Merve ŞEN, Hüseyin TAŞLI, Sefa ÇELİK
Health Sciences Quarterly - 2026;6(3):541-556
Rotavirus represents a predominant etiological agent of acute gastroenteritis among neonates and young pediatric populations. Rotavirus predominantly targets enterocytes, leading to diarrhea as a consequence of intestinal cellular impairment induced by the rotavirus nonstructural protein 4 (Nsp4) and subsequent stimulation of the enteric nervous system. Nsp4 serves as the principal protein accountable for the alterations in calcium (Ca²?) homeostasis within cells infected by rotavirus. This study investigated the effects of plantaricin A (PlnA), a Lactobacillus plantarum bacteriocin, on intracellular and extracellular Ca²? and anti-inflammatory and proinflammatory cytokine levels in the Caco-2 intestinal cell line treated with the Nsp4 protein, which causes diarrhea and damage to enterocytes through various mechanisms in rotavirus infections. Nsp4 increased intracellular and extracellular Ca²? levels over time, and PlnA suppressed this effect when applied with Nsp4. Consequently, PlnA has the capacity to diminish cytosolic Ca²?, a critical element utilized by the virus for replication during the initial phases of infection. PlnA increased the gene expression and protein levels of proinflammatory cytokines. In a comparable manner, PlnA elevated the transcriptional activity and protein concentrations of the anti-inflammatory cytokine IL-10, indicating that PlnA may exert an anti-inflammatory influence. If supported by in vivo studies, PlnA could be a therapeutic agent for treating viral enteritis.
