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Table 1 Respective neuroinflammatory and neuropathological effects observed under each experimental condition in preterm-like versus term-like brains.

From: Developmental regulation of the neuroinflammatory responses to LPS and/or hypoxia-ischemia between preterm and term neonates: An experimental study

Insult P1 preterm-like forebrain P12 term-like forebrain
  Pattern of neuroinflammatory response Neuropathological correlate Pattern of neuroinflammatory response Neuropathological correlate
LPS IL-1β (weak) increase with parallel IL-1ra decrease in gray matter; lack of modulation of other pro- (TNF-α) or anti-inflammatory cytokines. MCP-1 induction (gray & white matter) likely via IL-1β/IL-1ra unbalance. No visible change by hematoxylin staining. Transient (4 h) and diffuse IL-1β (high) increase with dyscoordinated TNF-α decrease (48 h) predominant in white matter. No modulation of anti-inflammatory cytokines. Transient (4 h) MCP-1 increase, mainly in gray matter, likely via IL-1β. No visible change seen by hematoxylin staining.
HI IL-1β (weak) increase (gray & white matters) with parallel IL-1ra decrease (gray matter). No modulation of other pro- (TNF-α) or anti-inflammatory cytokines. No modulation of MCP-1 and CINC-1; no PMN or CD68+ cell infiltration. Slight degree of laminar or columnar neuronal necrosis in neocortex and basal ganglia; foci of white matter damage. Possible direct and indirect neurotoxicity of IL-1β. Sustained (4-48 h) IL-1β (high) and TNF-α (weak) responses in gray & white matter with late (24-48 h) increase of anti-inflammatory cytokines in both gray & white matter. MCP-1 (4-24 h; high) and CINC-1 (48 h; moderate) inductions (possibly via IL-1β), only in gray matter & subsequent PMN and CD68+ cell infiltration (moderate). Infarcted areas in neocortex and underlying white matter. Possible neurotoxic effects of PMN and/or IL-1β.
LPS +HI IL-1β (moderate) and TNF-α (weak) increase (predominant in white matter) with parallel decrease of TGF-β1, IL-1ra (gray matter) and IL-6 (diffuse). No IL-10 response. Brief CINC-1 and MCP-1 inductions (high) in gray matter, likely via IL-1β, without any PMN or CD68+ cell infiltration. Compared to HI, more severe and abundant laminar or columnar areas of neuronal necrosis in neocortex and basal ganglia. Foci of white matter damage. Possible direct and indirect neurotoxicity of IL-1β. Sustained (4-48 h) IL-1β (very high) and TNF-α (moderate) responses with late (24-48 h) increase of all anti-inflammatory cytokines in both gray & white matter. MCP-1 and CINC-1 increase (very high and sustained (4-48 h)), possibly IL-1-induced, within gray matter & subsequent PMN and CD68+ cell infiltrations (high). Compared to HI, more extended infarcted areas in neocortex and adjacent white matter areas. Possible neurotoxic effects of PMN and/or IL-1β.