et al, 2007). In fact, in AD, neurons themselves induce the production of inflammatory molecules, such as interleukin (IL)-1, IL-6, TNF-, and complement proteins (Li et al, 2000;Tchelingerian et al, 1996;Yu et al, 2002).Further, A can attract and activate microglia, affecting the recruitment of microglia to A plaques, and increase the secretion of proinflammatory molecules, such as IL-1, IL-6, and IL-8 (Rogers and Lue, 2001). Astrocytes are also activated by A peptide to produce proinflammatory cytokines and chemokines in AD (Smits et al, 2002).…”