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Effects of intravaginal infusion of the osteopontin peptide possessing integrin-binding motifs on an inflammation-like response in the endometrium of dairy cows.

Created on 19 Oct 2026

Authors

Takashi Tanida, Tomochika Sugiura, Kenichiro Sakaguchi, Yojiro Yanagawa, Seiji Katagiri

Published in

The Journal of reproduction and development. Oct 16, 2026. Epub Oct 16, 2026.

Abstract

Intravaginal infusion of a peptide possessing the integrin-binding motifs of osteopontin (OPN peptide), a seminal protein, restored fertility in dairy cows by restoring the endometrial epidermal growth factor profile. Hypothetically, this treatment induces an inflammation-like response in the endometrium, which may modulate endometrial function. The present study aimed to determine whether intravaginal treatment with OPN peptide induces an inflammation-like response in the endometrium. Holstein lactating cows were infused with OPN peptide (peptide, n = 7) or vehicle only (control, n = 7) into the vagina 16-24 h after the second gonadotropin-releasing hormone treatment using the Ovsynch protocol. Endometrial, vaginal, and peripheral blood mononuclear cells (PBMC) were collected immediately before and 4 h after treatment. Endometrial gene expression of IL1A,IL1B,IL8, and TNF and the percentage of polymorphonuclear cells (PMN%) in smears were evaluated. Gene expression in the vagina and in PBMCs and PMNs, and PMN% in vaginal smears, were also examined in some cows. The results revealed that the OPN peptide increased endometrial IL1B and IL8 expression and PMN%. In vaginal samples, the OPN peptide increased PMN%, despite no differences in cytokine expression between the groups. IL1A and IL1B expression in PBMCs decreased after treatment in both groups; however, their degrees of decrease in the peptide group were smaller than that in the control group. These data demonstrate that intravaginal infusion of OPN peptide induces an inflammation-like response in the endometrium as well as vaginal and potentially systemic immune responses in cows.

PMID:
42893853
Bibliographic data and abstract were imported from PubMed on 19 Oct 2026.

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