CM from <i>L. plantarum</i>, <i>L. acidophilus</i>, and <i>B. infantis</i> suppressed NF-κB signaling and preserved IκBα expression.

<p>Intestines from healthy dam-fed controls and experimental intestinal injury pups treated with vehicle or different CM were IHC stained for the active/phosphorylated form of NF-κB p65 (p-NF-κB) and IκBα or lysed for immunoblotting for IκBα. <b><i>A.</i></b> Representative IHC staining (at 400×) shows that CM decreased IEC NF-κB activity/nuclear p-NF-κB (arrows) in experimental pups with or without intestinal injury (n = 3 per group). <b><i>B.</i></b> NF-κB activity from <b><i>A.</i></b> was quantified by percentage of nuclear p-NF-κB-positive IEC in three fields of each intestinal section (n = 3). <b><i>C.</i></b> Representative IHC staining shows La/Bi CM and all CM protection of IEC IκBα expression in experimental pups with or without intestinal injury, respectively, (n = 3 per group). <b><i>D.</i></b> IHC intensity of IκBα from <b><i>C.</i></b> was scored on a 0–4 scale to relatively quantify levels of IκBα. <b><i>E.</i></b> Immunoblotting shows CM protection of IEC IκBα expression in experimental pups. Intestines of vehicle- and CM-treated experimental pups with disease and healthy dam-fed pups were lysed and subjected to IκBα immunoblotting. IκBα protein levels were quantified by densitometry using ImageJ software and normalized to GAPDH and presented in <b><i>F.</i></b> Results are presented as mean of percentages, scores, or relative density ± SE. “*” depicts p<0.05 compared to the vehicle group by one-way ANOVA with Bonferroni correction.